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MYBL2 in synergy with CDC20 promotes the proliferation and inhibits apoptosis of gastric cancer cells.

BACKGROUND
Gastric cancer (GC) is a common malignant tumor with a high morbidity and mortality worldwide. It has been reported that V-Myb avian myeloblastosis viral oncogene homolog-like 2 (MYBL2) could be a promising prognostic biomarker for GC. However, the specific role of MYBL2 in GC progression remains unclear.


OBJECTIVES
To examine the role of MYBL2 in GC progression and investigate the underlying mechanisms.


MATERIAL AND METHODS
The mRNA levels of target genes were detected using quantitative real-time polymerase chain reaction (RT-qPCR) and protein expression was measured with western blot analysis. Cell Counting Kit-8 (CCK-8) and colony formation assays were employed to inspect HGC-27 cell proliferation, and cellular apoptosis was determined with TUNEL staining. Finally, the interaction of MYBL2 and cell division cycle 20 (CDC20) was verified with immunoprecipitation.


RESULTS
MYBL2 was confirmed to be overexpressed in GC cells. MYBL2 knockdown inhibited HGC-27 cell proliferation and promoted cellular apoptosis, and these effects were reversed by CDC20 overexpression. Interestingly, MYBL2 interacted with CDC20 and regulated its expression. MYBL2 knockdown also inhibited activation of the Wnt/β-catenin signaling pathway, while CDC20 overexpression showed the opposite effect.


CONCLUSIONS
In summary, the synergy between MYBL2 and CDC20 induced the proliferation of GC cells and inhibited cell apoptosis; these effects may have involved the Wnt/β-catenin signaling pathway. Thus, MYBL2 may be a promising target for GC treatment.