Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease

Background Hirschsprung’s disease (HSCR) is a common birth defect caused by dysplasia of neural crest cells in the gut. Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases,...
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Autor*in:	Li, Long [verfasserIn] Li, Xiao Wang, Xiaoqing Liu, Wei Wu, Rongde

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	LINC00346 HSCR ceRNA miR-148a-3p Dnmt1

Anmerkung:	© The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022

Übergeordnetes Werk:	Enthalten in: Pediatric surgery international - Berlin : Springer, 1986, 38(2022), 9 vom: 14. Juli, Seite 1273-1281
Übergeordnetes Werk:	volume:38 ; year:2022 ; number:9 ; day:14 ; month:07 ; pages:1273-1281

Links:	Volltext

DOI / URN:	10.1007/s00383-022-05144-9

Katalog-ID:	SPR047772654

Internformat


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100	1		\|a Li, Long \|e verfasserin \|0 (orcid)0000-0002-8208-5313 \|4 aut
245	1	0	\|a Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease
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520			\|a Background Hirschsprung’s disease (HSCR) is a common birth defect caused by dysplasia of neural crest cells in the gut. Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. Together, these findings indicate that LINC00346 could affect the occurrence of HSCR by participating in the development of enteric neural crest cells.
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author_variant	l l ll x l xl x w xw w l wl r w rw
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allfields	10.1007/s00383-022-05144-9 doi (DE-627)SPR047772654 (SPR)s00383-022-05144-9-e DE-627 ger DE-627 rakwb eng Li, Long verfasserin (orcid)0000-0002-8208-5313 aut Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022 Background Hirschsprung’s disease (HSCR) is a common birth defect caused by dysplasia of neural crest cells in the gut. Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. Together, these findings indicate that LINC00346 could affect the occurrence of HSCR by participating in the development of enteric neural crest cells. LINC00346 (dpeaa)DE-He213 HSCR (dpeaa)DE-He213 ceRNA (dpeaa)DE-He213 miR-148a-3p (dpeaa)DE-He213 Dnmt1 (dpeaa)DE-He213 Li, Xiao aut Wang, Xiaoqing aut Liu, Wei aut Wu, Rongde aut Enthalten in Pediatric surgery international Berlin : Springer, 1986 38(2022), 9 vom: 14. Juli, Seite 1273-1281 (DE-627)254638937 (DE-600)1463010-2 1437-9813 nnns volume:38 year:2022 number:9 day:14 month:07 pages:1273-1281 https://dx.doi.org/10.1007/s00383-022-05144-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 38 2022 9 14 07 1273-1281
spelling	10.1007/s00383-022-05144-9 doi (DE-627)SPR047772654 (SPR)s00383-022-05144-9-e DE-627 ger DE-627 rakwb eng Li, Long verfasserin (orcid)0000-0002-8208-5313 aut Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022 Background Hirschsprung’s disease (HSCR) is a common birth defect caused by dysplasia of neural crest cells in the gut. Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. Together, these findings indicate that LINC00346 could affect the occurrence of HSCR by participating in the development of enteric neural crest cells. LINC00346 (dpeaa)DE-He213 HSCR (dpeaa)DE-He213 ceRNA (dpeaa)DE-He213 miR-148a-3p (dpeaa)DE-He213 Dnmt1 (dpeaa)DE-He213 Li, Xiao aut Wang, Xiaoqing aut Liu, Wei aut Wu, Rongde aut Enthalten in Pediatric surgery international Berlin : Springer, 1986 38(2022), 9 vom: 14. Juli, Seite 1273-1281 (DE-627)254638937 (DE-600)1463010-2 1437-9813 nnns volume:38 year:2022 number:9 day:14 month:07 pages:1273-1281 https://dx.doi.org/10.1007/s00383-022-05144-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 38 2022 9 14 07 1273-1281
allfields_unstemmed	10.1007/s00383-022-05144-9 doi (DE-627)SPR047772654 (SPR)s00383-022-05144-9-e DE-627 ger DE-627 rakwb eng Li, Long verfasserin (orcid)0000-0002-8208-5313 aut Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022 Background Hirschsprung’s disease (HSCR) is a common birth defect caused by dysplasia of neural crest cells in the gut. Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. Together, these findings indicate that LINC00346 could affect the occurrence of HSCR by participating in the development of enteric neural crest cells. LINC00346 (dpeaa)DE-He213 HSCR (dpeaa)DE-He213 ceRNA (dpeaa)DE-He213 miR-148a-3p (dpeaa)DE-He213 Dnmt1 (dpeaa)DE-He213 Li, Xiao aut Wang, Xiaoqing aut Liu, Wei aut Wu, Rongde aut Enthalten in Pediatric surgery international Berlin : Springer, 1986 38(2022), 9 vom: 14. Juli, Seite 1273-1281 (DE-627)254638937 (DE-600)1463010-2 1437-9813 nnns volume:38 year:2022 number:9 day:14 month:07 pages:1273-1281 https://dx.doi.org/10.1007/s00383-022-05144-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 38 2022 9 14 07 1273-1281
allfieldsGer	10.1007/s00383-022-05144-9 doi (DE-627)SPR047772654 (SPR)s00383-022-05144-9-e DE-627 ger DE-627 rakwb eng Li, Long verfasserin (orcid)0000-0002-8208-5313 aut Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022 Background Hirschsprung’s disease (HSCR) is a common birth defect caused by dysplasia of neural crest cells in the gut. Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. Together, these findings indicate that LINC00346 could affect the occurrence of HSCR by participating in the development of enteric neural crest cells. LINC00346 (dpeaa)DE-He213 HSCR (dpeaa)DE-He213 ceRNA (dpeaa)DE-He213 miR-148a-3p (dpeaa)DE-He213 Dnmt1 (dpeaa)DE-He213 Li, Xiao aut Wang, Xiaoqing aut Liu, Wei aut Wu, Rongde aut Enthalten in Pediatric surgery international Berlin : Springer, 1986 38(2022), 9 vom: 14. Juli, Seite 1273-1281 (DE-627)254638937 (DE-600)1463010-2 1437-9813 nnns volume:38 year:2022 number:9 day:14 month:07 pages:1273-1281 https://dx.doi.org/10.1007/s00383-022-05144-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 38 2022 9 14 07 1273-1281
allfieldsSound	10.1007/s00383-022-05144-9 doi (DE-627)SPR047772654 (SPR)s00383-022-05144-9-e DE-627 ger DE-627 rakwb eng Li, Long verfasserin (orcid)0000-0002-8208-5313 aut Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022 Background Hirschsprung’s disease (HSCR) is a common birth defect caused by dysplasia of neural crest cells in the gut. Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. Together, these findings indicate that LINC00346 could affect the occurrence of HSCR by participating in the development of enteric neural crest cells. LINC00346 (dpeaa)DE-He213 HSCR (dpeaa)DE-He213 ceRNA (dpeaa)DE-He213 miR-148a-3p (dpeaa)DE-He213 Dnmt1 (dpeaa)DE-He213 Li, Xiao aut Wang, Xiaoqing aut Liu, Wei aut Wu, Rongde aut Enthalten in Pediatric surgery international Berlin : Springer, 1986 38(2022), 9 vom: 14. Juli, Seite 1273-1281 (DE-627)254638937 (DE-600)1463010-2 1437-9813 nnns volume:38 year:2022 number:9 day:14 month:07 pages:1273-1281 https://dx.doi.org/10.1007/s00383-022-05144-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 38 2022 9 14 07 1273-1281
language	English
source	Enthalten in Pediatric surgery international 38(2022), 9 vom: 14. Juli, Seite 1273-1281 volume:38 year:2022 number:9 day:14 month:07 pages:1273-1281
sourceStr	Enthalten in Pediatric surgery international 38(2022), 9 vom: 14. Juli, Seite 1273-1281 volume:38 year:2022 number:9 day:14 month:07 pages:1273-1281
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	LINC00346 HSCR ceRNA miR-148a-3p Dnmt1
isfreeaccess_bool	false
container_title	Pediatric surgery international
authorswithroles_txt_mv	Li, Long @@aut@@ Li, Xiao @@aut@@ Wang, Xiaoqing @@aut@@ Liu, Wei @@aut@@ Wu, Rongde @@aut@@
publishDateDaySort_date	2022-07-14T00:00:00Z
hierarchy_top_id	254638937
id	SPR047772654
language_de	englisch
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Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. 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author	Li, Long
spellingShingle	Li, Long misc LINC00346 misc HSCR misc ceRNA misc miR-148a-3p misc Dnmt1 Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease
authorStr	Li, Long
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topic_title	Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease LINC00346 (dpeaa)DE-He213 HSCR (dpeaa)DE-He213 ceRNA (dpeaa)DE-He213 miR-148a-3p (dpeaa)DE-He213 Dnmt1 (dpeaa)DE-He213
topic	misc LINC00346 misc HSCR misc ceRNA misc miR-148a-3p misc Dnmt1
topic_unstemmed	misc LINC00346 misc HSCR misc ceRNA misc miR-148a-3p misc Dnmt1
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title	Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease
ctrlnum	(DE-627)SPR047772654 (SPR)s00383-022-05144-9-e
title_full	Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease
author_sort	Li, Long
journal	Pediatric surgery international
journalStr	Pediatric surgery international
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author_browse	Li, Long Li, Xiao Wang, Xiaoqing Liu, Wei Wu, Rongde
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author-letter	Li, Long
doi_str_mv	10.1007/s00383-022-05144-9
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title_sort	aberrant expression of linc00346 regulates cell migration and proliferation via competitively binding to mirna-148a-3p/dnmt1 in hirschsprung’s disease
title_auth	Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease
abstract	Background Hirschsprung’s disease (HSCR) is a common birth defect caused by dysplasia of neural crest cells in the gut. Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. Together, these findings indicate that LINC00346 could affect the occurrence of HSCR by participating in the development of enteric neural crest cells. © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022
abstractGer	Background Hirschsprung’s disease (HSCR) is a common birth defect caused by dysplasia of neural crest cells in the gut. Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. Together, these findings indicate that LINC00346 could affect the occurrence of HSCR by participating in the development of enteric neural crest cells. © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022
abstract_unstemmed	Background Hirschsprung’s disease (HSCR) is a common birth defect caused by dysplasia of neural crest cells in the gut. Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. Together, these findings indicate that LINC00346 could affect the occurrence of HSCR by participating in the development of enteric neural crest cells. © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022
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container_issue	9
title_short	Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease
url	https://dx.doi.org/10.1007/s00383-022-05144-9
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author2	Li, Xiao Wang, Xiaoqing Liu, Wei Wu, Rongde
author2Str	Li, Xiao Wang, Xiaoqing Liu, Wei Wu, Rongde
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doi_str	10.1007/s00383-022-05144-9
up_date	2024-07-03T14:53:34.951Z
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Long noncoding RNAs (lncRNAs) play an important role in cellular processes, including development and disease. Despite the known engagement of LINC00346 in several human diseases, its biological function in HSCR remains unknown. Methods The relative expression levels of LINC00346, miR-148a-3p and Dnmt1 in HSCR colon tissues were detected by quantitative real-time PCR. Western blot assays were conducted to investigate the Dnmt1 protein expression level. Knockdown of LINC00346 and overexpression of miR-148a-3p in SH-SY5Y and SK-N-BE(2) cell lines was conducted. Cell proliferation and migration were detected by cell counting Kit-8 assays, 5-ethynyl-2′-deoxyuridine assays and transwell assays. Cell apoptosis was verified by flow cytometric analysis. Furthermore, the competing endogenous RNA (ceRNA) activity of LINC00346 on miR-148a-5p was investigated via bioinformatics analysis and luciferase reporter assays. Result Downregulation of LINC00346 and Dnmt1 was detected in HSCR tissues. Knockdown of LINC00346 and overexpression of miR-148a-3p in SK-N-BE(2) and SH-SY5Y cells inhibited cell migration and proliferation and promoted apoptosis. Moreover, the miR-148a-3p inhibitor rescued the downregulation of Dnmt1 in LINC00346 knockdown cell lines, which was evidence of the ceRNA regulatory mechanism of Dnmt1 by LINC00346. Conclusions LINC00346 was downregulated in HSCR colon tissues and acted as a ceRNA to regulate the expression of Dnmt1 in vitro. 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Aberrant expression of LINC00346 regulates cell migration and proliferation via competitively binding to miRNA-148a-3p/Dnmt1 in Hirschsprung’s disease

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