CSE1L promotes proliferation and migration in oral cancer through positively regulating MITF.

OBJECTIVE: CSE1L (human chromosomal segregation 1-like) is reported to be able to affect cell apoptosis, invasiveness, and migration. The purpose of this study was to uncover the regulatory effects of CSE1L on cell phenotypes of oral cancer and the underlying mechanism.

MATERIALS AND METHODS: CSE1L levels in oral cancer cells were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. CSE1L overexpression and knockdown models were constructed in CAL-27 and HN6 cells, respectively. Changes in proliferative and migratory abilities in oral cancer cells affected by CSE1L and microphthalmia-associated transcription factor (MITF) were assessed by cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and wound healing assay. Meanwhile, potential influences of CSE1L and MITF on relative levels of E-cadherin and Vimentin in oral cancer cells were detected. Finally, regulatory effects of CSE1L and MITF on the Akt/mTOR pathway were evaluated by detecting expression levels of p-Akt, Akt, p-mTOR, and mTOR.

RESULTS: CSE1L was upregulated in oral cancer cells. Knockdown of CSE1L in HN6 cells attenuated proliferative and migratory abilities, as well as downregulated Vimentin and upregulated E-cadherin. Overexpression of CSE1L in CAL-27 cells yielded the opposite results. MIFT level was positively regulated by CSE1L. Overexpression of MITF partially reversed regulatory effects of CSE1L on proliferative ability of oral cancer cells. Moreover, silence of CSE1L suppressed the Akt/mTOR pathway, which was reversed by overexpression of MITF.

CONCLUSIONS: CSE1L promotes the proliferative and migratory abilities in oral cancer cells by positively regulating MITF, thus activating the Akt/mTOR pathway.