Downregulated miR‑130a enhances the sensitivity of acute myeloid leukemia cells to Adriamycin
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Published on: June 17, 2022
Huimin Liu1, Min Liu1, Jiangzhao Zhang1
1Department of Hematology, Jingzhou Central Hospital, Jingzhou, Hubei 434020, P.R. China.
Abstract:
MicroRNA (miR)‑130a has been reported to promote cancer growth; however, its role during acute myeloid leukemia (AML) is not completely understood. In the present study, the effects of miR‑130a on the sensitivity of AML cells to Adriamycin (Adr) were investigated. 5‑Aza‑2'‑deoxycytidine (5‑Aza‑dC) was used to stimulate Adr resistance in AML cells, and cell viability and miR‑130a expression were determined using the Cell Counting Kit‑8 (CCK‑8) assay and reverse transcription‑quantitative PCR, respectively. miR‑130a overexpression and knockdown in Adr‑resistant AML cells was performed to investigate the proliferative and invasive abilities of the cells using CCK‑8 and Transwell assays, respectively. Furthermore, the effects of miR‑130a on the expression of epithelial‑mesenchymal transition (EMT)‑related proteins in Adr‑resistant AML cells were detected using western blot analysis. Pre‑treatment with 5‑Aza‑dC enhanced the cell viability and miR‑130a expression of Adr‑treated AML cells. Adr and miR‑130a expression showed a dose‑dependent relationship, with miR‑130a expression decreasing with increasing Adr concentrations. Moreover, miR‑130a overexpression alleviated the inhibitory effects of Adr on cell viability and invasion, while miR‑130a knockdown enhanced the sensitivity of AML cells to Adr. Furthermore, Adr exerted an inhibitory effect on EMT in AML cells, which was rescued by miR‑130a overexpression and enhanced by miR‑130a knockdown. miR‑130a knockdown also increased the sensitivity of AML cells to Adr by decreasing cell viability, invasion and EMT. Therefore, miR‑130a knockdown is a potential therapeutic strategy for Adr‑resistant AML.
Insights
MicroRNA-130a (miR-130a) plays a role in acute myeloid leukemia (AML) drug resistance. Knocking down miR-130a enhances Adriamycin (Adr) sensitivity in AML cells, suggesting it as a potential therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA (miR)-130a's role in cancer growth is known, but its specific function in acute myeloid leukemia (AML) remains unclear.
- Understanding miR-130a's impact on AML cell sensitivity to chemotherapy is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the effect of miR-130a on the sensitivity of AML cells to Adriamycin (Adr).
- To explore miR-130a's influence on cell viability, invasion, and epithelial-mesenchymal transition (EMT) in Adr-resistant AML cells.
Main Methods:
- AML cells were treated with 5-Aza-2'-deoxycytidine (5-Aza-dC) to induce Adriamycin (Adr) resistance.
- Cell Counting Kit-8 (CCK-8) and Transwell assays were used to assess cell viability and invasion.
- Reverse transcription-quantitative PCR and western blot analysis were employed to measure miR-130a and epithelial-mesenchymal transition (EMT)-related protein expression.
Main Results:
- Pre-treatment with 5-Aza-dC increased cell viability and miR-130a expression in Adr-treated AML cells.
- miR-130a overexpression reduced Adr's inhibitory effects on cell viability and invasion, while miR-130a knockdown increased sensitivity to Adr.
- miR-130a modulated the epithelial-mesenchymal transition (EMT) process in Adr-resistant AML cells, with knockdown enhancing Adr sensitivity.
Conclusions:
- miR-130a overexpression alleviates Adriamycin (Adr) resistance in acute myeloid leukemia (AML) cells.
- miR-130a knockdown enhances AML cell sensitivity to Adr by reducing viability, invasion, and epithelial-mesenchymal transition (EMT).
- Targeting miR-130a presents a potential therapeutic strategy for overcoming Adr resistance in AML.
