HPV-YAP1 oncogenic alliance drives malignant transformation of fallopian tube epithelial cells.

IF 6.5 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

EMBO Reports Pub Date : 2024-09-13 DOI:10.1038/s44319-024-00233-3

Chunbo He,Xiangmin Lv,Jiyuan Liu,Jinpeng Ruan,Peichao Chen,Cong Huang,Peter C Angeletti,Guohua Hua,Madelyn Leigh Moness,Davie Shi,Anjali Dhar,Siyi Yang,Savannah Murphy,Isabelle Montoute,Xingcheng Chen,Kazi Nazrul Islam,Sophia George,Tan A Ince,Ronny Drapkin,Chittibabu Guda,John S Davis,Cheng Wang

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引用次数: 0

Abstract

High grade serous ovarian carcinoma (HGSOC) is the most common and aggressive ovarian malignancy. Accumulating evidence indicates that HGSOC may originate from human fallopian tube epithelial cells (FTECs), although the exact pathogen(s) and/or molecular mechanism underlying the malignant transformation of FTECs is unclear. Here we show that human papillomavirus (HPV), which could reach FTECs via retrograde menstruation or sperm-carrying, interacts with the yes-associated protein 1 (YAP1) to drive the malignant transformation of FTECs. HPV prevents FTECs from natural replicative and YAP1-induced senescence, thereby promoting YAP1-induced malignant transformation of FTECs. HPV also stimulates proliferation and drives metastasis of YAP1-transformed FTECs. YAP1, in turn, stimulates the expression of the putative HPV receptors and suppresses the innate immune system to facilitate HPV acquisition. These findings provide critical clues for developing new strategies to prevent and treat HGSOC.

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HPV-YAP1 致癌联盟驱动输卵管上皮细胞恶性转化。

高级别浆液性卵巢癌（HGSOC）是最常见的侵袭性卵巢恶性肿瘤。越来越多的证据表明，高级别浆液性卵巢癌可能起源于人类输卵管上皮细胞（FTECs），但输卵管上皮细胞恶性转化的确切病原体和/或分子机制尚不清楚。在这里，我们发现人类乳头瘤病毒（HPV）可通过逆行性月经或精子携带到达输卵管上皮细胞，并与是相关蛋白1（YAP1）相互作用，驱动输卵管上皮细胞恶性转化。HPV 阻止 FTEC 自然复制和 YAP1 诱导的衰老，从而促进 YAP1 诱导的 FTEC 恶性转化。HPV 还刺激 YAP1 转化的 FTEC 增殖并推动其转移。反过来，YAP1 又会刺激假定的 HPV 受体的表达，抑制先天性免疫系统，从而促进 HPV 的获得。这些发现为开发预防和治疗 HGSOC 的新策略提供了重要线索。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

EMBO Reports 生物-生化与分子生物学

CiteScore

11.20

自引率

1.30%

发文量

267

审稿时长

1 months

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