CMPD1 inhibited human gastric cancer cell proliferation by inducing apoptosis and G2/M cell cycle arrest

• Published in: Biological research 2018-04, Vol.51 (1), p.11-11, Article 11
• Main Authors: Li, Yu, Zhang, Depeng, Yu, Kaikai, Hu, Yudong, Wu, Qiong, Qian, Feng, Wang, Zishu
• Format: Article
• Language: English
• Subjects: Antineoplastic Agents - pharmacology; Apoptosis; Apoptosis - drug effects; Apoptosis Regulatory Proteins - pharmacology; BIOLOGY; Blotting, Western; Care and treatment; Cell cycle; Cell cycle arrest; Cell Line, Tumor; Cell proliferation; Cell Proliferation - drug effects; CMPD1; Cytochromes - drug effects; Down-Regulation - drug effects; Flow Cytometry - methods; G2 Phase Cell Cycle Checkpoints - drug effects; Health aspects; Humans; Intracellular Signaling Peptides and Proteins - pharmacology; MKN-45; Phosphorylation; Proliferation; Protein-Serine-Threonine Kinases - pharmacology; Reproducibility of Results; SOX9 Transcription Factor - pharmacology; Stomach cancer; Stomach Neoplasms - drug therapy; Stomach Neoplasms - pathology; Up-Regulation - drug effects
• ISSN: 0717-6287; 0716-9760; 0717-6287
• DOI: 10.1186/s40659-018-0159-6

Gastric cancer occupies the fourth highest morbidity rate of cancers worldwide. Clinical therapies of gastric cancer remain limited because of uncertainty of mechanisms and shortness of effective medicine. Thus, new drug candidates for gastric cancer treatment is urgently needed. In this study, CMPD1 as a wildly used MK2 phosphorylation inhibitor was employed to find its impact on gastric cancer cell proliferation, apoptosis and cell cycle using colony formation assay and flow cytometry analysis. Along with its anti-proliferation effect on gastric cancer cell line MKN-45 and SGC7901, CMPD1 also induced massive apoptosis and significant G2/M phase arrest in a time-dependent and dose-dependent manner in MKN-45 cells respectively. Furthermore, Western blot confirmed that the expression of anti-apoptotic proteins Bcl-2 was decreased while BAX, cytochrome c release and cleaved PARP were increased. In addition, oncogene c-Myc was downregulated in response to CMPD1 treatment. Our results demonstrated that CMPD1 has anti-tumor effect on human gastric cancer cell line MKN-45 possibly via downregulating oncogene c-Myc expression and CMPD1 could be applied as a potential candidate for treating gastric malignancy. To the best of our knowledge, it is the first report of anti-tumor effect of CMPD-1 on human gastric cancer cells.