Upregulation of microRNA-143 reverses drug resistance in human breast cancer cells via inhibition of cytokine-induced apoptosis inhibitor 1

Wang, Jing‐Hao; Wang, Xiuwen; Qu, Di; Sun, Ji‐Wen; Guo, Fei‐Xiao; Lü, Dan

doi:10.3892/ol.2017.6078

Cited by 7 publications

(6 citation statements)

References 20 publications

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“…An inverse association between miRNA-143 and CIAPIN1 protein expression levels has been observed in a number of breast cancer cell lines. Overexpression of CIAPIN1 has been associated with multidrug resistance, and this was supported in the study by Wang and colleagues [180]. Furthermore, studies have shown that the miRNA-145/143 cluster targets the 3 -UTR of the ERBB2 gene, which has been linked with breast cancer multidrug resistance in a subtype dependent manner [181].…”

Section: Reduced Mirna-143 Contributes To Breast Cancer Drug Resistanmentioning

confidence: 83%

MiRNAs as Novel Adipokines: Obesity-Related Circulating MiRNAs Influence Chemosensitivity in Cancer Patients

Withers

Dewhurst

Hammond

et al. 2020

ncRNA

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Adipose tissue is an endocrine organ, capable of regulating distant physiological processes in other tissues via the release of adipokines into the bloodstream. Recently, circulating adipose-derived microRNAs (miRNAs) have been proposed as a novel class of adipokine, due to their capacity to regulate gene expression in tissues other than fat. Circulating levels of adipokines are known to be altered in obese individuals compared with typical weight individuals and are linked to poorer health outcomes. For example, obese individuals are known to be more prone to the development of some cancers, and less likely to achieve event-free survival following chemotherapy. The purpose of this review was twofold; first to identify circulating miRNAs which are reproducibly altered in obesity, and secondly to identify mechanisms by which these obesity-linked miRNAs might influence the sensitivity of tumors to treatment. We identified 8 candidate circulating miRNAs with altered levels in obese individuals (6 increased, 2 decreased). A second literature review was then performed to investigate if these candidates might have a role in mediating resistance to cancer treatment. All of the circulating miRNAs identified were capable of mediating responses to cancer treatment at the cellular level, and so this review provides novel insights which can be used by future studies which aim to improve obese patient outcomes.

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Section: Reduced Mirna-143 Contributes To Breast Cancer Drug Resistanmentioning

confidence: 83%

MiRNAs as Novel Adipokines: Obesity-Related Circulating MiRNAs Influence Chemosensitivity in Cancer Patients

Withers

Dewhurst

Hammond

et al. 2020

ncRNA

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“…A preliminary in vitro study highlighted the significance of hsa-miRNA-143-3p, finding that its expression levels were negatively correlated with paclitaxel resistance in TNBC and upregulating its expression could notably strengthen the ability of paclitaxel to kill tumor cells [ 17 ]. This previous study first demonstrated that the expression profile of hsa-miRNA-143-3p could provide MDR information and also acted as a reserve force to reverse MDR.…”

Section: Discussionmentioning

confidence: 99%

“…BT-20, MDA-MB-231, MCF7, SKBr-3, Lovo, HepG2A549, 293T, and MRC-5 cells were obtained from the Shanghai Institute of Biochemistry and Cell Biology (Shanghai, China). MDA-MB-231/Tax cell lines were established in a previous experiment [ 17 ] and passaged with trypsin digestion. MDA-MB-231/Tax cell lines in logarithmic growth phase at passage 3 were prepared into cell suspensions at 1×10 8 /mL and preserved at 4℃.…”

Section: Methodsmentioning

confidence: 99%

“…Subsequent studies indicated that this protein has important functions in MDR development in multiple tumor types, such as colon cancer [ 13 ], gastric cancer [ 14 ], leukemia [ 15 ], and breast cancer [ 16 ]. Surprisingly, in a preliminary in vitro study, we found that hsa-miRNA-143-3p has the CIAPIN1 gene mRNA 3′-UTR seed binding site in TNBC cells [ 17 ], which suggests that CIAPIN1 may be a target of hsamiRNA-143-3p.…”

Section: Introductionmentioning

confidence: 99%

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Hsa-miRNA-143-3p Reverses Multidrug Resistance of Triple-Negative Breast Cancer by Inhibiting the Expression of Its Target Protein Cytokine-Induced Apoptosis Inhibitor 1In Vivo

Deng

Hao

et al. 2018

J Breast Cancer

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PurposeMultidrug resistance (MDR) remains a major obstacle in the treatment of triple-negative breast cancer (TNBC) with conventional chemotherapeutic agents. A previous study demonstrated that hsa-miRNA-143-3p plays a vital role in drug resistance of TNBC. Downregulation of hsa-miRNA-143-3p upregulated the expression of its target protein cytokine-induced apoptosis inhibitor 1 (CIAPIN1) in order to activate MDR, while upregulation of hsa-miRNA-143-3p effectively enhances the sensitivity of drug-resistant TNBC cells to chemotherapeutics. The present study aimed to further verify these findings in vivo.MethodsWe established a hypodermic tumor nude mice model using paclitaxel-resistant TNBC cells. We expressed ectopic hsa-miRNA-143-3p under the control of a breast cancer-specific human mammaglobin promoter that guided the efficient expression of exogenous hsa-miRNA-143-3p only in breast cancer cells. Thereafter, we overexpressed hsa-miRNA-143-3p in xenografts using a recombinant virus system and quantified the expression of hsa-miRNA-143-3p, CIAPIN1 protein, and proteins encoded by related functional genes by western blot.ResultsWe successfully completed the prospective exploration of the intravenous virus injection pattern from extensive expression to targeted expression. The overexpression of hsa-miRNA-143-3p significantly alleviated chemoresistance of TNBC by inhibiting viability. In addition, we observed that the expression of CIAPIN1 as a hsa-miRNA-143-3p target protein was remarkably decreased.ConclusionWe partly illustrated the mechanism underlying the hsa-miRNA-143-3p/CIAPIN1 drug resistance pathway. HsamiRNA-143-3p as a tumor suppressive microRNA may be a novel target to effectively reverse MDR of TNBC in vivo.

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“…The ndings show that miR-143 controls the growth, invasion, and migration of breast cancer cells via interacting with MAPK7 [21]. As well as by blocking CIAPIN1, miR-143 contributes to the reversal of Taxol-induced drug-resistant (TDR) in human breast cancer cells and inhibits the development of breast cancer TDR cells [22]. Therefore, the present study aimed to explore the synergistic effects of miR-143 and miR-99a based expression plasmid for breast cancer inhibition.…”

Section: Introductionmentioning

confidence: 99%

Synergistic effects of miR-143 with miR-99a inhibited cell proliferation and induced apoptosis in breast cancer

Doosti

Ebrahimi

Ghahfarokhi

et al. 2023

Preprint

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Introduction: Breast cancer (BC) is the most common cancer type and the fifth leading cause of cancer-related death. The primary goals of BC treatment are to remove the tumor and prevent metastasis. Despite advances in BC treatment, more effective therapies are required. miRNAs can regulate many targets involved in biological processes and tumor progression; these molecules have emerged as a promising cancer treatment strategy. In the present study, we investigated the effects of miR-99a and miR-143 in based single expression plasmids for BC inhibition. Methods: In this study, the precursor structure of miRNAs in the expression vector pEGFP-N1 entered single and double states, and MCF7 and T47D cells were transfected. The miRNAs expression level after transfection was then measured using qPCR. The MultiMiR package was used to obtain predicted and validated miRNA targets. MTT assay, qRT-PCR, migration test, and flow cytometry were used to assess the effect of miRNA and gene modulation. Results: The qPCR results revealed that miRNA constructs were significantly expressed after the transfection of both cell lines. The biological function of miRNAs showed that upregulation of miR-99a and miR-143 in any of the two selected BC cells inhibited their proliferation and migration rate, significantly inducing apoptosis (p<0.01). Also, miR-99a/-143 co-treatment has a synergistic anticancer effect in cancer cells via Akt1 and CDK6 targeting. Conclusion: These findings suggest that miR-99a/-143 plays synergistic regulatory roles in BC, possibly via a shared signaling pathway, providing a therapeutic strategy for BC treatment.

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Upregulation of microRNA-143 reverses drug resistance in human breast cancer cells via inhibition of cytokine-induced apoptosis inhibitor 1

Cited by 7 publications

References 20 publications

MiRNAs as Novel Adipokines: Obesity-Related Circulating MiRNAs Influence Chemosensitivity in Cancer Patients

MiRNAs as Novel Adipokines: Obesity-Related Circulating MiRNAs Influence Chemosensitivity in Cancer Patients

Hsa-miRNA-143-3p Reverses Multidrug Resistance of Triple-Negative Breast Cancer by Inhibiting the Expression of Its Target Protein Cytokine-Induced Apoptosis Inhibitor 1In Vivo

Synergistic effects of miR-143 with miR-99a inhibited cell proliferation and induced apoptosis in breast cancer

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