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lncRNA FOXD2-AS1 敲低抑制乳腺癌细胞的增殖、迁移和耐药性。

Knockdown of lncRNA FOXD2-AS1 Inhibits Proliferation, Migration, and Drug Resistance of Breast Cancer Cells.

机构信息

Department of Oncology, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518036, China.

出版信息

Comput Math Methods Med. 2021 Nov 27;2021:9674761. doi: 10.1155/2021/9674761. eCollection 2021.

Abstract

OBJECTIVE

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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

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.

摘要

目的

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。

方法

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。

结果

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。

结论

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e80/8643235/4288eb089f31/CMMM2021-9674761.001.jpg

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