TNFR1 Regulates Ovarian Cancer Cell Tumorigenicity Through PIK3CB-p110Beta

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:

Keywords: EGF pathway, independent on TNF-α, Ovarian cancer, PIK3-P110beta, TNFR1, tumorigenicity.

Abstract: 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.

Cite this article as:

Peng C., Su J., Zeng W., Zhang X. and Chen X., TNFR1 Regulates Ovarian Cancer Cell Tumorigenicity Through PIK3CB-p110Beta, Current Molecular Medicine 2015; 15 (5) . https://dx.doi.org/10.2174/1566524015666150630125734