Department of Thyroid and Breast Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
J BUON. 2020 Mar-Apr;25(2):621-626.
A number of studies have provided concrete evidence about the role of Long noncoding RNAs (LncRNAs) in the development and progression of cancer. As such LncRNAs are believed to exhibit the potential to be used as therapeutic targets for the treatment of cancer. This study was undertaken to investigate the role and therapeutic implication of LncRNA PCAT29 in triple-negative breast cancer.
The breast cancer cell lines MDA-MB-231, MDA-MB-436, BT20, HCC70 and HCC38 and non-cancer cell line MB157 were used in this study. Gene expression analysis was performed by qRT-PCR. Cell proliferation was monitored by MTT and colony formation assays. Apoptosis was detected by annexin V/propidium iodide (PI) assay. Cell migration and Invasion was detected by wound heal and transwell assays.
The expression of LncRNA PCAT29 was significantly suppressed in the breast cancer tissues and the triple-negative breast cancer cell lines. PCAT29 overexpression caused inhibition of the proliferation rate and colony formation of the MDA-MB-231 cells. The proliferation of MD-MB-231 cells was inhibited by apoptotic cell death which was accompanied by elevation of Bax and depletion of Bcl-2 expression. The wound healing assay showed that PCAT29 caused remarkable inhibition of the MDA-MB-231 cell migration. The transwell assay showed that PCAT29 overexpression resulted in 65% inhibition of the MDA-MB-231 cell invasion.
PCAT29 regulates the proliferation, migration and invasion of breast cancer cells and may point to a novel therapeutic target in triple-negative breast cancer.
许多研究为长链非编码 RNA（LncRNA）在癌症的发生和发展中的作用提供了具体证据。因此，LncRNA 被认为具有作为癌症治疗的治疗靶点的潜力。本研究旨在探讨 LncRNA PCAT29 在三阴性乳腺癌中的作用和治疗意义。
本研究使用了乳腺癌细胞系 MDA-MB-231、MDA-MB-436、BT20、HCC70 和 HCC38 以及非癌细胞系 MB157。通过 qRT-PCR 进行基因表达分析。通过 MTT 和集落形成测定监测细胞增殖。通过 Annexin V/PI 检测法检测细胞凋亡。通过划痕愈合和 Transwell 测定法检测细胞迁移和侵袭。
LncRNA PCAT29 在乳腺癌组织和三阴性乳腺癌细胞系中的表达明显受到抑制。PCAT29 的过表达导致 MDA-MB-231 细胞的增殖率和集落形成受到抑制。增殖的 MD-MB-231 细胞通过凋亡细胞死亡受到抑制，同时伴随着 Bax 的升高和 Bcl-2 表达的耗尽。划痕愈合试验表明，PCAT29 导致 MDA-MB-231 细胞迁移显著抑制。Transwell 测定表明，PCAT29 的过表达导致 MDA-MB-231 细胞侵袭抑制了 65%。
PCAT29 调节乳腺癌细胞的增殖、迁移和侵袭，可能为三阴性乳腺癌提供新的治疗靶点。
