摘要
有研究表明,TNFR1在肿瘤微环境是一个关键的因素,即肿瘤发生依赖TNF-α引发的级联。在目前的研究中,我们发现TNFR1在卵巢癌中高表达,这与临床生存率和无疾病状态均有关。TNFR1抑制可显著减弱的恶性表型,包括和卵巢癌细胞的在软琼脂集落的生长、增殖,以及糖酵解。出乎意料,抑制TNFR1是通过PIK3-p110beta而不是p110alpha表达阻碍表皮生长因子诱导的p-Akt及p-p70S6K的表达和表皮生长因子诱导的细胞转化。总之,我们的数据提供的证据表明TNFR1在卵巢癌起关键作用,EGF诱导的信号通路是独立于TNF-α触发级联信号的,因此,TNFR1可作为卵巢癌预后的分子。
关键词: EGF通路,独立于TNF-α,卵巢癌,PIK3-P110beta,TNFR1,致瘤性。
Current Molecular Medicine
Title:TNFR1 Regulates Ovarian Cancer Cell Tumorigenicity Through PIK3CB-p110Beta
Volume: 15 Issue: 5
Author(s): C. Peng, J. Su, W. Zeng, X. Zhang and X. Chen
Affiliation:
关键词: EGF通路,独立于TNF-α,卵巢癌,PIK3-P110beta,TNFR1,致瘤性。
摘要: Studies have shown that TNFR1 is a key factor in the tumor microenvironment that is dependent on the TNF-α-initiated cascade for tumorigenesis. In this present study, we found that TNFR1 is over-expressed in ovarian cancer, which is relevant to both clinical survival and disease free status. Knockdown of TNFR1 dramatically attenuates malignant phenotypes, including proliferation and colony growth in soft agar, as well as glycolysis in ovarian cancer cells. Unexpectedly, knocking down TNFR1 blocks EGF-induced p-AKT and p-p70S6K expression and EGF-induced cell transformation through PIK3-p110beta rather than p110alpha expression. Taken together, our data provide evidence that TNFR1 plays a critical role in ovarian cancer and show that the EGF induced signaling pathway is independent of the TNF-α triggering cascade signal. Therefore, TNFR1 may serve as a prognostic molecule in ovarian cancer.
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Cite this article as:
C. Peng, J. Su, W. Zeng, X. Zhang and X. Chen , TNFR1 Regulates Ovarian Cancer Cell Tumorigenicity Through PIK3CB-p110Beta, Current Molecular Medicine 2015; 15 (5) . https://dx.doi.org/10.2174/1566524015666150630125734
DOI https://dx.doi.org/10.2174/1566524015666150630125734 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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