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通过 GSK-3β/CyclinD1 通路鉴定 GSPT1 作为预后生物标志物和恶性结肠癌细胞表型的促进因子。

Identification of GSPT1 as prognostic biomarker and promoter of malignant colon cancer cell phenotypes via the GSK-3β/CyclinD1 pathway.

机构信息

Department of General Surgery, Mianyang Central Hospital, Mianyang Central Hospital of Chongqing Medical University, Mianyang 621000, Sichuan Province, P.R. China.

Department of Gastroenterological Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Yuzhong 400016, Chongqing, P.R. China.

出版信息

Aging (Albany NY). 2021 Apr 4;13(7):10354-10368. doi: 10.18632/aging.202796.

DOI:10.18632/aging.202796
PMID:33819920
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8064227/
Abstract

Colon cancer is the third most common malignant tumor and its mortality rate ranks fourth among all malignant tumor types. Bioinformatics analysis has shown that is dysregulated in colon cancer and is associated with tumor progression. However, the underlying mechanism remains unclear. To address this research gap, we examined the impact of on cell proliferation, apoptosis, migration, and invasion as well as tumor growth in colon cancer by using a Cell Counting Kit-8 assay, flow cytometry, transwell migration assay, transwell invasion assay, and tumor xenograft model-based analysis, respectively. was significantly up-regulated in colon cancer tissues and cell lines. High GSPT1 expression was correlated with a larger tumor size. Depletion of GSPT1 suppressed cell proliferation, migration, and invasion-induced colon cancer cell apoptosis and restrained tumorigenicity in HCT116 colon cancer cells. Taken together, our findings suggest that the GSPT1/GSK pathway exerts tumor-promoting actions in colon cancer oncogenesis and progression. The GSPT1/GSK pathway may thus be an effective target for controlling colon cancer.

摘要

结直肠癌是第三大常见恶性肿瘤,其死亡率在所有恶性肿瘤类型中排名第四。生物信息学分析表明,在结直肠癌中失调,并与肿瘤进展相关。然而,其潜在的机制尚不清楚。为了解决这一研究空白,我们通过使用细胞计数试剂盒-8 检测、流式细胞术、Transwell 迁移实验、Transwell 侵袭实验和基于肿瘤异种移植模型的分析,分别检测了对细胞增殖、凋亡、迁移和侵袭以及肿瘤生长的影响。在结直肠癌组织和细胞系中显著上调。高 GSPT1 表达与更大的肿瘤大小相关。GSPT1 的耗竭抑制了细胞增殖、迁移和侵袭诱导的结肠癌细胞凋亡,并抑制了 HCT116 结肠癌细胞的致瘤性。总之,我们的研究结果表明,GSPT1/GSK 通路在结直肠癌的发生和发展中发挥着促进肿瘤的作用。因此,GSPT1/GSK 通路可能是控制结直肠癌的有效靶点。

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