Yu Tianwen, Huang Changhao, Lai Chen, He Qing, Yuan Weijie, Chen Zihua
Department of Gastrointestinal Surgery, Xiangya Hospital, Central South University, Changsha, China.
The Hunan Provincial Key Lab of Precision Diagnosis and Treatment for Gastrointestinal Tumor, Xiangya Hospital, Central South University, Changsha, China.
Front Oncol. 2023 Jul 4;13:1166444. doi: 10.3389/fonc.2023.1166444. eCollection 2023.
Colorectal cancer (CRC) is currently the third most common cancer in the world, and its prevalence and mortality rate continue to increase.
Based on an analysis of The Cancer Genome Atlas database, Tumor Immune Estimation Resource and Gene Expression Profiling Interactive Analysis, we explored the expression of CPNE7 in tumors. Immunohistochemistry and quantitative polymerase chain reaction analysis the expression of CPNE7 in colorectal cancer. Our study explored how CPNE7 promotes CRC cell proliferation and migration in vitro and in vivo. Transcriptome sequencing and Co-IP assay explored the underlying mechinaism of CPNE7 founction.
We found the CPNE7 was overexpressed in CRC by database and IHC. CPNE7 promoted CRC cells proliferstion and migration in vitro and in vivo. Comparing and analyzing transcriptome sequencing between exogenous up-/downregulated CPNE7 CRC cells and the controls, we found that CPNE7 activates mitogen-activated protein kinase (MAPK) signaling pathway stimulating cancer cell proliferation. Coimmunoprecipitation experiments revealed an interaction between CPNE7 and pyruvate kinase muscle protein (PKM2). We also found the activity of MAPK signaling is regulated by exogenous CPNE7 expression.
These results imply that CPNE7 may promote the progression of CRC by interacting with PKM2 and initiating the MAPK signaling pathway.
结直肠癌（CRC）是目前全球第三大常见癌症，其发病率和死亡率持续上升。
基于对癌症基因组图谱数据库、肿瘤免疫评估资源和基因表达谱交互式分析的分析，我们探究了CPNE7在肿瘤中的表达。免疫组织化学和定量聚合酶链反应分析了结直肠癌中CPNE7的表达。我们的研究探讨了CPNE7如何在体外和体内促进CRC细胞增殖和迁移。转录组测序和免疫共沉淀实验探究了CPNE7功能的潜在机制。
我们通过数据库和免疫组织化学发现CPNE7在CRC中过表达。CPNE7在体外和体内促进CRC细胞增殖和迁移。比较和分析外源性上调/下调CPNE7的CRC细胞与对照之间的转录组测序，我们发现CPNE7激活丝裂原活化蛋白激酶（MAPK）信号通路刺激癌细胞增殖。免疫共沉淀实验揭示了CPNE7与丙酮酸激酶肌肉型蛋白（PKM2）之间的相互作用。我们还发现外源性CPNE7表达调节MAPK信号的活性。
这些结果表明，CPNE7可能通过与PKM2相互作用并启动MAPK信号通路来促进CRC的进展。
