OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma

<p<Abstract</p< <p<Background</p< <p<OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.</p<...
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Autor*in:	Cao Lu [verfasserIn] Li Chunguang [verfasserIn] Shen Shuwen [verfasserIn] Yan Yan [verfasserIn] Ji Weidan [verfasserIn] Wang Jinghan [verfasserIn] Qian Haihua [verfasserIn] Jiang Xiaoqing [verfasserIn] Li Zhigang [verfasserIn] Wu Mengchao [verfasserIn] Zhang Ying [verfasserIn] Su Changqing [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2013

Schlagwörter:	Transcription factor Cell cycle Cell apoptosis Cancer biotherapy Hepatocellular carcinoma

Übergeordnetes Werk:	In: BMC Cancer - BMC, 2003, 13(2013), 1, p 82
Übergeordnetes Werk:	volume:13 ; year:2013 ; number:1, p 82

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2407-13-82

Katalog-ID:	DOAJ038603128

Internformat


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520			\|a <p<Abstract</p< <p<Background</p< <p<OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.</p< <p<Methods</p< <p<By manipulating OCT4 and BIRC5 expression in hepatocellular carcinoma (HCC) cell lines, the regulatory mechanism of OCT4 on BIRC5 and CCND1 were investigated.</p< <p<Results</p< <p<Increasing or decreasing OCT4 expression could enhance or suppress BIRC5 expression, respectively, by regulating the activity of BIRC5 promoter. Because there is no binding site for OCT4 within BIRC5 promoter, the effect of OCT4 on BIRC5 promoter is indirect. An octamer motif for OCT4 in the CCND1 promoter has directly and partly participated in the regulation of CCND1 promoter activity, suggesting that OCT4 also could upregulated the expression of CCND1. Co-suppression of OCT4 and BIRC5 induced cancer cell apoptosis and cell cycle arrest, thereby efficiently inhibiting the proliferative activity of cancer cells and suppressing the growth of HCC xenogrfts in nude mice.</p< <p<Conclusion</p< <p<OCT4 can upregulate BIRC5 and CCND1 expression by increasing their promoter activity. These factors collusively promotes HCC cell proliferation, and co-suppression of OCT4 and BIRC5 is potentially beneficial for HCC treatment.</p<
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653		0	\|a Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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allfields	10.1186/1471-2407-13-82 doi (DE-627)DOAJ038603128 (DE-599)DOAJ0f5fa028630b4202af087df6217d6d41 DE-627 ger DE-627 rakwb eng RC254-282 Cao Lu verfasserin aut OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.</p< <p<Methods</p< <p<By manipulating OCT4 and BIRC5 expression in hepatocellular carcinoma (HCC) cell lines, the regulatory mechanism of OCT4 on BIRC5 and CCND1 were investigated.</p< <p<Results</p< <p<Increasing or decreasing OCT4 expression could enhance or suppress BIRC5 expression, respectively, by regulating the activity of BIRC5 promoter. Because there is no binding site for OCT4 within BIRC5 promoter, the effect of OCT4 on BIRC5 promoter is indirect. An octamer motif for OCT4 in the CCND1 promoter has directly and partly participated in the regulation of CCND1 promoter activity, suggesting that OCT4 also could upregulated the expression of CCND1. Co-suppression of OCT4 and BIRC5 induced cancer cell apoptosis and cell cycle arrest, thereby efficiently inhibiting the proliferative activity of cancer cells and suppressing the growth of HCC xenogrfts in nude mice.</p< <p<Conclusion</p< <p<OCT4 can upregulate BIRC5 and CCND1 expression by increasing their promoter activity. These factors collusively promotes HCC cell proliferation, and co-suppression of OCT4 and BIRC5 is potentially beneficial for HCC treatment.</p< Transcription factor Cell cycle Cell apoptosis Cancer biotherapy Hepatocellular carcinoma Neoplasms. Tumors. Oncology. Including cancer and carcinogens Li Chunguang verfasserin aut Shen Shuwen verfasserin aut Yan Yan verfasserin aut Ji Weidan verfasserin aut Wang Jinghan verfasserin aut Qian Haihua verfasserin aut Jiang Xiaoqing verfasserin aut Li Zhigang verfasserin aut Wu Mengchao verfasserin aut Zhang Ying verfasserin aut Su Changqing verfasserin aut In BMC Cancer BMC, 2003 13(2013), 1, p 82 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:13 year:2013 number:1, p 82 https://doi.org/10.1186/1471-2407-13-82 kostenfrei https://doaj.org/article/0f5fa028630b4202af087df6217d6d41 kostenfrei http://www.biomedcentral.com/1471-2407/13/82 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 13 2013 1, p 82
spelling	10.1186/1471-2407-13-82 doi (DE-627)DOAJ038603128 (DE-599)DOAJ0f5fa028630b4202af087df6217d6d41 DE-627 ger DE-627 rakwb eng RC254-282 Cao Lu verfasserin aut OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.</p< <p<Methods</p< <p<By manipulating OCT4 and BIRC5 expression in hepatocellular carcinoma (HCC) cell lines, the regulatory mechanism of OCT4 on BIRC5 and CCND1 were investigated.</p< <p<Results</p< <p<Increasing or decreasing OCT4 expression could enhance or suppress BIRC5 expression, respectively, by regulating the activity of BIRC5 promoter. Because there is no binding site for OCT4 within BIRC5 promoter, the effect of OCT4 on BIRC5 promoter is indirect. An octamer motif for OCT4 in the CCND1 promoter has directly and partly participated in the regulation of CCND1 promoter activity, suggesting that OCT4 also could upregulated the expression of CCND1. Co-suppression of OCT4 and BIRC5 induced cancer cell apoptosis and cell cycle arrest, thereby efficiently inhibiting the proliferative activity of cancer cells and suppressing the growth of HCC xenogrfts in nude mice.</p< <p<Conclusion</p< <p<OCT4 can upregulate BIRC5 and CCND1 expression by increasing their promoter activity. These factors collusively promotes HCC cell proliferation, and co-suppression of OCT4 and BIRC5 is potentially beneficial for HCC treatment.</p< Transcription factor Cell cycle Cell apoptosis Cancer biotherapy Hepatocellular carcinoma Neoplasms. Tumors. Oncology. Including cancer and carcinogens Li Chunguang verfasserin aut Shen Shuwen verfasserin aut Yan Yan verfasserin aut Ji Weidan verfasserin aut Wang Jinghan verfasserin aut Qian Haihua verfasserin aut Jiang Xiaoqing verfasserin aut Li Zhigang verfasserin aut Wu Mengchao verfasserin aut Zhang Ying verfasserin aut Su Changqing verfasserin aut In BMC Cancer BMC, 2003 13(2013), 1, p 82 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:13 year:2013 number:1, p 82 https://doi.org/10.1186/1471-2407-13-82 kostenfrei https://doaj.org/article/0f5fa028630b4202af087df6217d6d41 kostenfrei http://www.biomedcentral.com/1471-2407/13/82 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 13 2013 1, p 82
allfields_unstemmed	10.1186/1471-2407-13-82 doi (DE-627)DOAJ038603128 (DE-599)DOAJ0f5fa028630b4202af087df6217d6d41 DE-627 ger DE-627 rakwb eng RC254-282 Cao Lu verfasserin aut OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.</p< <p<Methods</p< <p<By manipulating OCT4 and BIRC5 expression in hepatocellular carcinoma (HCC) cell lines, the regulatory mechanism of OCT4 on BIRC5 and CCND1 were investigated.</p< <p<Results</p< <p<Increasing or decreasing OCT4 expression could enhance or suppress BIRC5 expression, respectively, by regulating the activity of BIRC5 promoter. Because there is no binding site for OCT4 within BIRC5 promoter, the effect of OCT4 on BIRC5 promoter is indirect. An octamer motif for OCT4 in the CCND1 promoter has directly and partly participated in the regulation of CCND1 promoter activity, suggesting that OCT4 also could upregulated the expression of CCND1. Co-suppression of OCT4 and BIRC5 induced cancer cell apoptosis and cell cycle arrest, thereby efficiently inhibiting the proliferative activity of cancer cells and suppressing the growth of HCC xenogrfts in nude mice.</p< <p<Conclusion</p< <p<OCT4 can upregulate BIRC5 and CCND1 expression by increasing their promoter activity. These factors collusively promotes HCC cell proliferation, and co-suppression of OCT4 and BIRC5 is potentially beneficial for HCC treatment.</p< Transcription factor Cell cycle Cell apoptosis Cancer biotherapy Hepatocellular carcinoma Neoplasms. Tumors. Oncology. Including cancer and carcinogens Li Chunguang verfasserin aut Shen Shuwen verfasserin aut Yan Yan verfasserin aut Ji Weidan verfasserin aut Wang Jinghan verfasserin aut Qian Haihua verfasserin aut Jiang Xiaoqing verfasserin aut Li Zhigang verfasserin aut Wu Mengchao verfasserin aut Zhang Ying verfasserin aut Su Changqing verfasserin aut In BMC Cancer BMC, 2003 13(2013), 1, p 82 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:13 year:2013 number:1, p 82 https://doi.org/10.1186/1471-2407-13-82 kostenfrei https://doaj.org/article/0f5fa028630b4202af087df6217d6d41 kostenfrei http://www.biomedcentral.com/1471-2407/13/82 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 13 2013 1, p 82
allfieldsGer	10.1186/1471-2407-13-82 doi (DE-627)DOAJ038603128 (DE-599)DOAJ0f5fa028630b4202af087df6217d6d41 DE-627 ger DE-627 rakwb eng RC254-282 Cao Lu verfasserin aut OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.</p< <p<Methods</p< <p<By manipulating OCT4 and BIRC5 expression in hepatocellular carcinoma (HCC) cell lines, the regulatory mechanism of OCT4 on BIRC5 and CCND1 were investigated.</p< <p<Results</p< <p<Increasing or decreasing OCT4 expression could enhance or suppress BIRC5 expression, respectively, by regulating the activity of BIRC5 promoter. Because there is no binding site for OCT4 within BIRC5 promoter, the effect of OCT4 on BIRC5 promoter is indirect. An octamer motif for OCT4 in the CCND1 promoter has directly and partly participated in the regulation of CCND1 promoter activity, suggesting that OCT4 also could upregulated the expression of CCND1. Co-suppression of OCT4 and BIRC5 induced cancer cell apoptosis and cell cycle arrest, thereby efficiently inhibiting the proliferative activity of cancer cells and suppressing the growth of HCC xenogrfts in nude mice.</p< <p<Conclusion</p< <p<OCT4 can upregulate BIRC5 and CCND1 expression by increasing their promoter activity. These factors collusively promotes HCC cell proliferation, and co-suppression of OCT4 and BIRC5 is potentially beneficial for HCC treatment.</p< Transcription factor Cell cycle Cell apoptosis Cancer biotherapy Hepatocellular carcinoma Neoplasms. Tumors. Oncology. Including cancer and carcinogens Li Chunguang verfasserin aut Shen Shuwen verfasserin aut Yan Yan verfasserin aut Ji Weidan verfasserin aut Wang Jinghan verfasserin aut Qian Haihua verfasserin aut Jiang Xiaoqing verfasserin aut Li Zhigang verfasserin aut Wu Mengchao verfasserin aut Zhang Ying verfasserin aut Su Changqing verfasserin aut In BMC Cancer BMC, 2003 13(2013), 1, p 82 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:13 year:2013 number:1, p 82 https://doi.org/10.1186/1471-2407-13-82 kostenfrei https://doaj.org/article/0f5fa028630b4202af087df6217d6d41 kostenfrei http://www.biomedcentral.com/1471-2407/13/82 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 13 2013 1, p 82
allfieldsSound	10.1186/1471-2407-13-82 doi (DE-627)DOAJ038603128 (DE-599)DOAJ0f5fa028630b4202af087df6217d6d41 DE-627 ger DE-627 rakwb eng RC254-282 Cao Lu verfasserin aut OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.</p< <p<Methods</p< <p<By manipulating OCT4 and BIRC5 expression in hepatocellular carcinoma (HCC) cell lines, the regulatory mechanism of OCT4 on BIRC5 and CCND1 were investigated.</p< <p<Results</p< <p<Increasing or decreasing OCT4 expression could enhance or suppress BIRC5 expression, respectively, by regulating the activity of BIRC5 promoter. Because there is no binding site for OCT4 within BIRC5 promoter, the effect of OCT4 on BIRC5 promoter is indirect. An octamer motif for OCT4 in the CCND1 promoter has directly and partly participated in the regulation of CCND1 promoter activity, suggesting that OCT4 also could upregulated the expression of CCND1. Co-suppression of OCT4 and BIRC5 induced cancer cell apoptosis and cell cycle arrest, thereby efficiently inhibiting the proliferative activity of cancer cells and suppressing the growth of HCC xenogrfts in nude mice.</p< <p<Conclusion</p< <p<OCT4 can upregulate BIRC5 and CCND1 expression by increasing their promoter activity. These factors collusively promotes HCC cell proliferation, and co-suppression of OCT4 and BIRC5 is potentially beneficial for HCC treatment.</p< Transcription factor Cell cycle Cell apoptosis Cancer biotherapy Hepatocellular carcinoma Neoplasms. Tumors. Oncology. Including cancer and carcinogens Li Chunguang verfasserin aut Shen Shuwen verfasserin aut Yan Yan verfasserin aut Ji Weidan verfasserin aut Wang Jinghan verfasserin aut Qian Haihua verfasserin aut Jiang Xiaoqing verfasserin aut Li Zhigang verfasserin aut Wu Mengchao verfasserin aut Zhang Ying verfasserin aut Su Changqing verfasserin aut In BMC Cancer BMC, 2003 13(2013), 1, p 82 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:13 year:2013 number:1, p 82 https://doi.org/10.1186/1471-2407-13-82 kostenfrei https://doaj.org/article/0f5fa028630b4202af087df6217d6d41 kostenfrei http://www.biomedcentral.com/1471-2407/13/82 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 13 2013 1, p 82
language	English
source	In BMC Cancer 13(2013), 1, p 82 volume:13 year:2013 number:1, p 82
sourceStr	In BMC Cancer 13(2013), 1, p 82 volume:13 year:2013 number:1, p 82
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Transcription factor Cell cycle Cell apoptosis Cancer biotherapy Hepatocellular carcinoma Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	BMC Cancer
authorswithroles_txt_mv	Cao Lu @@aut@@ Li Chunguang @@aut@@ Shen Shuwen @@aut@@ Yan Yan @@aut@@ Ji Weidan @@aut@@ Wang Jinghan @@aut@@ Qian Haihua @@aut@@ Jiang Xiaoqing @@aut@@ Li Zhigang @@aut@@ Wu Mengchao @@aut@@ Zhang Ying @@aut@@ Su Changqing @@aut@@
publishDateDaySort_date	2013-01-01T00:00:00Z
hierarchy_top_id	326643710
id	DOAJ038603128
language_de	englisch
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callnumber-first	R - Medicine
author	Cao Lu
spellingShingle	Cao Lu misc RC254-282 misc Transcription factor misc Cell cycle misc Cell apoptosis misc Cancer biotherapy misc Hepatocellular carcinoma misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma
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topic_title	RC254-282 OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma Transcription factor Cell cycle Cell apoptosis Cancer biotherapy Hepatocellular carcinoma
topic	misc RC254-282 misc Transcription factor misc Cell cycle misc Cell apoptosis misc Cancer biotherapy misc Hepatocellular carcinoma misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc Transcription factor misc Cell cycle misc Cell apoptosis misc Cancer biotherapy misc Hepatocellular carcinoma misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_browse	misc RC254-282 misc Transcription factor misc Cell cycle misc Cell apoptosis misc Cancer biotherapy misc Hepatocellular carcinoma misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma
ctrlnum	(DE-627)DOAJ038603128 (DE-599)DOAJ0f5fa028630b4202af087df6217d6d41
title_full	OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma
author_sort	Cao Lu
journal	BMC Cancer
journalStr	BMC Cancer
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author_browse	Cao Lu Li Chunguang Shen Shuwen Yan Yan Ji Weidan Wang Jinghan Qian Haihua Jiang Xiaoqing Li Zhigang Wu Mengchao Zhang Ying Su Changqing
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author-letter	Cao Lu
doi_str_mv	10.1186/1471-2407-13-82
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title_sort	oct4 increases birc5 and ccnd1 expression and promotes cancer progression in hepatocellular carcinoma
callnumber	RC254-282
title_auth	OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma
abstract	<p<Abstract</p< <p<Background</p< <p<OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.</p< <p<Methods</p< <p<By manipulating OCT4 and BIRC5 expression in hepatocellular carcinoma (HCC) cell lines, the regulatory mechanism of OCT4 on BIRC5 and CCND1 were investigated.</p< <p<Results</p< <p<Increasing or decreasing OCT4 expression could enhance or suppress BIRC5 expression, respectively, by regulating the activity of BIRC5 promoter. Because there is no binding site for OCT4 within BIRC5 promoter, the effect of OCT4 on BIRC5 promoter is indirect. An octamer motif for OCT4 in the CCND1 promoter has directly and partly participated in the regulation of CCND1 promoter activity, suggesting that OCT4 also could upregulated the expression of CCND1. Co-suppression of OCT4 and BIRC5 induced cancer cell apoptosis and cell cycle arrest, thereby efficiently inhibiting the proliferative activity of cancer cells and suppressing the growth of HCC xenogrfts in nude mice.</p< <p<Conclusion</p< <p<OCT4 can upregulate BIRC5 and CCND1 expression by increasing their promoter activity. These factors collusively promotes HCC cell proliferation, and co-suppression of OCT4 and BIRC5 is potentially beneficial for HCC treatment.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.</p< <p<Methods</p< <p<By manipulating OCT4 and BIRC5 expression in hepatocellular carcinoma (HCC) cell lines, the regulatory mechanism of OCT4 on BIRC5 and CCND1 were investigated.</p< <p<Results</p< <p<Increasing or decreasing OCT4 expression could enhance or suppress BIRC5 expression, respectively, by regulating the activity of BIRC5 promoter. Because there is no binding site for OCT4 within BIRC5 promoter, the effect of OCT4 on BIRC5 promoter is indirect. An octamer motif for OCT4 in the CCND1 promoter has directly and partly participated in the regulation of CCND1 promoter activity, suggesting that OCT4 also could upregulated the expression of CCND1. Co-suppression of OCT4 and BIRC5 induced cancer cell apoptosis and cell cycle arrest, thereby efficiently inhibiting the proliferative activity of cancer cells and suppressing the growth of HCC xenogrfts in nude mice.</p< <p<Conclusion</p< <p<OCT4 can upregulate BIRC5 and CCND1 expression by increasing their promoter activity. These factors collusively promotes HCC cell proliferation, and co-suppression of OCT4 and BIRC5 is potentially beneficial for HCC treatment.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.</p< <p<Methods</p< <p<By manipulating OCT4 and BIRC5 expression in hepatocellular carcinoma (HCC) cell lines, the regulatory mechanism of OCT4 on BIRC5 and CCND1 were investigated.</p< <p<Results</p< <p<Increasing or decreasing OCT4 expression could enhance or suppress BIRC5 expression, respectively, by regulating the activity of BIRC5 promoter. Because there is no binding site for OCT4 within BIRC5 promoter, the effect of OCT4 on BIRC5 promoter is indirect. An octamer motif for OCT4 in the CCND1 promoter has directly and partly participated in the regulation of CCND1 promoter activity, suggesting that OCT4 also could upregulated the expression of CCND1. Co-suppression of OCT4 and BIRC5 induced cancer cell apoptosis and cell cycle arrest, thereby efficiently inhibiting the proliferative activity of cancer cells and suppressing the growth of HCC xenogrfts in nude mice.</p< <p<Conclusion</p< <p<OCT4 can upregulate BIRC5 and CCND1 expression by increasing their promoter activity. These factors collusively promotes HCC cell proliferation, and co-suppression of OCT4 and BIRC5 is potentially beneficial for HCC treatment.</p<
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container_issue	1, p 82
title_short	OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma
url	https://doi.org/10.1186/1471-2407-13-82 https://doaj.org/article/0f5fa028630b4202af087df6217d6d41 http://www.biomedcentral.com/1471-2407/13/82 https://doaj.org/toc/1471-2407
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