RBM38 is negatively regulated by miR‑320b and enhances Adriamycin resistance in breast cancer cells
- Jing Ke
- Kan Ni
- Huimin Xue
- Jia Li
Affiliations: Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226021, P.R. China
- Published online on: November 19, 2021 https://doi.org/10.3892/ol.2021.13145
Copyright: © Ke
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Breast cancer (BC) is a common type of malignant tumor that is frequently accompanied by drug resistance, which is a significant challenge in the treatment of BC. Adriamycin (ADM) is a commonly used drug for the treatment of BC. The aim of the present study was to demonstrate the association between RNA binding motif protein 38 (RBM38) and ADM resistance in BC. The results revealed that the expression levels of RBM38 were significantly upregulated in ADM‑resistant BC tissues and the ADM‑resistant cell line, MCF‑7/A, as demonstrated using reverse transcription‑quantitative PCR and western blotting. In addition, the results of the MTT assay revealed that the overexpression of RBM38 enhanced the resistance of MCF‑7/A cells to ADM, promoted invasiveness, as determined using a Transwell assay, inhibited the apoptosis of resistant cells, as determined using flow cytometry, and accelerated cell cycle progression from the G0 to the S phase. The results of the dual luciferase reporter assay demonstrated the binding relationship between microRNA (miR)‑320b and RBM38, and the expression levels of miR‑320b were significantly downregulated in ADM‑resistant BC tissues and MCF‑7/A cells. Overexpression of miR‑320b reversed ADM resistance, suppressed invasiveness, promoted apoptosis and arrested MCF‑7/A cells in the G0 phase. In addition, RBM38 was discovered to be negatively regulated by miR‑320b, which was able to restore the sensitivity of BC cells to ADM by downregulating RBM38. Further exploration of the underlying regulatory mechanism revealed that the miR‑320b/RBM38 signaling axis mediated the development of ADM resistance in BC by altering the expression of cell cycle‑, drug resistance‑ and PI3K/AKT signaling pathway‑related proteins. In conclusion, the results of the present study suggested that RBM38 may be negatively regulated by miR‑320b, which accelerates drug resistance in BC.