Objective: To explore the role of RN181 in the pathogenesis of oral squamous cell carcinoma (OSCC) cells via mediating ERK/MAPK signaling.
Methods: The expression of RN181 was detected in OSCC tissues and cells. CAL27 and SCC-15 cells were divided into Control, Empty, RN181, si-RN181, U0126 (an inhibitor of ERK/MAPK pathway) and si-RN181 + U0126 groups. MTT was used to determine cell proliferation, flow cytometry to determine cell cycle and apoptosis, Transwell assay and wound healing test to determine cell invasion and migration, respectively. Western blotting was used to measure the protein expression. Furthermore, a xenograft tumor model was established to observe the effect of RN181 on the in vivo growth of OSCC cells.
Results: RN181 was down-regulated in OSCC tissues and cells. As compared to the Control group, CAL27 and SCC-15 cells in the RN181 group and U0126 group presented with decreases in the proliferation, invasion and migration, but increases in the cell ratio at the G0/G1 phase and apoptosis, while the p-ERK 1/2/ERK 1/2 was down-regulated. Cells in the si-RN181 group manifested the opposite changes. U0126 could reverse the positive effect of si-RN181 on the growth of OSCC cells. In vivo experiment demonstrated that the tumor growth and weight were reduced in the RN181 group, with decreased Ki67 positive expression and elevated TUNEL positive cells.
Conclusion: RN181 was down-regulated in OSCC, and it could inhibit the proliferation, invasion and migration, cause the G0/G1 arrest, while promote the apoptosis of OSCC cells via inhibiting ERK/MAPK pathway.
Keywords: ERK/MAPK signaling pathway; OSCC; RN181.
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