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miR-4461 通过调节 EGFR/AKT 信号通路抑制胆囊癌的进展。

miR-4461 inhibits the progression of Gallbladder carcinoma via regulating EGFR/AKT signaling.

机构信息

Department of Biliary Tract Surgery, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.

Department of Critical Care Medicine, Huadong Hospital, Shanghai, China.

出版信息

Cell Cycle. 2022 Jun;21(11):1166-1177. doi: 10.1080/15384101.2022.2042775. Epub 2022 Feb 23.

Abstract

Increasing evidence has demonstrated that microRNAs (miRNAs) participated in the tumorigenesis, progression and recurrence of various malignancies including Gallbladder carcinoma (GBC). miR-4461 was reported to work as a tumor suppressor gene in renal cell carcinoma. However, the role of miR-4461 in GBC remains unknown. Herein, we show that miR-4461 is downregulated in gallbladder cancer stem cells (CSCs). Forced miR-4461 expression attenuates the self-renewal, tumorigenicity of gallbladder CSCs, and inhibits proliferation and metastasis of GBC cells. Conversely, miR-4461 knockdown promotes the self-renewal of gallbladder CSCs, and facilities proliferation and metastasis of GBC cells. Mechanistically, miR-4461 inhibits GBC progression via downregulating EGFR/AKT pathway. Special EGFR siRNA or AKT overexpression virus abolishes the discrepancy of self-renewal, tumorigenesis, growth, and metastasis between miR-4461 overexpression GBC cells and their control cells. In conclusion, miR-4461 suppresses GBC cells self-renewal, tumorigenicity, proliferation, and metastasis by inactivating EGFR/AKT signaling, and may therefore prove to be a potential therapeutic target for GBC patients.

摘要

越来越多的证据表明,微小 RNA(miRNA)参与了各种恶性肿瘤的发生、发展和复发,包括胆囊癌(GBC)。miR-4461 被报道在肾细胞癌中作为一种肿瘤抑制基因发挥作用。然而,miR-4461 在 GBC 中的作用尚不清楚。本文显示 miR-4461 在胆囊癌干细胞(CSCs)中下调。强制表达 miR-4461 可减弱胆囊 CSCs 的自我更新、致瘤性,并抑制 GBC 细胞的增殖和转移。相反,miR-4461 的下调促进了胆囊 CSCs 的自我更新,并促进了 GBC 细胞的增殖和转移。机制上,miR-4461 通过下调 EGFR/AKT 通路抑制 GBC 进展。特殊的 EGFR siRNA 或 AKT 过表达病毒消除了 miR-4461 过表达 GBC 细胞与其对照细胞之间在自我更新、致瘤性、生长和转移方面的差异。总之,miR-4461 通过失活 EGFR/AKT 信号抑制 GBC 细胞的自我更新、致瘤性、增殖和转移,因此可能成为 GBC 患者的潜在治疗靶点。

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