Department of Oncology, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518036, China.
Comput Math Methods Med. 2021 Nov 27;2021:9674761. doi: 10.1155/2021/9674761. eCollection 2021.
In order to investigate the effect of lncRNA FOXD2-AS1 on breast cancer cells proliferation, migration, and drug resistance as well as its molecular mechanism.
Real-time PCR was used to detect the expression of breast cancer tissues and cells from patients admitted to our hospital and the expression of lncRNA FOXD2-AS1 in MCF-7/ADR in adriamycin- (ADR-) resistant breast cancer cells. After interfering with or overexpressing lncRNA FOXD2-AS1 in MCF-7/ADR cells, cell proliferation, apoptosis, invasion, and migration were detected using CCK-8, flow cytometry, Transwell assay, and scratch test, respectively. The protein levels of PI3K, p-PI3K, AKT, and p-AKT in the PI3K/AKT signaling pathway were detected by Western blot.
lncRNA FOXD2-AS1 was upregulated in breast cancer tissues and cells and increased cell drug resistance to ADR. Downregulation of lncRNA FOXD2-AS1 inhibited invasion and migration of MCF-7/ADR cells, promoted apoptosis, increased chemosensitivity of MCF-7/ADR cells, and inhibited the activity of PI3K/AKT signaling pathway in MCF-7/ADR cells.
lncRNA FOXD2-AS1 can promote the proliferation, invasion, migration, and drug resistance of breast cancer cells, inhibit apoptosis, and accelerate the development of breast cancer by positively regulating the PI3K/AKT signaling pathway.
探讨长链非编码 RNA FOXD2-AS1 对乳腺癌细胞增殖、迁移和耐药性的影响及其分子机制。
采用实时 PCR 检测我院收治的乳腺癌患者组织和细胞中 lncRNA FOXD2-AS1 的表达,以及阿霉素(ADR)耐药乳腺癌细胞 MCF-7/ADR 中 lncRNA FOXD2-AS1 的表达。干扰或过表达 MCF-7/ADR 细胞中的 lncRNA FOXD2-AS1 后,分别采用 CCK-8、流式细胞术、Transwell 实验和划痕实验检测细胞增殖、凋亡、侵袭和迁移,Western blot 检测 PI3K/AKT 信号通路中 PI3K、p-PI3K、AKT 和 p-AKT 的蛋白水平。
lncRNA FOXD2-AS1 在乳腺癌组织和细胞中上调,并增加了 ADR 对细胞的耐药性。下调 lncRNA FOXD2-AS1 抑制 MCF-7/ADR 细胞的侵袭和迁移,促进凋亡,增加 MCF-7/ADR 细胞的化疗敏感性,并抑制 MCF-7/ADR 细胞中 PI3K/AKT 信号通路的活性。
lncRNA FOXD2-AS1 可通过正向调控 PI3K/AKT 信号通路,促进乳腺癌细胞的增殖、侵袭、迁移和耐药性,抑制凋亡,加速乳腺癌的发展。