首页> 外文期刊>European review for medical and pharmacological sciences. >Long noncoding RNA-JPX predicts the poor prognosis of ovarian cancer patients and promotes tumor cell proliferation, invasion and migration by the PI3K/Akt/mTOR signaling pathway
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Long noncoding RNA-JPX predicts the poor prognosis of ovarian cancer patients and promotes tumor cell proliferation, invasion and migration by the PI3K/Akt/mTOR signaling pathway

机译:较长的非编码RNA-JPX通过PI3K / Akt / mTOR信号通路预测卵巢癌患者预后不良,并促进肿瘤细胞增殖,侵袭和迁移

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OBJECTIVE: To investigate the clinical functions and the detailed mechanism of long noncoding RNA (lncRNA) JPX in human ovarian cancer cell lines. PATIENTS AND METHODS: The expression of JPX in ovarian cancer tissues and cell lines was detected by Real-time polymerase chain reaction (RT-PCR). The correlation between JPX expression and prognosis was analyzed by follow-up data. The OVCAR-3 cell proliferation, invasion and migration were measured by methyl thiazolyl tetrazolium (MTT) assay, cloning formation assay and scratch assay. The cell apoptosis was detected by Bcl-2, Bax, and Caspase-3 activity. PI3K/mTOR inhibitor treatment and Western blot proved that JPX functions associated with PI3K/Akt/mTOR signaling and test the protein levels of p-PI3K, p-Akt, p-mTOR. RESULTS: RT-PCR results showed that the expression of JPX was upregulated in ovarian cancer tissues and ovarian cancer cell lines (p 0.05), and it was significantly increased in large tumor tissues and metastatic lymph nodes (p 0.05). The survival rate of high JPX expression patients was much lower than low JPX expression patients (p 0.05), indicating that high expression of JPX predicted poor prognosis in patients with ovarian cancer. MTT assay, colony formation and scratch assay showed the repression of JPX and resulted with significantly decreased in cell proliferation, invasion and migration of OVCAR-3 cells compared with the control (p 0.05). PI3K/mTOR inhibitor treatment showed overexpression of JPX could activate the PI3K/Akt/mTOR signaling pathway. Western blot assay showed that the expressions of p-PI3K, p-Akt, p-mTOR were significantly increased after overexpression of JPX (p 0.05), and after the inhibition of PI3K/Akt/mTOR signaling pathway and overexpression of JPX, the tumor cell proliferation, invasion and migration were significantly repressed, compared with the control (p 0.05). CONCLUSIONS: JPX could predict the poor prognosis in patients with ovarian cancer, which could promote the tumor cell proliferation, invasion and migration in human ovarian cancer cell lines and inhibited the cell apoptosis through activating PI3K/Akt/mTOR signaling pathway.
机译:目的:探讨长链非编码RNA(IncRNA)JPX在人卵巢癌细胞系中的临床功能和详细机制。病人和方法:通过实时聚合酶链反应(RT-PCR)检测JPX在卵巢癌组织和细胞系中的表达。通过随访数据分析了JPX表达与预后之间的相关性。 OVCAR-3细胞的增殖,侵袭和迁移通过甲基噻唑基四唑(MTT)测定,克隆形成测定和刮擦测定来测量。通过Bcl-2,Bax和Caspase-3活性检测细胞凋亡。 PI3K / mTOR抑制剂的处理和Western blot证明JPX功能与PI3K / Akt / mTOR信号相关,并测试p-PI3K,p-Akt,p-mTOR的蛋白质水平。结果:RT-PCR结果显示,JPX在卵巢癌组织和卵巢癌细胞系中表达上调(p <0.05),在大肿瘤组织和转移性淋巴结中明显升高(p <0.05)。高JPX表达患者的生存率远低于低JPX表达患者(p <0.05),表明高表达JPX预测卵巢癌患者预后不良。 MTT法,集落形成和刮擦法显示出JPX的抑制,并且与对照相比,OVCAR-3细胞的细胞增殖,侵袭和迁移显着降低(p <0.05)。 PI3K / mTOR抑制剂治疗表明JPX的过表达可以激活PI3K / Akt / mTOR信号通路。 Western blot检测表明,JPX过表达后p-PI3K,p-Akt,p-mTOR的表达显着增加(p <0.05),PI3K / Akt / mTOR信号通路被抑制和JPX过表达后,p-PI3K,p-Akt,p-mTOR的表达显着增加。与对照组相比,肿瘤细胞的增殖,侵袭和迁移得到了显着抑制(p <0.05)。结论:JPX可预测卵巢癌患者的预后不良,可通过激活PI3K / Akt / mTOR信号通路促进卵巢癌细胞株肿瘤细胞的增殖,侵袭和迁移,并抑制其凋亡。

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