lncRNA HSD52在卵巢癌组织中的表达及其对卵巢癌细胞增殖和侵袭的影响

Expression of lncRNA HSD52 in ovarian cancer tissue and its effect on proliferation and invasion of ovarian cancer cells

目的观察长链非编码RNA(long-chain non-coding RNA,lncRNA)HSD52在卵巢癌组织的表达,探讨lncRNA HSD52对卵巢癌细胞增殖和侵袭能力的影响及分子作用机制。方法实时荧光定量聚合酶链反应(qRT-PCR)检测lncRNA HSD52在卵巢癌组织、5种卵巢癌细胞株中的表达。将载有lncRNA HSD52序列的质粒和阴性对照质粒分别转染至lncRNA HSD52表达最低的卵巢癌细胞,分别命名为实验组和对照组。MTT法、Matrigel侵袭实验分别检测上调lncRNA HSD52对卵巢癌细胞增殖、侵袭能力的影响。生物信息学软件预测lncRNA HSD52的分子作用机制。qRT-PCR和Western Blot检测上调lncRNA HSD52对下游基因表达的影响。结果 lncRNA HSD52在卵巢癌组织中的表达明显低于癌旁组织(P <0.01)。lncRNA HSD52在卵巢癌细胞株中的表达明显低于正常卵巢上皮细胞(P<0.05),SKOV-3细胞中lncRNA HSD52的表达最低(P <0.01)。上调lncRNA HSD52可明显抑制SKOV-3细胞的增殖(P <0.05)和侵袭能力(P <0.01)。生物信息学软件显示,lncRNA HSD52可配对结合miR-498-5p,miR-498-5p可配对结合内皮素3(Endothelin 3,EDN3)。上调lncRNA HSD52可明显降低SKOV-3细胞中miR-498-5p的表达(P <0.01),增加EDN3 mRNA和蛋白的表达(P <0.01)。结论 lncRNA HSD52在卵巢癌组织和细胞株中低表达,上调lncRNA HSD52可明显抑制卵巢癌细胞系SKOV-3的增殖和侵袭能力,其分子作用机制可能是lncRNA HSD52特异性吸附miR-498-5p间接调控EDN3基因的表达。

Objective To observe the expression of long-chain non-coding RNA(lncRNA)HSD52 in ovarian cancer tissues,and to explore the effect and molecular mechanism of lncRNA HSD52 on the proliferation and invasion ability of ovarian cancer cells. Methods Real-time fluorescent quantitative polymerase chain reaction(qRT-PCR)was used to detect the expression of lncRNA HSD52 in ovarian cancer tissues and five ovarian cancer cell lines. The plasmid carrying the lncRNA HSD52 sequence and the negative control plasmid were transfected into ovarian cancer cells with the lowest lncRNA HSD52 expression,respectively,and were included into experimental group and control group,respectively. MTT method and Matrigel invasion test were used to detect the effects of up-regulation of lncRNA HSD52 on the proliferation and invasion ability of ovarian cancer cells. Bioinformatics software was employed to predict the molecular mechanism of lncRNA HSD52. qRT-PCR and Western Blot were used to detect the effects of up-regulated lncRNA HSD52 on downstream gene expression. Result The expression of lncRNA HSD52 in ovarian cancer tissue was significantly lower than that in adjacent tissues(P < 0.01). The expression of lncRNA HSD52 in ovarian cancer cell lines was significantly lower than that in normal ovarian epithelial cells(P < 0.05),and the expression of lncRNA HSD52 was the lowest in SKOV-3 cells(P < 0.01). Upregulation of lncRNA HSD52 can significantly inhibit the proliferation(P < 0.05)and invasive ability of SKOV-3 cells(P < 0.01). Bioinformatics showed that lncRNA HSD52 can pair with miR-498-5 p,and miR-498-5 p can pair with endothelin 3(EDN3). Up-regulation of lncRNA HSD52 can significantly reduce the expression of miR-498-5 p in SKOV-3 cells(P < 0.01)but increase the expression of EDN3 m RNA and protein(P < 0.01). Conclusions lncRNA HSD52 is lowly-expressed in ovarian cancer tissues and cell lines. The up-regulation of lncRNA HSD52 can significantly inhibit the proliferation and invasion of ovarian cancer cell line SKOV-3. The molecular mechanism may be that lncRNA HSD52 specifically adsorbs miR-498-5 p to indirectly regulate EDN3 expression.