Introduction: Cervical cancer (CC) is the third most commonly occurring cancer and the fourth most common cause of cancer-related death in women. Squamous cell carcinoma (SCC) comprises ~70% of CC cases; however, its detailed molecular mechanisms are still unclear. Methods: 24 pairs of SCC and para-tumor tissues were detected with RT-qPCR, respectively. MTT and EdU assays were performed to demonstrate the role of MYH9 in SCC cell proliferation. Transwell and Boyden were performed to demonstrate the role of MYH9 in SCC cell progression. A Western blot was performed to demonstrate the mechanism of MYH9 in SCC. Results: The results showed that mRNA and protein levels of MYH9 were higher in SCC samples than in para-tumor samples, and MYH9 knockdown suppressed the proliferation of SCC cells, and suppressed the migration and invasion of the Siha cell line, but not the C-33A cell line. Mechanistic assays showed that knockdown of MYH9 inhibited the epithelial-mesenchymal transition (EMT) and downstream cell-cycle factors, including c-Jun and cyclin-D1. Discussion: MYH9 expression was upregulated in samples with SCC. Furthermore, the in vitro assays demonstrated that MYH9 had roles in promoting the proliferation of the SCC Siha and C- 33A cell lines and inducing the migration and invasion of Siha cells via regulating EMT signals and downstream cell-cycle factors. Conclusion: MYH9 acts as an oncogenic gene in SCC, which promotes the carcinogenesis and progression of SCC cells via EMT signaling, and it may serve as a valuable patent for targeted treatment biomarker of SCC.
Yi et al. (Thu,) studied this question.