Norrin maintains malignancy of gastric cancer cells in part through activating AKT signaling

Liu, Lei; Qin, Zhong-yi; Liu, Qin; Wen, Liangzhi; Guo, Yan; Zhou, Yin-Bin; Wang, Bin; Chen, Dongfeng; Wang, Tao

doi:10.1016/j.bbrc.2019.03.044

Cited by 2 publications

(1 citation statement)

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“…Generally, multiple proteins involved in DNA repair, cell proliferation, angiogenesis, as well as mitogenesis are highly expressed in cervical intraepithelial neoplasia (CIN) and tumour [ 7 ]. Recently, He et al reported that the Hippo-Yap signalling pathway plays an important role in the development of cervical tumours [ 57 ]. In the Hippo signalling cascade, the HPV E6 directly binds with the Yes-associated protein (YAP1) to initiate and accelerate tumour progression in cervical oncogenesis.…”

Section: Discussionmentioning

confidence: 99%

IRF-1 Inhibits Angiogenic Activity of HPV16 E6 Oncoprotein in Cervical Cancer

Rho

Lee

Byun

et al. 2020

IJMS

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HPV16 E6 oncoprotein is a member of the human papillomavirus (HPV) family that contributes to enhanced cellular proliferation and risk of cervical cancer progression via viral infection. In this study, interferon regulatory factor-1 (IRF-1) regulates cell growth inhibition and transcription factors in immune response, and acts as an HPV16 E6-binding cellular molecule. Over-expression of HPV16 E6 elevated cell growth by attenuating IRF-1-induced apoptosis and repressing p21 and p53 expression, but activating cyclin D1 and nuclear factor kappa B (NF-κB) expression. The promoter activities of p21 and p53 were suppressed, whereas NF-κB activities were increased by HPV16 E6. Additionally, the cell viability of HPV16 E6 was diminished by IRF-1 in a dose-dependent manner. We found that HPV16 E6 activated vascular endothelial growth factor (VEGF)-induced endothelial cell migration and proliferation as well as phosphorylation of VEGFR-2 via direct interaction in vitro. HPV16 E6 exhibited potent pro-angiogenic activity and clearly enhanced the levels of hypoxia-inducible factor-1α (HIF-1α). By contrast, the loss of function of HPV16 E6 by siRNA-mediated knockdown inhibited the cellular events. These data provide direct evidence that HPV16 E6 facilitates tumour growth and angiogenesis. HPV16 E6 also activates the PI3K/mTOR signalling cascades, and IRF-1 suppresses HPV16 E6-induced tumourigenesis and angiogenesis. Collectively, these findings suggest a biological mechanism underlying the HPV16 E6-related activity in cervical tumourigenesis.

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Section: Discussionmentioning

confidence: 99%