INHBA knockdown inhibits proliferation and invasion of nasopharyngeal carcinoma SUNE1 cells in vitro.

Up-regulated expression of INHBA has been reported in multiple malignant tumors. However, in nasopharyngeal carcinoma (NPC), the expression pattern and clinical significance of INHBA are still unclear. This study aimed to detect the expression of INHBA and its prognostic significance in NPC, then explore the tumor-associated functions of INHBA gene and the potential mechanism. The INHBA expression of mRNA levels in tumor tissues and noncancerous nasopharyngeal tissues was investigated by RT-qPCR. The protein expression in cells were detected by western blot. Cell proliferation was detected by CCK assay and cell invasion ability was evaluated by Transwell assay. The expression of INHBA in paraffin-embedded NPC tissues was detected by immunohistochemistry (IHC). Statistical analyses were further applied to assess the clinical significance of INHBA expression. The result reveals INHBA mRNA level is elevated in NPC tissues compared to those in noncancerous nasopharyngeal epithelial tissues. In paraffin-embedded NPC tissues, immunoreactivity of INHBA was primarily detected in 53.70% (58/108) of these patients. The overexpression was notably associated with the clinical stage (UICC) (P=0.048), N classification (P=0.042), carotid sheath involvement (P=0.016), and decreased disease-free survival (DFS) (P=0.004) and overall survival (OS) (P=0.010). Multivariate analysis revealed that INHBA expression was an independent prognostic factor for DFS (P=0.028). CCK assay showed SUNE1 cells' proliferation was decreased in INHBA knockdown group than control. Transwell assay showed the invasion of SUNE1 cells was decreased in INHBA knockdown group by comparison with control. Further study showed knockdown of INHBA expression in SUNE1 cells could block the TGF-β signaling pathway. In conclusion, INHBA is up-regulated in NPC, and is significantly correlated with clinical stage (UICC), N stage, carotid sheath involvement, and survival. Knockdown INHBA in SUNE1 cells could inhibit the cells' proliferation and invasion. The underlying mechanism may be blockade of the TGF-β signaling pathway.