SNX16 通过调节 EGFR-AKT 信号通路促进肝癌细胞的存活。
SNX16 is required for hepatocellular carcinoma survival via modulating the EGFR-AKT signaling pathway.
机构信息
Department of General Surgery, Jiangxi Medical College, The Second Affiliated Hospital of Nanchang University, Nanchang University, Nanchang, 330006, China.
Oncology Department, First Affiliated Hospital of Jiangxi Medical College, Nanchang University, Nanchang, 330006, China.
出版信息
Sci Rep. 2024 Jun 7;14(1):13093. doi: 10.1038/s41598-024-64015-6.
Sorting nexin 16 (SNX16), a pivotal sorting nexin, emerges in tumor progression complexity, fueling research interest. However, SNX16's biological impact and molecular underpinnings in hepatocellular carcinoma (HCC) remain elusive. This study probes SNX16's function, clinical relevance via mRNA, and protein expression in HCC. Overexpression/knockdown assays of SNX16 were employed to elucidate impacts on HCC cell invasion, proliferation, and EMT. Additionally, the study delved into SNX16's regulation of the EGFR-AKT signaling cascade mechanism. SNX16 overexpression in HCC correlates with poor patient survival; enhancing proliferation, migration, invasion, and tumorigenicity, while SNX16 knockdown suppresses these processes. SNX16 downregulation curbs phospho-EGFR, dampening AKT signaling. EGFR suppression counters SNX16-overexpression-induced HCC proliferation, motility, and invasiveness. Our findings delineate SNX16's regulatory role in HCC, implicating it as a prospective therapeutic target.
分选连接蛋白 16（SNX16）是一种关键的分选连接蛋白，在肿瘤进展的复杂性中出现，引起了研究兴趣。然而，SNX16 在肝细胞癌（HCC）中的生物学影响和分子基础仍不清楚。本研究通过 HCC 中的 mRNA 和蛋白表达水平，探究了 SNX16 的功能和临床相关性。通过 SNX16 的过表达/敲低实验，阐明了其对 HCC 细胞侵袭、增殖和 EMT 的影响。此外，该研究还探讨了 SNX16 对 EGFR-AKT 信号级联机制的调节作用。SNX16 在 HCC 中的过表达与患者预后不良相关；增强了增殖、迁移、侵袭和致瘤性，而 SNX16 的敲低则抑制了这些过程。SNX16 的下调抑制了磷酸化 EGFR，减弱了 AKT 信号。EGFR 抑制作用逆转了 SNX16 过表达诱导的 HCC 增殖、迁移和侵袭。我们的研究结果描绘了 SNX16 在 HCC 中的调节作用，表明其可能成为一种有前途的治疗靶点。
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