Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line

Background Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficac...
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Autor*in:	Kim, Seung Tae [verfasserIn] Kim, Sun Young Lee, Jeeyun Kim, Kyung Park, Se Hoon Park, Young Suk Lim, Ho Yeong Kang, Won Ki Park, Joon Oh

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	Patient derived cells (PDCs) Triptolide Chk2

Anmerkung:	© The Author(s). 2018

Übergeordnetes Werk:	Enthalten in: BMC cancer - London : BioMed Central, 2001, 18(2018), 1 vom: 12. Nov.
Übergeordnetes Werk:	volume:18 ; year:2018 ; number:1 ; day:12 ; month:11

Links:	Volltext

DOI / URN:	10.1186/s12885-018-4995-0

Katalog-ID:	SPR027705455

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520			\|a Background Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients. Results In vitro cell viability assay for triptolide in 6 PC cell lines, the $ IC_{50} $ was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients. Conclusions Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). More robust biomarkers such as KRAS mutation and Chk2 phosphorylation and careful clinical trial design using triptolide (minnelide) are warranted.
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Indexfelder

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publishDate	2018
allfields	10.1186/s12885-018-4995-0 doi (DE-627)SPR027705455 (SPR)s12885-018-4995-0-e DE-627 ger DE-627 rakwb eng Kim, Seung Tae verfasserin aut Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients. Results In vitro cell viability assay for triptolide in 6 PC cell lines, the $ IC_{50} $ was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients. Conclusions Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). More robust biomarkers such as KRAS mutation and Chk2 phosphorylation and careful clinical trial design using triptolide (minnelide) are warranted. Patient derived cells (PDCs) (dpeaa)DE-He213 Triptolide (dpeaa)DE-He213 Chk2 (dpeaa)DE-He213 Kim, Sun Young aut Lee, Jeeyun aut Kim, Kyung aut Park, Se Hoon aut Park, Young Suk aut Lim, Ho Yeong aut Kang, Won Ki aut Park, Joon Oh aut Enthalten in BMC cancer London : BioMed Central, 2001 18(2018), 1 vom: 12. Nov. (DE-627)326643710 (DE-600)2041352-X 1471-2407 nnns volume:18 year:2018 number:1 day:12 month:11 https://dx.doi.org/10.1186/s12885-018-4995-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 12 11
spelling	10.1186/s12885-018-4995-0 doi (DE-627)SPR027705455 (SPR)s12885-018-4995-0-e DE-627 ger DE-627 rakwb eng Kim, Seung Tae verfasserin aut Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients. Results In vitro cell viability assay for triptolide in 6 PC cell lines, the $ IC_{50} $ was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients. Conclusions Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). More robust biomarkers such as KRAS mutation and Chk2 phosphorylation and careful clinical trial design using triptolide (minnelide) are warranted. Patient derived cells (PDCs) (dpeaa)DE-He213 Triptolide (dpeaa)DE-He213 Chk2 (dpeaa)DE-He213 Kim, Sun Young aut Lee, Jeeyun aut Kim, Kyung aut Park, Se Hoon aut Park, Young Suk aut Lim, Ho Yeong aut Kang, Won Ki aut Park, Joon Oh aut Enthalten in BMC cancer London : BioMed Central, 2001 18(2018), 1 vom: 12. Nov. (DE-627)326643710 (DE-600)2041352-X 1471-2407 nnns volume:18 year:2018 number:1 day:12 month:11 https://dx.doi.org/10.1186/s12885-018-4995-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 12 11
allfields_unstemmed	10.1186/s12885-018-4995-0 doi (DE-627)SPR027705455 (SPR)s12885-018-4995-0-e DE-627 ger DE-627 rakwb eng Kim, Seung Tae verfasserin aut Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients. Results In vitro cell viability assay for triptolide in 6 PC cell lines, the $ IC_{50} $ was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients. Conclusions Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). More robust biomarkers such as KRAS mutation and Chk2 phosphorylation and careful clinical trial design using triptolide (minnelide) are warranted. Patient derived cells (PDCs) (dpeaa)DE-He213 Triptolide (dpeaa)DE-He213 Chk2 (dpeaa)DE-He213 Kim, Sun Young aut Lee, Jeeyun aut Kim, Kyung aut Park, Se Hoon aut Park, Young Suk aut Lim, Ho Yeong aut Kang, Won Ki aut Park, Joon Oh aut Enthalten in BMC cancer London : BioMed Central, 2001 18(2018), 1 vom: 12. Nov. (DE-627)326643710 (DE-600)2041352-X 1471-2407 nnns volume:18 year:2018 number:1 day:12 month:11 https://dx.doi.org/10.1186/s12885-018-4995-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 12 11
allfieldsGer	10.1186/s12885-018-4995-0 doi (DE-627)SPR027705455 (SPR)s12885-018-4995-0-e DE-627 ger DE-627 rakwb eng Kim, Seung Tae verfasserin aut Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients. Results In vitro cell viability assay for triptolide in 6 PC cell lines, the $ IC_{50} $ was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients. Conclusions Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). More robust biomarkers such as KRAS mutation and Chk2 phosphorylation and careful clinical trial design using triptolide (minnelide) are warranted. Patient derived cells (PDCs) (dpeaa)DE-He213 Triptolide (dpeaa)DE-He213 Chk2 (dpeaa)DE-He213 Kim, Sun Young aut Lee, Jeeyun aut Kim, Kyung aut Park, Se Hoon aut Park, Young Suk aut Lim, Ho Yeong aut Kang, Won Ki aut Park, Joon Oh aut Enthalten in BMC cancer London : BioMed Central, 2001 18(2018), 1 vom: 12. Nov. (DE-627)326643710 (DE-600)2041352-X 1471-2407 nnns volume:18 year:2018 number:1 day:12 month:11 https://dx.doi.org/10.1186/s12885-018-4995-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 12 11
allfieldsSound	10.1186/s12885-018-4995-0 doi (DE-627)SPR027705455 (SPR)s12885-018-4995-0-e DE-627 ger DE-627 rakwb eng Kim, Seung Tae verfasserin aut Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients. Results In vitro cell viability assay for triptolide in 6 PC cell lines, the $ IC_{50} $ was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients. Conclusions Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). More robust biomarkers such as KRAS mutation and Chk2 phosphorylation and careful clinical trial design using triptolide (minnelide) are warranted. Patient derived cells (PDCs) (dpeaa)DE-He213 Triptolide (dpeaa)DE-He213 Chk2 (dpeaa)DE-He213 Kim, Sun Young aut Lee, Jeeyun aut Kim, Kyung aut Park, Se Hoon aut Park, Young Suk aut Lim, Ho Yeong aut Kang, Won Ki aut Park, Joon Oh aut Enthalten in BMC cancer London : BioMed Central, 2001 18(2018), 1 vom: 12. Nov. (DE-627)326643710 (DE-600)2041352-X 1471-2407 nnns volume:18 year:2018 number:1 day:12 month:11 https://dx.doi.org/10.1186/s12885-018-4995-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 12 11
language	English
source	Enthalten in BMC cancer 18(2018), 1 vom: 12. Nov. volume:18 year:2018 number:1 day:12 month:11
sourceStr	Enthalten in BMC cancer 18(2018), 1 vom: 12. Nov. volume:18 year:2018 number:1 day:12 month:11
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Patient derived cells (PDCs) Triptolide Chk2
isfreeaccess_bool	true
container_title	BMC cancer
authorswithroles_txt_mv	Kim, Seung Tae @@aut@@ Kim, Sun Young @@aut@@ Lee, Jeeyun @@aut@@ Kim, Kyung @@aut@@ Park, Se Hoon @@aut@@ Park, Young Suk @@aut@@ Lim, Ho Yeong @@aut@@ Kang, Won Ki @@aut@@ Park, Joon Oh @@aut@@
publishDateDaySort_date	2018-11-12T00:00:00Z
hierarchy_top_id	326643710
id	SPR027705455
language_de	englisch
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However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients. Results In vitro cell viability assay for triptolide in 6 PC cell lines, the $ IC_{50} $ was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients. Conclusions Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). 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author	Kim, Seung Tae
spellingShingle	Kim, Seung Tae misc Patient derived cells (PDCs) misc Triptolide misc Chk2 Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line
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topic_title	Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line Patient derived cells (PDCs) (dpeaa)DE-He213 Triptolide (dpeaa)DE-He213 Chk2 (dpeaa)DE-He213
topic	misc Patient derived cells (PDCs) misc Triptolide misc Chk2
topic_unstemmed	misc Patient derived cells (PDCs) misc Triptolide misc Chk2
topic_browse	misc Patient derived cells (PDCs) misc Triptolide misc Chk2
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title	Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line
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title_full	Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line
author_sort	Kim, Seung Tae
journal	BMC cancer
journalStr	BMC cancer
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author_browse	Kim, Seung Tae Kim, Sun Young Lee, Jeeyun Kim, Kyung Park, Se Hoon Park, Young Suk Lim, Ho Yeong Kang, Won Ki Park, Joon Oh
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format_se	Elektronische Aufsätze
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doi_str_mv	10.1186/s12885-018-4995-0
title_sort	triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line
title_auth	Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line
abstract	Background Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients. Results In vitro cell viability assay for triptolide in 6 PC cell lines, the $ IC_{50} $ was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients. Conclusions Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). More robust biomarkers such as KRAS mutation and Chk2 phosphorylation and careful clinical trial design using triptolide (minnelide) are warranted. © The Author(s). 2018
abstractGer	Background Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients. Results In vitro cell viability assay for triptolide in 6 PC cell lines, the $ IC_{50} $ was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients. Conclusions Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). More robust biomarkers such as KRAS mutation and Chk2 phosphorylation and careful clinical trial design using triptolide (minnelide) are warranted. © The Author(s). 2018
abstract_unstemmed	Background Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer. Methods We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients. Results In vitro cell viability assay for triptolide in 6 PC cell lines, the $ IC_{50} $ was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients. Conclusions Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). More robust biomarkers such as KRAS mutation and Chk2 phosphorylation and careful clinical trial design using triptolide (minnelide) are warranted. © The Author(s). 2018
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title_short	Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line
url	https://dx.doi.org/10.1186/s12885-018-4995-0
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up_date	2024-07-03T14:37:50.150Z
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