MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met

Abstract Metastasis is the leading cause of death in patients with breast cancer and aberrantly expressed microRNAs (miRNAs) are highly associated with this process. A previous study has shown that miR-335 is downregulated in breast cancer and can suppress tumor invasion and metastasis. Emerging evi...
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Gespeichert in:

Autor*in:	Gao, Yue [verfasserIn] Zeng, Fan Wu, Jia-Yan Li, Hai-Yu Fan, Jian-Jun Mai, Li Zhang, Ji Ma, Dong-Mei Li, Yun Song, Fang-zhou

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Breast cancer miR-335 c-Met HGF Metastasis 5-AZA-CdR

Anmerkung:	© International Society of Oncology and BioMarkers (ISOBM) 2014

Übergeordnetes Werk:	Enthalten in: Tumor biology - Amsterdam : IOS Press, 1987, 36(2014), 4 vom: 10. Dez., Seite 2875-2883
Übergeordnetes Werk:	volume:36 ; year:2014 ; number:4 ; day:10 ; month:12 ; pages:2875-2883

Links:	Volltext

DOI / URN:	10.1007/s13277-014-2917-6

Katalog-ID:	SPR03115588X

Internformat


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allfields	10.1007/s13277-014-2917-6 doi (DE-627)SPR03115588X (SPR)s13277-014-2917-6-e DE-627 ger DE-627 rakwb eng Gao, Yue verfasserin aut MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract Metastasis is the leading cause of death in patients with breast cancer and aberrantly expressed microRNAs (miRNAs) are highly associated with this process. A previous study has shown that miR-335 is downregulated in breast cancer and can suppress tumor invasion and metastasis. Emerging evidences indicate that c-Met is implicated in cell scattering, migration, and invasion. However, little is known about the relationship between miR-335 expression and c-Met alteration in breast cancer. In the present study, we found that miR-335 expression was downregulated and c-Met protein expression was upregulated in two human breast cell lines. MiR-335 was found to negatively regulate c-Met protein level by directly targeting its 3′ untranslated region (UTR). Forced expression of miR-335 decreased c-Met expression at protein levels and consequently diminished hepatocyte growth factor (HGF)-induced phosphorylation of c-Met and subsequently inhibited HGF promotion of breast cancer cell migration in a c-Met-dependent manner. MiR-335 expression was increased after 5-aza-2′-deoxycytidine (5-AZA-CdR) treatment, and 5-AZA-CdR treatment resulted in the same phenotype as the effect of miR-335 overexpression. Taken together, these results demonstrate that miR-335 suppresses breast cancer cell migration by negatively regulating the HGF/c-Met pathway. Breast cancer (dpeaa)DE-He213 miR-335 (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 HGF (dpeaa)DE-He213 Metastasis (dpeaa)DE-He213 5-AZA-CdR (dpeaa)DE-He213 Zeng, Fan aut Wu, Jia-Yan aut Li, Hai-Yu aut Fan, Jian-Jun aut Mai, Li aut Zhang, Ji aut Ma, Dong-Mei aut Li, Yun aut Song, Fang-zhou aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 36(2014), 4 vom: 10. Dez., Seite 2875-2883 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:36 year:2014 number:4 day:10 month:12 pages:2875-2883 https://dx.doi.org/10.1007/s13277-014-2917-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 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_4012 GBV_ILN_4035 GBV_ILN_4037 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_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 36 2014 4 10 12 2875-2883
spelling	10.1007/s13277-014-2917-6 doi (DE-627)SPR03115588X (SPR)s13277-014-2917-6-e DE-627 ger DE-627 rakwb eng Gao, Yue verfasserin aut MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract Metastasis is the leading cause of death in patients with breast cancer and aberrantly expressed microRNAs (miRNAs) are highly associated with this process. A previous study has shown that miR-335 is downregulated in breast cancer and can suppress tumor invasion and metastasis. Emerging evidences indicate that c-Met is implicated in cell scattering, migration, and invasion. However, little is known about the relationship between miR-335 expression and c-Met alteration in breast cancer. In the present study, we found that miR-335 expression was downregulated and c-Met protein expression was upregulated in two human breast cell lines. MiR-335 was found to negatively regulate c-Met protein level by directly targeting its 3′ untranslated region (UTR). Forced expression of miR-335 decreased c-Met expression at protein levels and consequently diminished hepatocyte growth factor (HGF)-induced phosphorylation of c-Met and subsequently inhibited HGF promotion of breast cancer cell migration in a c-Met-dependent manner. MiR-335 expression was increased after 5-aza-2′-deoxycytidine (5-AZA-CdR) treatment, and 5-AZA-CdR treatment resulted in the same phenotype as the effect of miR-335 overexpression. Taken together, these results demonstrate that miR-335 suppresses breast cancer cell migration by negatively regulating the HGF/c-Met pathway. Breast cancer (dpeaa)DE-He213 miR-335 (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 HGF (dpeaa)DE-He213 Metastasis (dpeaa)DE-He213 5-AZA-CdR (dpeaa)DE-He213 Zeng, Fan aut Wu, Jia-Yan aut Li, Hai-Yu aut Fan, Jian-Jun aut Mai, Li aut Zhang, Ji aut Ma, Dong-Mei aut Li, Yun aut Song, Fang-zhou aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 36(2014), 4 vom: 10. Dez., Seite 2875-2883 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:36 year:2014 number:4 day:10 month:12 pages:2875-2883 https://dx.doi.org/10.1007/s13277-014-2917-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 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_4012 GBV_ILN_4035 GBV_ILN_4037 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_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 36 2014 4 10 12 2875-2883
allfields_unstemmed	10.1007/s13277-014-2917-6 doi (DE-627)SPR03115588X (SPR)s13277-014-2917-6-e DE-627 ger DE-627 rakwb eng Gao, Yue verfasserin aut MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract Metastasis is the leading cause of death in patients with breast cancer and aberrantly expressed microRNAs (miRNAs) are highly associated with this process. A previous study has shown that miR-335 is downregulated in breast cancer and can suppress tumor invasion and metastasis. Emerging evidences indicate that c-Met is implicated in cell scattering, migration, and invasion. However, little is known about the relationship between miR-335 expression and c-Met alteration in breast cancer. In the present study, we found that miR-335 expression was downregulated and c-Met protein expression was upregulated in two human breast cell lines. MiR-335 was found to negatively regulate c-Met protein level by directly targeting its 3′ untranslated region (UTR). Forced expression of miR-335 decreased c-Met expression at protein levels and consequently diminished hepatocyte growth factor (HGF)-induced phosphorylation of c-Met and subsequently inhibited HGF promotion of breast cancer cell migration in a c-Met-dependent manner. MiR-335 expression was increased after 5-aza-2′-deoxycytidine (5-AZA-CdR) treatment, and 5-AZA-CdR treatment resulted in the same phenotype as the effect of miR-335 overexpression. Taken together, these results demonstrate that miR-335 suppresses breast cancer cell migration by negatively regulating the HGF/c-Met pathway. Breast cancer (dpeaa)DE-He213 miR-335 (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 HGF (dpeaa)DE-He213 Metastasis (dpeaa)DE-He213 5-AZA-CdR (dpeaa)DE-He213 Zeng, Fan aut Wu, Jia-Yan aut Li, Hai-Yu aut Fan, Jian-Jun aut Mai, Li aut Zhang, Ji aut Ma, Dong-Mei aut Li, Yun aut Song, Fang-zhou aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 36(2014), 4 vom: 10. Dez., Seite 2875-2883 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:36 year:2014 number:4 day:10 month:12 pages:2875-2883 https://dx.doi.org/10.1007/s13277-014-2917-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 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_4012 GBV_ILN_4035 GBV_ILN_4037 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_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 36 2014 4 10 12 2875-2883
allfieldsGer	10.1007/s13277-014-2917-6 doi (DE-627)SPR03115588X (SPR)s13277-014-2917-6-e DE-627 ger DE-627 rakwb eng Gao, Yue verfasserin aut MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract Metastasis is the leading cause of death in patients with breast cancer and aberrantly expressed microRNAs (miRNAs) are highly associated with this process. A previous study has shown that miR-335 is downregulated in breast cancer and can suppress tumor invasion and metastasis. Emerging evidences indicate that c-Met is implicated in cell scattering, migration, and invasion. However, little is known about the relationship between miR-335 expression and c-Met alteration in breast cancer. In the present study, we found that miR-335 expression was downregulated and c-Met protein expression was upregulated in two human breast cell lines. MiR-335 was found to negatively regulate c-Met protein level by directly targeting its 3′ untranslated region (UTR). Forced expression of miR-335 decreased c-Met expression at protein levels and consequently diminished hepatocyte growth factor (HGF)-induced phosphorylation of c-Met and subsequently inhibited HGF promotion of breast cancer cell migration in a c-Met-dependent manner. MiR-335 expression was increased after 5-aza-2′-deoxycytidine (5-AZA-CdR) treatment, and 5-AZA-CdR treatment resulted in the same phenotype as the effect of miR-335 overexpression. Taken together, these results demonstrate that miR-335 suppresses breast cancer cell migration by negatively regulating the HGF/c-Met pathway. Breast cancer (dpeaa)DE-He213 miR-335 (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 HGF (dpeaa)DE-He213 Metastasis (dpeaa)DE-He213 5-AZA-CdR (dpeaa)DE-He213 Zeng, Fan aut Wu, Jia-Yan aut Li, Hai-Yu aut Fan, Jian-Jun aut Mai, Li aut Zhang, Ji aut Ma, Dong-Mei aut Li, Yun aut Song, Fang-zhou aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 36(2014), 4 vom: 10. Dez., Seite 2875-2883 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:36 year:2014 number:4 day:10 month:12 pages:2875-2883 https://dx.doi.org/10.1007/s13277-014-2917-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 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_4012 GBV_ILN_4035 GBV_ILN_4037 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_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 36 2014 4 10 12 2875-2883
allfieldsSound	10.1007/s13277-014-2917-6 doi (DE-627)SPR03115588X (SPR)s13277-014-2917-6-e DE-627 ger DE-627 rakwb eng Gao, Yue verfasserin aut MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract Metastasis is the leading cause of death in patients with breast cancer and aberrantly expressed microRNAs (miRNAs) are highly associated with this process. A previous study has shown that miR-335 is downregulated in breast cancer and can suppress tumor invasion and metastasis. Emerging evidences indicate that c-Met is implicated in cell scattering, migration, and invasion. However, little is known about the relationship between miR-335 expression and c-Met alteration in breast cancer. In the present study, we found that miR-335 expression was downregulated and c-Met protein expression was upregulated in two human breast cell lines. MiR-335 was found to negatively regulate c-Met protein level by directly targeting its 3′ untranslated region (UTR). Forced expression of miR-335 decreased c-Met expression at protein levels and consequently diminished hepatocyte growth factor (HGF)-induced phosphorylation of c-Met and subsequently inhibited HGF promotion of breast cancer cell migration in a c-Met-dependent manner. MiR-335 expression was increased after 5-aza-2′-deoxycytidine (5-AZA-CdR) treatment, and 5-AZA-CdR treatment resulted in the same phenotype as the effect of miR-335 overexpression. Taken together, these results demonstrate that miR-335 suppresses breast cancer cell migration by negatively regulating the HGF/c-Met pathway. Breast cancer (dpeaa)DE-He213 miR-335 (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 HGF (dpeaa)DE-He213 Metastasis (dpeaa)DE-He213 5-AZA-CdR (dpeaa)DE-He213 Zeng, Fan aut Wu, Jia-Yan aut Li, Hai-Yu aut Fan, Jian-Jun aut Mai, Li aut Zhang, Ji aut Ma, Dong-Mei aut Li, Yun aut Song, Fang-zhou aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 36(2014), 4 vom: 10. Dez., Seite 2875-2883 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:36 year:2014 number:4 day:10 month:12 pages:2875-2883 https://dx.doi.org/10.1007/s13277-014-2917-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 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_4012 GBV_ILN_4035 GBV_ILN_4037 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_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 36 2014 4 10 12 2875-2883
language	English
source	Enthalten in Tumor biology 36(2014), 4 vom: 10. Dez., Seite 2875-2883 volume:36 year:2014 number:4 day:10 month:12 pages:2875-2883
sourceStr	Enthalten in Tumor biology 36(2014), 4 vom: 10. Dez., Seite 2875-2883 volume:36 year:2014 number:4 day:10 month:12 pages:2875-2883
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Breast cancer miR-335 c-Met HGF Metastasis 5-AZA-CdR
isfreeaccess_bool	false
container_title	Tumor biology
authorswithroles_txt_mv	Gao, Yue @@aut@@ Zeng, Fan @@aut@@ Wu, Jia-Yan @@aut@@ Li, Hai-Yu @@aut@@ Fan, Jian-Jun @@aut@@ Mai, Li @@aut@@ Zhang, Ji @@aut@@ Ma, Dong-Mei @@aut@@ Li, Yun @@aut@@ Song, Fang-zhou @@aut@@
publishDateDaySort_date	2014-12-10T00:00:00Z
hierarchy_top_id	300897855
id	SPR03115588X
language_de	englisch
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author	Gao, Yue
spellingShingle	Gao, Yue misc Breast cancer misc miR-335 misc c-Met misc HGF misc Metastasis misc 5-AZA-CdR MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met
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topic_title	MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met Breast cancer (dpeaa)DE-He213 miR-335 (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 HGF (dpeaa)DE-He213 Metastasis (dpeaa)DE-He213 5-AZA-CdR (dpeaa)DE-He213
topic	misc Breast cancer misc miR-335 misc c-Met misc HGF misc Metastasis misc 5-AZA-CdR
topic_unstemmed	misc Breast cancer misc miR-335 misc c-Met misc HGF misc Metastasis misc 5-AZA-CdR
topic_browse	misc Breast cancer misc miR-335 misc c-Met misc HGF misc Metastasis misc 5-AZA-CdR
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title	MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met
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title_full	MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met
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author_browse	Gao, Yue Zeng, Fan Wu, Jia-Yan Li, Hai-Yu Fan, Jian-Jun Mai, Li Zhang, Ji Ma, Dong-Mei Li, Yun Song, Fang-zhou
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doi_str_mv	10.1007/s13277-014-2917-6
title_sort	mir-335 inhibits migration of breast cancer cells through targeting oncoprotein c-met
title_auth	MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met
abstract	Abstract Metastasis is the leading cause of death in patients with breast cancer and aberrantly expressed microRNAs (miRNAs) are highly associated with this process. A previous study has shown that miR-335 is downregulated in breast cancer and can suppress tumor invasion and metastasis. Emerging evidences indicate that c-Met is implicated in cell scattering, migration, and invasion. However, little is known about the relationship between miR-335 expression and c-Met alteration in breast cancer. In the present study, we found that miR-335 expression was downregulated and c-Met protein expression was upregulated in two human breast cell lines. MiR-335 was found to negatively regulate c-Met protein level by directly targeting its 3′ untranslated region (UTR). Forced expression of miR-335 decreased c-Met expression at protein levels and consequently diminished hepatocyte growth factor (HGF)-induced phosphorylation of c-Met and subsequently inhibited HGF promotion of breast cancer cell migration in a c-Met-dependent manner. MiR-335 expression was increased after 5-aza-2′-deoxycytidine (5-AZA-CdR) treatment, and 5-AZA-CdR treatment resulted in the same phenotype as the effect of miR-335 overexpression. Taken together, these results demonstrate that miR-335 suppresses breast cancer cell migration by negatively regulating the HGF/c-Met pathway. © International Society of Oncology and BioMarkers (ISOBM) 2014
abstractGer	Abstract Metastasis is the leading cause of death in patients with breast cancer and aberrantly expressed microRNAs (miRNAs) are highly associated with this process. A previous study has shown that miR-335 is downregulated in breast cancer and can suppress tumor invasion and metastasis. Emerging evidences indicate that c-Met is implicated in cell scattering, migration, and invasion. However, little is known about the relationship between miR-335 expression and c-Met alteration in breast cancer. In the present study, we found that miR-335 expression was downregulated and c-Met protein expression was upregulated in two human breast cell lines. MiR-335 was found to negatively regulate c-Met protein level by directly targeting its 3′ untranslated region (UTR). Forced expression of miR-335 decreased c-Met expression at protein levels and consequently diminished hepatocyte growth factor (HGF)-induced phosphorylation of c-Met and subsequently inhibited HGF promotion of breast cancer cell migration in a c-Met-dependent manner. MiR-335 expression was increased after 5-aza-2′-deoxycytidine (5-AZA-CdR) treatment, and 5-AZA-CdR treatment resulted in the same phenotype as the effect of miR-335 overexpression. Taken together, these results demonstrate that miR-335 suppresses breast cancer cell migration by negatively regulating the HGF/c-Met pathway. © International Society of Oncology and BioMarkers (ISOBM) 2014
abstract_unstemmed	Abstract Metastasis is the leading cause of death in patients with breast cancer and aberrantly expressed microRNAs (miRNAs) are highly associated with this process. A previous study has shown that miR-335 is downregulated in breast cancer and can suppress tumor invasion and metastasis. Emerging evidences indicate that c-Met is implicated in cell scattering, migration, and invasion. However, little is known about the relationship between miR-335 expression and c-Met alteration in breast cancer. In the present study, we found that miR-335 expression was downregulated and c-Met protein expression was upregulated in two human breast cell lines. MiR-335 was found to negatively regulate c-Met protein level by directly targeting its 3′ untranslated region (UTR). Forced expression of miR-335 decreased c-Met expression at protein levels and consequently diminished hepatocyte growth factor (HGF)-induced phosphorylation of c-Met and subsequently inhibited HGF promotion of breast cancer cell migration in a c-Met-dependent manner. MiR-335 expression was increased after 5-aza-2′-deoxycytidine (5-AZA-CdR) treatment, and 5-AZA-CdR treatment resulted in the same phenotype as the effect of miR-335 overexpression. Taken together, these results demonstrate that miR-335 suppresses breast cancer cell migration by negatively regulating the HGF/c-Met pathway. © International Society of Oncology and BioMarkers (ISOBM) 2014
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title_short	MiR-335 inhibits migration of breast cancer cells through targeting oncoprotein c-Met
url	https://dx.doi.org/10.1007/s13277-014-2917-6
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author2	Zeng, Fan Wu, Jia-Yan Li, Hai-Yu Fan, Jian-Jun Mai, Li Zhang, Ji Ma, Dong-Mei Li, Yun Song, Fang-zhou
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up_date	2024-07-03T22:18:28.199Z
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