LINC00707通过靶向miR-382-5p/LRRK2轴来促进卵巢癌症细胞的多药耐药性。

IF 1.4 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Min-Wen Zhao, Chang-Jie Lin, Jian-Ping Qiu
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引用次数: 0

摘要

多药耐药性严重限制了卵巢癌症(OC)治疗的疗效。最近的研究揭示了LINC00707 RNA的致癌作用。然而,LINC00707在OC多药耐药性发展中的作用尚未阐明。因此,本研究的目的是研究LINC00707与OC多药耐药性之间的关系,这有助于开发新的治疗剂来有效解决这一问题。通过qRT-PCR检测SKOV3(人OC细胞系)细胞中LINC00707、miR-382-5p和富含亮氨酸重复激酶2(LRRK2)的RNA表达。通过MTT法和集落形成法测定LINC00707对SKOV3细胞增殖和活力的影响。LINC00707、miR-382-5p和LRRK2的相互作用是生物信息学预测的,并用双荧光素酶报告基因分析进行验证。此外,还探讨了LINC00707通过靶向miR-382-5p/LRRK2轴对SKOV3细胞耐药性的影响。LINC00707和LRRK2在SKOV3细胞中的表达显著增加,而miR-382-5p的表达显著降低。生物信息学预测和集落形成测定的结果表明,LINC00707可以通过靶向miR-382-5p来调节SKOV3细胞中LRRK2的表达。此外,敲低LINC00707显著增加了miR-382-5p的表达,降低了LRRK2的表达,增加了SKOV3细胞的细胞增殖和活力,以及对化疗药物的敏感性。值得注意的是,与单独敲低LINC00707相比,同时敲低LINC0707和miR-382-5p的这些表现更加明显。LINC00707在SKOV3细胞中过表达,并通过靶向miR-382-5p/LRRK2轴促进SKOV3的细胞增殖和对化疗药物的耐药性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LINC00707 promotes multidrug resistance of ovarian cancer cells by targeting the miR-382-5p/LRRK2 axis.

Multidrug resistance severely limits the efficacy of ovarian cancer (OC) treatment. Recent studies have revealed the carcinogenic role of LINC00707 RNA. However, the role of LINC00707 in the development of multidrug resistance in OC has not been clarified. Therefore, the aim of this study was to investigate the relationship between LINC00707 and multidrug resistance in OC, which can facilitate the development of new therapeutic agents for effectively addressing this issue. The RNA expression of LINC00707, miR-382-5p and leucine-rich repeat kinase 2 (LRRK2) in SKOV3 (a human OC cell line) cells was detected by qRT-PCR. The effects of LINC00707 on the proliferation and viability of SKOV3 cells were determined by MTT assay and colony formation assay. The interaction of LINC00707, miR-382-5p, and LRRK2 was bioinformatically predicted and verified with dual-luciferase reporter assay. In addition, the effect of LINC00707 on drug resistance in SKOV3 cells through targeting the miR-382-5p/LRRK2 axis was explored. The expression of LINC00707 and LRRK2 was significantly increased in SKOV3 cells, while miR-382-5p expression was significantly decreased. The results of bioinformatic prediction and colony formation assay demonstrated that LINC00707 could regulate LRRK2 expression in SKOV3 cells by targeting miR-382-5p. Additionally, knockdown of LINC00707 markedly increased expression of miR-382-5p and decreased that of LRRK2, increased cell proliferation and viability, as well as sensitivity to chemotherapeutic agents in SKOV3 cells. Notably, these manifestations were more obvious with simultaneous knockdown of LINC00707 and miR-382-5p compared with knockdown of LINC00707 alone. LINC00707 is overexpressed in SKOV3 cells and promotes SKOV3 cell proliferation and resistance to chemotherapeutic drugs via targeting the miR-382-5p/LRRK2 axis.

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来源期刊
Acta biochimica Polonica
Acta biochimica Polonica 生物-生化与分子生物学
CiteScore
2.40
自引率
0.00%
发文量
99
审稿时长
4-8 weeks
期刊介绍: Acta Biochimica Polonica is a journal covering enzymology and metabolism, membranes and bioenergetics, gene structure and expression, protein, nucleic acid and carbohydrate structure and metabolism.
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