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目的探讨Ras相关蛋白23(Rab23)对Sa3鳞状细胞癌细胞侵袭能力的影响,以及Rab23是否通过调控Ras相关C3肉毒杆菌毒素底物1(Rac1)促进Sa3细胞的侵袭。方法用慢病毒感染的方式建立Rab23过表达和干涉的Sa3稳定感染细胞系。TranswellTM小室侵袭实验检测Rab23对Sa3细胞侵袭能力的影响;Western blot法检测Rab23对Rac1表达的影响;在稳定感染细胞系中加入Rac1抑制剂ⅡZ62954982后,进行TranswellTM小室侵袭实验检测Rac1在Rab23促进Sa3细胞侵袭中的作用。结果过表达Rab23可以显著增强Sa3细胞的侵袭能力,而干涉Rab23则显著降低Sa3细胞侵袭能力。Rab23促进Rac1的表达。Rac1抑制剂显著抑制Rab23对Sa3细胞侵袭的促进作用。结论 Rab23通过上调Rac1的表达促进Sa3细胞的侵袭。
Objective To investigate the effect of Ras-related protein 23 (Rab23) on the invasiveness of Sa3 cells and whether Rab23 could promote the invasion of Sa3 cells by regulating the Ras-associated C3 botulinum toxin substrate 1 (Rac1). Methods Rab3 overexpressing and interfering Sa3 stable infected cell lines were established by lentivirus infection. The effect of Rab23 on the expression of Rac1 was detected by Western blot and the invasion assay was performed by TranswellTM invasion assay. TranswellTM cell invasion assay was used to detect the effect of Rac1 on the invasion of Sa3 cells The role of invasion. Results Overexpression of Rab23 significantly enhanced the invasion ability of Sa3 cells, while interference with Rab23 significantly reduced the invasion ability of Sa3 cells. Rab23 promotes Rac1 expression. Rac1 inhibitor significantly inhibits the promotion of Rab23 on Sa3 cell invasion. Conclusion Rab23 promotes the invasion of Sa3 cells by up-regulating the expression of Rac1.