Role and mechanism of in promoting malignant behaviors in gastric cancer.

BACKGROUND

Gastric cancer (GC) is one of the major malignancies threatening human lives and health. Non-SMC condensin II complex subunit D3 () plays a crucial role in the occurrence of many diseases. However, its role in GC remains unexplored.

MATERIALS AND METHODS

The Cancer Genome Atlas (TCGA) database, clinical samples, and cell lines were used to analyze expression in GC. was overexpressed and inhibited by lentiviral vectors and the CRISPR/Cas9 system, respectively. The biological functions of were investigated and . Gene microarray, Gene set enrichment analysis (GSEA) and ingenuity pathway analysis (IPA) were performed to establish the potential mechanisms.

RESULTS

was highly expressed in GC and was associated with a poor prognosis. upregulation significantly promoted the malignant biological behaviors of gastric cancer cell, while inhibition exerted a opposite effect. loss can directly inhibit CCND1 and ESR1 expression to downregulate the expression of downstream targets CDK6 and IRS1 and inhibit the proliferation of gastric cancer cells. Moreover, loss activates IRF7 and DDIT3 to regulate apoptosis in gastric cancer cells.

CONCLUSION

Our study revealed that silencing attenuates malignant phenotypes of GC and that it is a potential target for GC treatment.