Significance of desmoglein‐2 on cell malignant behaviors via mediating MAPK signaling in cervical cancer

Abstract

Abstract Desmoglein‐2 (DSG2) is an integral component of desmosomes, maintaining cell‐cell adhension in multiple cancers. It has been well studied in epithelial cells, cardiomyocytes and primary prostate cancer, colon cancer, skin squamous cell carcinoma, except for cervical cancer. Hence, we performed this study to examine the function of DSG2 in cervical cancer. We used TCGA and Oncomine databases to assess the expression level of DSG2 in cervical cancer cases. Kaplan‐Meier method with log‐rank test was utilized to plot overall survival (OS) curve. The reverse transcription‐quantitative polymerase chain reaction (qRT‐PCR) and western blotting were performed to detect the expression of DSG2 in cells. Cell Counting Kit‐8 (CCK‐8), wound‐healing analysis, and transwell assay were carried out to examine proliferation, migration, and invasion of cells. A higher level of DSG2 in cervical cancer was associated with lower OS rate. Knockdown of DSG2 inhibited cervical cancer cell proliferation, migration, and invasion, while DSG2 enhancement promoted cell proliferation, migration, and invasion. Moreover, the proteins expression of p‐MEK and p‐ERK that are required for mitogen‐activated protein kinases (MAPK) pathway were downregulated after reducing DSG2. In conclusion, these findings illustrated the importance of DSG2 in cervical cancer development and cell behaviors by mediating MAPK signaling pathway, suggesting DSG2 maybe a novel therapeutic target in control of cervical cancer.

Keywords

• cell viability
• cervical cancer
• desmoglein‐2
• MAPK