Guo Yuehui, Zhu Qingyun, Chen Shiwei, Li Yanxiang, Fu Daiquan, Qiao Delin, Ni Caifang
Department of Interventional Radiology, The First Affiliated Hospital of Soochow University, 188 Shizi Street, 215006 Suzhou, Jiangsu People's Republic of China.
Department of Interventioin, Gongli Hospital of Shanghai Pudong New Area, Shanghai, 200135 China.
3 Biotech. 2021 Mar;11(3):139. doi: 10.1007/s13205-021-02682-2. Epub 2021 Feb 23.
The G protein-coupled receptors (GPRs) have been shown to regulate several cancer related processes. The aberrant expression of GPRs has been linked to the development of several cancers. The present study was designed to examine the expression and decipher the role of GPR15 in the development of human colorectal cancer. The results revealed GPR15 to be significantly ( < 0.05) upregulated in colorectal cancer cells. The silencing of GPR15 inhibited the growth of the colorectal cancer cells via induction of apoptosis. Induction of apoptosis in colorectal cancer cells was associated increase in Bax and decrease in Bcl-2 expression. The silencing of GPR-15 also caused a significant ( < 0.05) decline in the migration and invasion of the colorectal cancer cells. Bioinformatic analysis and luciferase assay revealed that the expression of GPR15 to be post-transcriptionally regulated by microRNA-1225 (miR-1225). The expression of miR-1225 was found to significantly ( < 0.05) downregulated in colorectal cancer cells and its overexpression caused suppression of GPR15 and inhibited the proliferation of the colorectal cancer cells. Nonetheless, overexpression of GPR15 could avoid the growth inhibitory effects of miR-1225. The results suggest that the GPR15/miR-1225 axis play an important role in the development of colon rectal cancer and exhibit therapeutic implications for its treatment.
G蛋白偶联受体(GPRs)已被证明可调节多种癌症相关过程。GPRs的异常表达与多种癌症的发生有关。本研究旨在检测GPR15在人类结直肠癌发生中的表达并阐明其作用。结果显示,GPR15在结直肠癌细胞中显著上调(<0.05)。GPR15沉默通过诱导凋亡抑制结直肠癌细胞生长。结直肠癌细胞凋亡的诱导与Bax增加和Bcl-2表达减少有关。GPR-15沉默还导致结直肠癌细胞迁移和侵袭显著下降(<0.05)。生物信息学分析和荧光素酶检测显示,GPR15的表达受微小RNA-1225(miR-1225)转录后调控。发现miR-1225在结直肠癌细胞中显著下调(<0.05),其过表达导致GPR15抑制并抑制结直肠癌细胞增殖。然而,GPR15过表达可避免miR-1225的生长抑制作用。结果表明,GPR15/miR-1225轴在结直肠癌发生中起重要作用,并对其治疗具有潜在的治疗意义。