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.

中文翻译：

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RN181通过介导ERK/MAPK信号通路调控口腔鳞癌细胞生物学行为

客观的

探讨RN181通过介导ERK/MAPK信号通路在口腔鳞状细胞癌（OSCC）细胞发病机制中的作用。

方法

在OSCC组织和细胞中检测到RN181的表达。CAL27 和 SCC-15 细胞分为 Control、Empty、RN181、si-RN181、U0126（ERK/MAPK 通路抑制剂）和 si-RN181 + U0126 组。MTT用于确定细胞增殖，流式细胞仪用于确定细胞周期和细胞凋亡，Transwell测定和伤口愈合试验用于确定细胞侵袭和迁移，分别。Western印迹用于测量蛋白质表达。此外，建立异种移植肿瘤模型，观察RN181对OSCC细胞体内生长的影响。

结果

RN181 在 OSCC 组织和细胞中下调。与对照组相比，RN181组和U0126组CAL27、SCC-15细胞增殖、侵袭、迁移减少，G0/G1期细胞比例和凋亡增加，而p- ERK 1/2/ERK 1/2 被下调。si-RN181 组的细胞表现出相反的变化。U0126可以逆转si-RN181对OSCC细胞生长的积极作用。体内实验表明，RN181组的肿瘤生长和重量减少，Ki67阳性表达减少，TUNEL阳性细胞升高。

结论

RN181在OSCC中表达下调，可通过抑制ERK/MAPK通路抑制OSCC细胞的增殖、侵袭和迁移，引起G0/G1期阻滞，同时促进OSCC细胞的凋亡。