The miR-491-3p/Sp3/ABCB1 axis attenuates multidrug resistance of hepatocellular carcinoma

Zhao, Yang; Qi, Xinming; Chen, Jing; Wei, Wenxin; Yu, Cunzhi; Yan, Hong; Pu, Mengfan; Yu, Li; Miao, Lijing; Li, Chun‐Zhu; Ren, Jin

doi:10.1016/j.canlet.2017.08.027

Cited by 64 publications

(44 citation statements)

References 38 publications

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“…Breast cancer Over-expression of these miRNAs re-sensitizes the drug-resistant cells to doxorubicin [45] miR-199a-3p MTOR Cholangiocarcinoma Reconstitution of miR-199a-3p increases growth inhibition rate and apoptosis induced by cisplatin [39] miR-210-3p ABCC5 Pancreatic cancer Elevated miR-210-3p levels improve the overall cytotoxicity of gemcitabine [26] miR-218-5p PRKCE Gallbladder cancer Elevated miR-218-5p levels potentiate gemcitabine-mediated cell death and growth inhibition [38] miR-223-3p ABCB1 Hepatocellular carcinoma Down-regulation of miR-223-3p confers resistance to doxorubicin [18] miR-326 ABCC1 Hepatocellular carcinoma Over-expression of miR-326 leads to elevated cytotoxicity of doxorubicin [23] miR-328-3p ABCG2 Breast cancer Over-expression of miR-328-3p augments the sensitivity of drug-resistant cells to mitoxantrone [29] miR-491-3p ABCB1, SP3 Hepatocellular carcinoma Down-regulation of miR-491-3p decreases the sensitivity to doxorubicin and vinblastin [19] miR-495-3p ABCB1, UBE2C Ovarian cancer, Gastric cancer, Lung cancer…”

Section: Spin1mentioning

confidence: 99%

“…As noted above, miR-491-3p directly controls ABCB1 expression. Interestingly, miR-491-3p also transcriptionally represses ABCB1 levels by regulating Sp3, which is known as a transcription factor of ABCB1 [19]. In addition, it was intriguingly noted that miR-508-5p, which directly regulates ABCB1, also targets zinc ribbon domaincontaining 1 (ZNRD1), thereby negatively regulates the transcription of ABCB1 [21,43] (Figure 1 and Table 1).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Seo

Moeng

Sim³

et al. 2019

Cells

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The susceptibility of cancer cells to different types of treatments can be restricted by intrinsic and acquired therapeutic resistance, leading to the failure of cancer regression and remission. To overcome this problem, a combination therapy has been proposed as a fundamental strategy to improve therapeutic responses; however, resistance is still unavoidable. MicroRNA (miRNAs) are associated with cancer therapeutic resistance. The modulation of dysregulated miRNA levels through miRNA-based therapy comprising a replacement or inhibition approach has been proposed to sensitize cancer cells to other anti-cancer therapies. The combination of miRNA-based therapy with other anti-cancer therapies (miRNA-based combinatorial cancer therapy) is attractive, due to the ability of miRNAs to target multiple genes associated with the signaling pathways controlling therapeutic resistance. In this article, we present an overview of recent findings on the role of therapeutic resistance-related miRNAs in different types of cancer. We review the feasibility of utilizing dysregulated miRNAs in cancer cells and extracellular vesicles as potential candidates for miRNA-based combinatorial cancer therapy. We also discuss innate properties of miRNAs that need to be considered for more effective combinatorial cancer therapy.Cells 2020, 9, 29 2 of 32 to confer the ability to acquire CSC properties onto cancer cells, thereby contributing to therapeutic resistance [7]. Moreover, cell-to-cell communication via extracellular vesicles among different types of cells within the cancer microenvironment could affect the efficacy of cancer therapies by delivering miRNAs that regulate various signaling pathways connected to therapeutic resistance [8,9].Combination therapies have been proposed to overcome therapeutic resistance via the combined inhibition of different mechanisms. For example, the combination of cobimetinib and pictilisib was reported to be beneficial for the treatment of colorectal cancer cells. However, resistance is unavoidable even after the combination treatment [10]. Similarly, the simultaneous inhibition of phosphoinositide 3-kinase (PI3K) and a mechanistic target of rapamycin kinase (mTOR) was reported to activate extracellular signal-regulated kinase (ERK), a pro-survival factor, in acute myeloid leukemia [11]. Therefore, it is still necessary to explore new combination strategies to defeat therapeutic resistance. An improved understanding of the cellular basis of cancer therapeutic resistance can further provide promising opportunities to design and develop novel cancer treatment strategies to manage cancers.MicroRNAs (miRNAs) are widely recognized, small, regulatory RNAs modulating numerous intracellular signaling pathways in several diseases, including cancers. Based on the expression levels and intracellular functions of miRNAs, they could act as tumor-suppressive or oncogenic factors in cancer cells [12][13][14]. The abnormal expression of miRNAs is associated with therapeutic resistance in cancer, and the modulation of m...

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Section: Spin1mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Seo

Moeng

Sim³

et al. 2019

Cells

View full text Add to dashboard Cite

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“…In our study, XCT‐790 suppressed transcription of ABCB1 was abolished in cells transfected with si‐SP3. In addition, miR‐491‐3p, which can down‐regulate the expression of ABCB1 and its transcription factor Sp3 by directly targeting their 3′‐UTR, attenuated multidrug resistance of hepatocellular carcinoma . Furthermore, we found that XCT‐790 can increase the expression of miR‐9 and then trigger the decay of ABCB1 mRNA.…”

Section: Discussionmentioning

confidence: 73%

Oestrogen‐related receptor alpha mediates chemotherapy resistance of osteosarcoma cells via regulation of ABCB1

Chen

Zhang

Yang

et al. 2019

J Cellular Molecular Medi

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Chemotherapy resistance is one of the major challenges for the treatment of osteosarcoma ( OS ). The potential roles of oestrogenic signals in the chemoresistance of OS cells were investigated. As compare to the parental cells, the doxorubicin and cisplatin ( CDDP ) resistant OS cells had greater levels of oestrogen‐related receptors alpha ( ERR α). Targeted inhibition of ERR α by its specific si RNA s or inverse agonist XCT ‐790 can restore the sensitivity of OS resistant cells to chemotherapy. This might be due to that si‐ ERR α can decrease the expression of P‐glycoprotein (P‐gp, encoded by ABCB 1), one important ABC membrane transporter for drug efflux. XCT ‐790 can decrease the transcription and mRNA stability of ABCB 1, while had no effect on protein stability of P‐gp. ERR α can bind to the transcription factor of SP 3 to increase the transcription of ABCB 1. Furthermore, XCT ‐790 treatment decreased the expression of miR‐9, which can bind to the 3′ UTR of ABCB 1 and trigger its decay. Collectively, we found that ERR α can regulate the chemoresistance of OS cells via regulating the transcription and mRNA stability of ABCB 1. Targeted inhibition of ERR α might be a potential approach for OS therapy.

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“…MiR-491-3p has been reported to be involved in the pathogenesis of major depression or suicide [23]. In addition, previous study has found that miR-491-3p played a vital role in the modulation of multidrug resistance in hepatocellular carcinoma through regulating ABCB1 and Sp3 expression [19]. Moreover, miR-491-3p was discovered to suppress the growth and invasiveness of osteosarcoma [18] and glioblastoma [24] cells.…”

Section: Discussionmentioning

confidence: 98%

“…Thus, circulating miR-133a-3p might be regarded as an underlying non-invasive biomarker and therapy target in PMO [15]. Several reports documented the involvement of miR-491-3p in cancer, for example, miR-491-3p reduced multidrug resistance of hepatocellular carcinoma, inhibited the growth and invasion of osteosarcoma cells, regulated the chemo-sensitivity of human tongue cancer, and participated in the pathogenesis of clear cell renal cell carcinoma [16][17][18][19]. However, its role in PMO has yet not been investigated.…”

Section: Introductionmentioning

confidence: 99%

MiR-491-3p is down-regulated in postmenopausal osteoporosis and affects growth, differentiation and apoptosis of hFOB1.19 cells through targeting CTSS

Jiazheng

2020

Folia Histochem Cytobiol.

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Background. Postmenopausal osteoporosis (PMO) is a common disease related to aging, which has been paid increasing attention in recent years because of its serious complications. MiR-491-3p was found to play a crucial roles in several diseases. However, the role of miR-491-3p in PMO has yet not been studied. Our research intends to explore the impact of miR-491-3p on PMO in the in vitro model. Material and methods. The expression patterns of miR-491-3p and cathepsin S (CTSS) in patients with PMO were acquired from the GEO database. The human osteoblast cell hFOB1.19 was used to detect the function of miR-491-3p and CTSS in PMO. The viability and apoptosis of hFOB1.19 cells were measured by cell counting kit 8 and flow cytometry assays. The apoptosis and differentiation related proteins were analyzed by western blotting. The relationship between miR-491-3p and CTSS was predicted by appropriate software and affirmed by luciferase assay. Results. MiR-491-3p expression was lower in patients with PMO. The up-regulation of miR-491-3p in hFOB1.19 cells increased their viability and differentiation and inhibited their apoptosis. CTSS, which was highly expressed in patients with PMO, was confirmed as a direct target of miR-491-3p and was found to be inversely modulated by miR-491-3p. The rescue assays showed that overexpression of CTSS suppressed the promoting effects of miR-491-3p mimic on the proliferation and differentiation of hFOB1.19 cells, and repressed the inhibitory effects of miR-491-3p mimic on apoptosis of hFOB1.19 cells. Conclusions. The results of our study showed that miR-491-3p could ameliorate biological characteristics of hFOB1.19 cells by reducing CTSS expression suggesting that miR-491-3p/CTSS might be a potential biomarker for the diagnosis and treatment of PMO.

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The miR-491-3p/Sp3/ABCB1 axis attenuates multidrug resistance of hepatocellular carcinoma

Cited by 64 publications

References 38 publications

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Oestrogen‐related receptor alpha mediates chemotherapy resistance of osteosarcoma cells via regulation of ABCB1

MiR-491-3p is down-regulated in postmenopausal osteoporosis and affects growth, differentiation and apoptosis of hFOB1.19 cells through targeting CTSS

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