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Long non-coding RNA PVT1 regulates the proliferation and metastasis of human breast cancer via the Wnt/b-catenin signalling pathway

PVT1型 癌症研究 Wnt信号通路 乳腺癌 癌细胞 癌症 医学 转移 细胞生长 细胞凋亡 长非编码RNA 分子生物学 生物 基因 下调和上调 细胞生物学 信号转导 内科学 遗传学
作者
Nian-Qu Zhang,Qing Li,Shanmei Sun
出处
期刊:Archives of Medical Science [Termedia Sp. z.o.o.]
标识
DOI:10.5114/aoms/126557
摘要

Introduction The development of many human diseases has been implicated to be coupled by the dysregulation of long non-coding RNAs (lncRNAs). Considering this, the current study was aimed at identifying and then investigating the molecular role of a specific lncRNA from a set of such genetic elements in regulating the developmental aspects of human breast cancer. Material and methods The quantitative real-time polymerase chain reaction (qRT-PCR) method was used to deduce the gene expression levels. Proliferation of cancer cells was determined by the cell counting kit 8 (CCK8). The evaluation of apoptotic cell death in breast cancer cells was made through the acridine orange/ethidium bromide (AO/EB) and annexin V-FITC staining protocols. Transwell assays were used to monitor cell migration and invasion. Results Estimation of gene expression levels of a set of lncRNAs showed that lncRNA PVT1 is specifically overexpressed in the breast cancer tissues and cell lines. The downregulation of PVT1 in cancer cells negatively affected their proliferation rates, and cancer cells exhibited significantly lower viabilities due to induction of Bax/Bcl-2 signal arbitrated apoptotic cell death in the cancer cells. Moreover, the cancer cells showed significantly lower rates of migration and invasion when lncRNA PVT1 was repressed. The PVT1 repression-driven anti-cancer effects against the cancer cells were seen to be modulated through the Wnt/β-catenin signalling pathway. Conclusions The results of this work are indicative of the prognostic role of lncRNA PVT1 in breast cancer. Also, the molecular targeting of PVT1 might prove to be a vital step against the progression of human breast cancer.

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