ARHGAP 42 promotes cell migration and invasion involving PI 3K/Akt signaling pathway in nasopharyngeal carcinoma

Rho GTP ase‐activating protein 42 was identified as an inhibitor of RhoA to maintain normal blood pressure homeostasis. However, the effect of ARHGAP 42 in promoting cell malignancy in nasopharyngeal carcinoma is demonstrated in this study. Microarray and real‐time quantitative PCR were used for a mRNA profiling of ARHGAP 42 in nasopharyngeal primary and metastatic carcinoma tissues. Western blot and immunohistochemical staining were used for detecting the expression of ARHGAP 42 protein in nasopharyngeal carcinoma tissues and cell lines. The overexpression and silence experiments of ARHGAP 42 were performed in NPC cell lines using si RNA and expressive plasmid for evaluating cancer cell migration and invasion in vitro. Real‐time quantitative PCR , western blot, and transwell test were employed for with the function of ARHGAP 42 and its antisense lnc RNA uc010rul. We confirmed the elevated expression of ARHGAP 42 in metastatic NPC tissues of mRNA and protein for the first time. Immunohistochemical analysis indicated that NPC patients with highly ARHGAP 42 expression were significantly associated with shorter metastasis‐free survival. Knockdown of ARHGAP 42 resulted in significant inhibition of nasopharyngeal cancer cell migration and invasion in vitro, and the overexpression of ARHGAP 42 showed the opposite effects. In addition, the silence of uc010rul resulted in ARHGAP 42 expression decrease and significant inhibition of nasopharyngeal cancer cell migration and invasion. High expression of ARHGAP 42 is associated with poor metastasis‐free survival of nasopharyngeal carcinoma patients. ARHGAP 42 promotes migration and invasion of nasopharyngeal carcinoma cells in vitro ; the antisense lnc RNA may be involved in this effect.