MicroRNA-27b reverses docetaxel resistance of non-small cell lung carcinoma cells via targeting epithelial growth factor receptor

Chen, Shi; Wang, Qian; Zhou, Xianmei; Zhu, Ji-Xiao; Liu, Tian; Huang, Mao

doi:10.3892/mmr.2016.5332

Cited by 10 publications

(5 citation statements)

References 28 publications

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“…76 MiR-27b is shown to probably enhance cell viability and promote cell resistance to docetaxel treatment of NSCLC through directly targeting EGFR expression. Therefore, miR-27b may be a promising target for improving the effectiveness of docetaxel 77 (Table 1). Esophageal cancer patients accompanied with high level of miR-27b exert resistance to cisplatin and significantly correlate with shorter survival after treatment with cisplatin.…”

Section: Egfrmentioning

confidence: 99%

Promising therapeutic role of miR-27b in tumor

Ding

Yang

et al. 2017

Tumour Biol.

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MicroRNAs are small nonprotein-encoding RNAs ranging from 18 to 25 nucleotides in size and regulate multiple biological pathways via directly targeting a variety of associated genes in cancers. MicroRNA-27b is a highly conserved MicroRNA throughout vertebrates and there are two homologs (hsa-miR-27a and hsa-miR-27b) in humans. MicroRNA27b is an intragenic microRNA located on chromosome 9q22.1 within the C9orf3 gene, clustering with miR-23b and miR-24-1 in human. As a frequently dysregulated microRNA in human cancers, microRNA-27b could function as a tumor suppressor or an oncogenic microRNA. More and more studies indicate that microRNA-27b is involved in affecting various biological processes, such as angiogenesis, proliferation, metastasis, and drug resistance, and thus may act as a promising therapeutic target in human cancers. In this review, we discuss the role of microRNA-27b in detail and offer novel insights into molecular targeting therapy for cancers.

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Section: Egfrmentioning

confidence: 99%

Promising therapeutic role of miR-27b in tumor

Ding

Yang

et al. 2017

Tumour Biol.

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“…Studies in other cancer types have identified a number of miRNAs associated with docetaxel resistance. In non‐small cell lung cancer, increased expression of miR‐27b was found to promote docetaxel resistance through inhibition of EGFR expression . Zhang et al found that miR‐3646, miR‐3658, miR‐4438, miR‐1246, and miR‐574‐3p are all upregulated in docetaxel resistant breast cancer cells and inhibition of miR‐3646 was demonstrated to improve treatment response.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐181a promotes docetaxel resistance in prostate cancer cells

et al. 2017

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Background Docetaxel is one of the primary drugs used for treating castration resistant prostate cancer (CRPC). Unfortunately, over time patients invariably develop resistance to docetaxel therapy and their disease will continue to progress. The mechanisms by which resistance develops are still incompletely understood. This study seeks to determine the involvement of miRNAs, specifically miR-181a, in docetaxel resistance in CRPC. Methods Real-time PCR was used to measure miR-181a expression in parental and docetaxel resistant C4-2B and DU145 cells (TaxR and DU145-DTXR). miR-181a expression was modulated in parental or docetaxel resistant cells by transfecting them with miR-181a mimics or antisense, respectively. Following transfection, cell number was determined after 48 h with or without docetaxel. Cross resistance to cabazitaxel induced by miR-181a was also determined. Western blots were used to determine ABCB1 protein expression and rhodamine assays used to assess activity. Phospho-p53 expression was assessed by western blot and apoptosis was measured by ELISA in C4-2B TaxR and PC3 cells with inhibited or overexpressed miR-181a expression with or without docetaxel. Results miR-181a is significantly overexpressed in TaxR and DU145-DTXR cells compared to parental cells. Overexpression of miR-181a in parental cells confers docetaxel and cabazitaxel resistance and knockdown of miR-181a in TaxR cells re-sensitizes them to treatment with both docetaxel and cabazitaxel. miR-181a was not observed to impact ABCB1 expression or activity, a protein which was previously demonstrated to be highly involved in docetaxel resistance. Knockdown of miR-181a in TaxR cells induced phospho-p53 expression. Furthermore, miR-181a knockdown alone induced apoptosis in TaxR cells which could be further enhanced by the addition of DTX. Conclusions Overexpression of mir-181a in prostate cancer cells contributes to their resistance to docetaxel and cabazitaxel and inhibition of mir-181a expression can restore treatment response. This is due, in part, to modulation of p53 phosphorylation and apoptosis.

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“…At present, many studies have shown that miR-27b plays an important biological role in the growth, invasiveness and metastasis of colon cancer, bladder cancer, renal cell cancer and lung cancer. Its low expression in tumor cells is closely related to the proliferation and high invasiveness of tumor cells [ 22 , 33 – 36 ]. The expression of microRNA-27b is regulated by a variety of factors.…”

Section: Discussionmentioning

confidence: 99%

“…The total reaction system was 10 μL. qRT-PCR parameters were: 95 °C denaturation for 30 s, and 60 °C annealing for 40 s, for a total of 36 cycles [ 22 ].…”

Section: Methodsmentioning

confidence: 99%

Effect of miR-27b on the proliferation and apoptosis of diffuse large b-cell lymphoma cells by targeting the regulation of MET/PI3K/AKT pathway

Zhang

Huang

et al. 2022

Discov Onc

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Background This study aimed to explore the regulation of miR-27b expression on MET/PI3K/AKT pathway, and to explain its effect on biological functions of DLBCL cells. Methods The expressions of miR-27b and MET gene in DLBCL cells and normal human B cell lines were determined by qRT-PCR. miR-27b expression in DLBCL cell line Toledo was over-expressed with the cell transfection method. The proliferation of DLBCL cells was determined by MTT. And the invasiveness of DLBCL cells was determined by Transwell. The level of apoptosis in DLBCL cells was determined by ELISA. miR-27b targeting of MET was verified by dual- luciferase reporter assay. The activation of MET/PI3K/AKT pathway and the expression of downstream related proteins were determined by Western blot. Results The results showed that miR-27b was poorly expressed in DLBCL cell lines compared with normal human B cell lines, and was associated with its high proliferation, high invasiveness and low apoptosis level. High miR-27b expression can reduce the proliferation and increase the apoptosis level in DLBCL cells. By examining the effect of miR-27b over-expression on the MET/PI3K/AKT pathway, it was found that miR-27b can inhibit the proliferation and invasiveness and promote the apoptosis of DLBCL cells by targeting the inhibition of MET expression and the activation of PI3K/AKT pathway. Conclusion miR-27b can inhibit the proliferation and invasiveness of DLBCL cells and promote the apoptosis of the cells by targeting MET/PI3K/AKT pathway.

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MicroRNA-27b reverses docetaxel resistance of non-small cell lung carcinoma cells via targeting epithelial growth factor receptor

Cited by 10 publications

References 28 publications

Promising therapeutic role of miR-27b in tumor

Promising therapeutic role of miR-27b in tumor

MicroRNA‐181a promotes docetaxel resistance in prostate cancer cells

Effect of miR-27b on the proliferation and apoptosis of diffuse large b-cell lymphoma cells by targeting the regulation of MET/PI3K/AKT pathway

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