Ribosomal protein RPL5 regulates colon cancer cell proliferation and migration through MAPK/ERK signaling pathway.
Ribosomal protein RPL5 regulates colon cancer cell proliferation and migration through MAPK/ERK signaling pathway.
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核糖体蛋白RPL5通过MAPK/ERK信号通路调控结肠癌细胞增殖和迁移
DOI：
10.1186/s12860-022-00448-z
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发表时间：
2022-11-16
影响因子：
2.8
通讯作者：
中科院分区：
文献类型：
--
作者：
核糖体蛋白的异常表达对肿瘤的进展具有重要的调节作用。RPL5参与多种恶性肿瘤的发生发展，但RPL5在结肠癌中的作用尚不清楚。使用TCGA和GTEx数据库中的数据分析RPL5在泛癌中的表达。采用Western blotting检测RPL5在临床结肠癌组织和人结肠癌细胞系中的表达水平；设计针对RPL5的siRNA，通过Western blotting和RT-qPCR验证其干扰效率；采用CCK8实验、克隆形成实验、细胞周期分析和细胞划痕实验观察RPL5对结肠癌细胞增殖和迁移的影响；采用Western blotting检测MAPK/ERK信号通路相关蛋白的变化。RPL5在结肠癌组织和细胞系中的表达水平分别显著高于癌旁组织和NCM460细胞，在HCT116细胞和RKO细胞中的表达水平较高。RPL5基因敲除可显著抑制HCT16和RKO细胞的增殖和迁移，并使细胞周期停滞于G0/G1期。机制研究表明，下调RPL5后，p-MEK1/2、p-ERK、c-Myc表达下调，FOXO_3表达上调，ERK激动剂(TBHQ)可部分逆转siRPL5的上述作用。此外，TBHQ可部分逆转siRPL5对结肠癌细胞增殖和迁移的抑制作用。总的来说，RPL5至少部分地通过激活MAPK/ERK信号通路来促进结肠细胞的增殖和迁移。RPL5至少部分通过激活MAPK/ERK信号通路促进结肠癌细胞的增殖和迁移，MAPK/ERK信号通路可能成为肿瘤治疗的新靶点。网上版载有补充材料，可在10.1186/s12860022-00448-z上查阅。
Abnormal expression of ribosomal proteins has an important regulatory effect on the progression of cancer. RPL5 is involved in the progression of various malignancies, however, the role of RPL5 in colon cancer remains is still unclear. Data from TCGA and GTEx databases were used to analyze the RPL5 expression in pan-cancer. The expression level of RPL5 in clinical colon cancer tissue samples and human colon cancer cell lines was detected by western blotting; siRNA targeting RPL5 was designed, and its interference efficiency was verified by western blotting and RT-qPCR; CCK8 assay, clone formation assay, cell cycle assay, and cell scratch assay were used to observe the effect of RPL5 on colon cancer cell proliferation and migration; the changes of proteins related to MAPK/ERK signaling pathway were also detected using western blotting. The expression level of RPL5 in colon cancer tissues and cell lines was significantly higher than that in adjacent tissues and NCM460 cells, respectively, and its expression level was higher in HCT116 cells and RKO cells. Knockdown of RPL5 significantly inhibited the proliferation and migration of HCT16 and RKO cells, and arrested the cell cycle in G0/G1 phase. Mechanistic studies revealed that the expression of p-MEK1/2, p-ERK, c-Myc were down-regulated, and the expression of FOXO3 was up-regulated after down-regulation of RPL5, ERK activator (TBHQ) could partially reverse the above-mentioned effects caused by siRPL5. Moreover, TBHQ could partially reverse the inhibitory effect of siRPL5 on the proliferation and migration of colon cancer cells. Collectively, RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway. RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway, which may serve as a novel therapeutic target for cancers in which MAPK/ERK signaling is a dominant feature. The online version contains supplementary material available at 10.1186/s12860-022-00448-z.
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