Abstract
BackgroundGastric 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.ResultsIn 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.ConclusionsOur 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.
Highlights
Gastric cancer occupies the fourth highest morbidity rate of cancers worldwide
We revealed that CMPD1 caused a dose-dependent cell cycle arrest which mainly occurred in the G2/M phase possibly due to oncogene c-Myc downregulation
CMPD1 induces apoptosis in MKN‐45 cells We further investigated whether CMPD1 inhibited cell proliferation by inducing apoptosis in MKN-45 cells
Summary
Gastric cancer occupies the fourth highest morbidity rate of cancers worldwide. With poor prognosis and high morbidity, gastric cancer remains the second leading cause of cancer-related death and ranks the fourth in common types of malignancies worldwide [1, 2]. In China, gastric cancer occupies the second highest mortality and incidence rate [3]. Despite the decreased mortality rates and the advanced approaches to cure this illness, treatment of patients with gastric cancer is still limited with disappointing outcomes [4]. The occurrence of gastric cancer is the outcome of sequential genetic and epigenetic changes with resistance to DNA damage as one of the hallmarks [8,9,10].
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