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17β-Estradiol exerts anticancer effects in anoikis-resistant hepatocellular carcinoma cell lines by targeting IL-6/STAT3 signaling
DC Field | Value | Language |
---|---|---|
dc.contributor.advisor | 김윤준 | - |
dc.contributor.author | 이슬기 | - |
dc.date.accessioned | 2017-07-19T10:07:53Z | - |
dc.date.available | 2017-07-19T10:07:53Z | - |
dc.date.issued | 2016-08 | - |
dc.identifier.other | 000000135979 | - |
dc.identifier.uri | https://hdl.handle.net/10371/132311 | - |
dc.description | 학위논문 (석사)-- 서울대학교 대학원 : 협동과정 종양생물학전공, 2016. 8. 김윤준. | - |
dc.description.abstract | 17β-Estradiol (E2) has been proven to exert protective effects against HCC | - |
dc.description.abstract | however, its mechanism on HCC proliferation and suppression of invasion remains to be further explored. Because HCC up-regulates serum Interleukin-6 (IL-6) levels and Signal Transducer and Activator of Transcription 3 (STAT3), molecular agents that attenuate IL-6/STAT3 signaling can potentially suppress HCC development. In this study, we examined involvement of E2 in anoikis resistance that induces invasion capacities and chemo-resistance. Huh-BAT and HepG2 cells grown under anchorage-independent condition were selected. The anoikis-resistant (AR) cells showed stronger chemo-resistance against sorafenib, doxorubicin, 5-fluorouracil and cisplatin compared to adherent HCC cells. AR HCC cells exhibited decreased expression of E-cadherin and increased expression of the N-cadherin and vimentin compared to adherent HCC cells. We then demonstrated that E2 suppressed cell proliferation in AR HCC cells. IL-6 treatment enhanced invasive characteristics, and E2 reversed it. Regarding mechanism of E2, it decreased in the phosphorylation of STAT3 that overexpressed on AR HCC cells. The inhibitory effect of E2 on cell growth was accompanied with cell cycle arrest at G2/M phase and caspase-3/9/PARP activation through c-Jun N-terminal Kinase (JNK) phosphorylation. Taken together, these findings suggested that E2 inhibited the proliferation of AR HCC cells through down-regulation of IL-6/STAT3 signaling. Thus, E2 can be a potential therapeutic drug for treatment of HCC. | - |
dc.description.tableofcontents | Introdution 1
Materials and methods 4 Results 9 Discussion 28 References 31 Abstract in Korean 35 | - |
dc.format | application/pdf | - |
dc.format.extent | 1559500 bytes | - |
dc.format.medium | application/pdf | - |
dc.language.iso | en | - |
dc.publisher | 서울대학교 대학원 | - |
dc.subject | Hepatocellular carcinoma | - |
dc.subject | 17β-estradiol | - |
dc.subject | Interleukin-6 | - |
dc.subject | STAT3 | - |
dc.subject | Drug resistance | - |
dc.subject | Aniokis resistance | - |
dc.subject | EMT | - |
dc.subject.ddc | 616 | - |
dc.title | 17β-Estradiol exerts anticancer effects in anoikis-resistant hepatocellular carcinoma cell lines by targeting IL-6/STAT3 signaling | - |
dc.type | Thesis | - |
dc.description.degree | Master | - |
dc.citation.pages | 36 | - |
dc.contributor.affiliation | 의과대학 협동과정 종양생물학전공 | - |
dc.date.awarded | 2016-08 | - |
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