Department of Biliary Tract Surgery, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Department of Critical Care Medicine, Huadong Hospital, Shanghai, China.
Cell Cycle. 2022 Jun;21(11):1166-1177. doi: 10.1080/15384101.2022.2042775. Epub 2022 Feb 23.
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.
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。