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. 2021 Nov 27:2021:9674761.
doi: 10.1155/2021/9674761. eCollection 2021.

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

Qiaohong Nong  1 , Shaokang Yu  1 , Hui Hu  1 , Xue Hu  1
Affiliations

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

Qiaohong Nong et al. Comput Math Methods Med. .

Retraction in

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.

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Conflict of interest statement

The authors claim that there is no conflict of interest between them.

Figures

Figure 1
Figure 1
lncRNA FOXD2-AS1 highly expressed in breast cancer. (a) qRT-PCR detects the expression of lncRNA FOXD2-AS1 in breast cancer tissues and paracancer tissues; ∗∗P < 0.01, n = 60 per group. (b) The expression of lncRNA FOXD2-AS1 in normal breast cells (MCF-10A), breast cancer cells (MCF-7), and adriamycin-resistant strains of breast cancer was detected by qRT-PCR; ∗∗P < 0.01vs. the MCF-10A group, ##P < 0.01vs. MCF-7 group; (c) CCK-8 assay was used to detect cell viability. (d) The IC50 values in both cells; ∗∗P < 0.01vs. MCF-7 groups.
Figure 2
Figure 2
The effect of lncRNA FOXD2-AS1 on the invasion, migration, and apoptosis of MCF-7/ADR cells. (a) The expression of lncRNA FOXD2-AS1 in each group of MCF-7/ADR cells was detected by qRT-PCR; ∗P < 0.05vs. the MCF-7/ADR-vector group; ##P < 0.01 vs. the MCF-7/ADR-siNC group; (b) Transwell assay was used to evaluate the invasion ability of MCF-7/ADR cells in each group. (c) Scratch test was performed to detect the migration ability of MCF-7/ADR cells in each group; ∗∗P < 0.01vs. the MCF-7/ADR-NC group. (d) Flow cytometry was conducted to detect apoptosis of MCF-7/ADR cells in each group; ∗∗P < 0.01vs. the vector group; ##P < 0.01vs. the siNC group.
Figure 3
Figure 3
The effect of lncRNA FOXD2-AS1 expression on the chemical sensitivity of MCF-7-ADR cells. CCK-8 assay was used to detect the cell survival rate of each group of MCF-7/ADR cells under ADR (a), DDP (b), and 5-FU (c) treatment; CCK-8 assay was used to detect the IC50 value of cells of each group of MCF-7/ADR cells under ADR (d), DDP (e), and 5-FU (f) treatment. ∗P < 0.05vs. the MCF-7/ADR-vector group; ##P < 0.01vs. the MCF-7/ADR-siNC group.
Figure 4
Figure 4
The effect of lncRNA FOXD2-AS1 on the PI3K/AKT signaling pathway in MCF-7/ADR cells. The protein expression of p-PI3K, PI3K, p-AKT, and AKT in the ADR-resistant cells (MCF-7) was detected using Western blot. ∗∗P < 0.01vs. the vector group; ##P < 0.01vs. the siNC group.
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