Lnc-CRCMSL在结直肠癌中的表达及对癌细胞生长的影响

Expression of Lnc-CRCMSL in colorectal cancer cells and its effect on cancer cell growth

目的探讨长链非编码RNA-CRCMSL(Lnc-CRCMSL)在结直肠癌组织和癌细胞中的表达及对癌细胞生长的影响。方法采用实时定量PCR(qRT-PCR)检测Lnc-CRCMSL在结肠癌组织和癌旁正常组织、正常结肠上皮细胞及结直肠癌细胞中的表达特点。建立SW480耐药株SW480/DDP,并通过基因干扰实验过表达其Lnc-CRCMSL水平,采用流式细胞术测定细胞的凋亡率,CCK-8测定细胞的增殖活力,划痕愈合实验测定细胞的迁移能力,Transwell测定细胞的侵袭能力,免疫蛋白印迹实验测定基质金属蛋白酶2(MMP2)和基质金属蛋白酶9(MMP9)的蛋白表达。结果 Lnc-CRCMSL在结直肠癌组织的表达低于癌旁正常组织,在Ⅱ期、Ⅲ期结直肠癌组织中的表达低于Ⅰ期,且在结直肠癌细胞中的表达量低于正常结肠上皮细胞(P<0.05)。过表达Lnc-CRCMSL提高了SW480/DDP的凋亡率,抑制了SW480/DDP的增殖、迁移和侵袭活力(P<0.05)。同时,过表达Lnc-CRCMSL降低了SW480/DDP的MMP2和MMP9表达水平(P<0.05)。结论 Lnc-CRCMSL在结直肠癌中表达异常,对结直肠癌细胞的增殖、凋亡、迁移及侵袭行为具有调控作用。

Aim To investigate the expression of long non-coding RNA-CRCMSL(Lnc-CRCMSL) in colorectal cancer and cancer cells and its effect on cancer cell growth. Methods The expression of Lnc-CRCMSL in colon cancer tissues and adjacent healthy tissues, normal colon epithelial cells and colorectal cancer cells was detected by real-time quantitative PCR(qRT-PCR). SW480 resistant strain SW480/DDP was established, and the Lnc-CRCMSL level of SW480/DDP was overexpressed by gene interference. The apoptosis, proliferation, migration, and invasion of SW480/DDP cells were determined by flow cytometry, CCK-8 assay, scratch test, and Transwell chamber assay. Results The expression of Lnc-CRCMSL in colorectal cancer tissues was lower than that in adjacent healthy tissues, the expression of LNC-CRCMSL in stage Ⅱ and Ⅲ tissues was lower than that in stage I, and the expression level in colorectal cancer cells was lower than that in normal colon epithelial cells(P<0.05). Lnc-CRCMSL overexpression increased the apoptosis rate of SW480/DDP, while inhibited the proliferation, migration, and invasion activity of SW480/DDP(P<0.05). Meanwhile, Lnc-CRCMSL overexpression decreased the expression levels of MMP2 and MMP9 in SW480/DDP(P<0.05). Conclusion Lnc-CRCMSL showed abnormal expression in colorectal cancer, and may regulate the proliferation, apoptosis, migration and invasion of colorectal cancer cells.