Downregulation of TMOD1 promotes cell motility and cell proliferation in cervical cancer cells.

Abstract

Tropomodulin-1 (TMOD1) is a key regulator of actin dynamics, which caps the pointed end of actin filaments. TMOD1 has been reported to be involved in several cellular processes, including neurite outgrowth, spine formation and cell migration. Increasing evidence demonstrates that TMOD1 is implicated in several aspects of cancer development. The present study aimed to investigate the role of TMOD1 in cervical cancer. HeLa and CaSki cell lines, derived from human cervical cancer, were used to evaluate the function of TMOD1. Cell motility was measured via a wound-healing assay, with the TMOD1 short hairpin (sh)RNAs transfected cells. Subsequently, cell proliferation was assessed using low serum cell culture condition, while cell cycle distribution was analyzed via flow cytometry. The results demonstrated that downregulated TMOD1 promoted cell motility and proliferation, which is attributed to promotion of G1/S phase transition in HeLa and CaSki cells. Furthermore, it was indicated that co-expression of shRNA resistant TMOD1 rescued these phenomena. The clinical data demonstrated that high TMOD1 expression is associated with good pathological status in patients with cervical cancer. Overall, the results of the present study indicated that TMOD1 may act as a tumor suppressor in cervical cancer, whereby its downregulated expression was demonstrated to have direct effects on cell motility and cell proliferation. These results provide new evidence for the prognostic prediction of cervical cancer, which may serve as a promising therapeutic strategy for patients with cervical cancer.