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STK32C通过激活c-MYC信号通路促进结肠肿瘤进展。

STK32C promotes colon tumor progression through activating c-MYC signaling.

作者信息

Zhang Xin, Jin Mingxin, Chu Yali, Liu Fengjun, Qu Hui, Chen Cheng

机构信息

Department of General Surgery, Qilu Hospital of Shandong University, 107 West Wenhua Road, JiNan, 250012, China.

出版信息

Cell Mol Life Sci. 2025 Jun 14;82(1):235. doi: 10.1007/s00018-025-05773-y.

DOI:10.1007/s00018-025-05773-y
PMID:40515843
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12167181/
Abstract

Serine/threonine kinase 32C (STK32C) is a member of the AGC kinase family and has been identified as a potential promoter of cancer progression, though its role remains largely uncharacterized. This study explores the impact of STK32C on colorectal cancer (CRC) progression, particularly focusing on its influence on the MYC signaling pathway. Analysis of CRC samples and in vitro experiments revealed that STK32C expression is significantly elevated in cancerous tissues and associated with poor prognosis. Functional assays demonstrated that STK32C promotes proliferation, migration, and invasion of CRC cells, likely through phosphorylation of MYC at the S420 site, enhancing MYC stability and signaling activity. In vivo studies using a mouse xenograft model confirmed that STK32C knockdown suppresses tumor growth and MYC pathway activation. These findings suggest that STK32C contributes to CRC progression by modulating MYC signaling, highlighting its potential as a therapeutic target in CRC.

摘要

丝氨酸/苏氨酸激酶32C（STK32C）是AGC激酶家族的成员，尽管其作用在很大程度上仍未明确，但已被确定为癌症进展的潜在促进因子。本研究探讨了STK32C对结直肠癌（CRC）进展的影响，尤其关注其对MYC信号通路的影响。对CRC样本的分析和体外实验表明，STK32C在癌组织中的表达显著升高，且与预后不良相关。功能测定表明，STK32C可能通过在S420位点磷酸化MYC来促进CRC细胞的增殖、迁移和侵袭，增强MYC的稳定性和信号活性。使用小鼠异种移植模型的体内研究证实，敲低STK32C可抑制肿瘤生长和MYC通路激活。这些发现表明，STK32C通过调节MYC信号促进CRC进展，突出了其作为CRC治疗靶点的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/616eb23feba0/18_2025_5773_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/cde48fd2d742/18_2025_5773_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/e4920b86bbf6/18_2025_5773_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/803711263372/18_2025_5773_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/865379882f9c/18_2025_5773_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/bb5285b2c0d6/18_2025_5773_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/7d18764eb241/18_2025_5773_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/616eb23feba0/18_2025_5773_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/cde48fd2d742/18_2025_5773_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/e4920b86bbf6/18_2025_5773_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/803711263372/18_2025_5773_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/865379882f9c/18_2025_5773_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/bb5285b2c0d6/18_2025_5773_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/7d18764eb241/18_2025_5773_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa11/12167181/616eb23feba0/18_2025_5773_Fig7_HTML.jpg

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