Functional miRNAs in breast cancer drug resistance

Hu, Weizi; Tan, Chunli; He, Yunjie; Zhang, Guangqin; Xu, Yong; Tang, Jinhai

doi:10.2147/ott.s152462

Cited by 102 publications

(82 citation statements)

References 151 publications

(211 reference statements)

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“…Target gene expression is regulated by two mechanisms: (i) binding to the untranslated region (3'UTR) of the target messenger RNA (mRNA) 3' end, inhibiting its translation; and (ii) like small interfering RNA (siRNA), miRNA binds to the target and degrades target mRNA . Recent studies have found that miRNAs regulate drug resistance by mediating their targeting genes in various cancers . In recent years, abnormal expression of miR‐873 has been found in many kinds of tumors, such as breast and ovarian cancers, and glioma .…”

Section: Introductionmentioning

confidence: 99%

“…[17][18][19] Recent studies have found that miRNAs regulate drug resistance by mediating their targeting genes in various cancers. [20][21][22][23][24] In recent years, abnormal expression of miR-873 has been found in many kinds of tumors, such as breast and ovarian cancers, and glioma. [25][26][27] MiR-873 plays a role in promoting cancer or anticancer by regulating tumor cell invasion, migration, proliferation, apoptosis, and sensitivity to chemotherapeutic drugs.…”

Section: Introductionmentioning

confidence: 99%

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MiR‐873 inhibition enhances gefitinib resistance in non‐small cell lung cancer cells by targeting glioma‐associated oncogene homolog 1

Jin

et al. 2018

Thoracic Cancer

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BackgroundThe five‐year survival rate of non‐small cell lung cancer (NSCLC) patients is very low. MiR‐873 is involved in the growth, metastasis, and differentiation of tumors. Herein, we determined the target gene and influence of miR‐873 in NSCLC.MethodsMiRanda and Targetscan websites were used to predict the target gene of miR‐873 in NSCLC. Luciferase activity was examined using a dual luciferase reporter gene assay kit. The viability, tube formation, and proliferation of cells were analyzed by cell counting kit‐8, angiogenic analysis, and flow cytometry, respectively. The levels of miR‐873 and GLI1 were evaluated using quantitative real‐time PCR and Western blot assays.ResultsLow levels of GLI1 and high levels of miR‐873 were observed in an NSCLC cell line (PC9) highly sensitive to EGFR‐tyrosine kinase inhibitors. There was a negative correlation between miR‐873 and GLI1 expression in PC9 and PC9/GR cells. The inhibition of miR‐873 enhanced GLI1 levels. MiR‐873 expression was inhibited by gefitinib. Gefitinib markedly reduced the viability, tube formation, and cell number in PC9 cells. However, suppression of miR‐873 enhanced the resistance and knockdown of GLI1 enhanced the sensitivity of PC9 cells to gefitinib.Conclusions GLI1 is a target gene of miR‐873 in NSCLC. The inhibition of miR‐873 increased gefitinib resistance of NSCLC cells via the upregulation of GLI1. These results indicate that miR‐873‐GLI1 signaling is involved in gefitinib resistance in NSCLC.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MiR‐873 inhibition enhances gefitinib resistance in non‐small cell lung cancer cells by targeting glioma‐associated oncogene homolog 1

Jin

et al. 2018

Thoracic Cancer

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“…miRNAs, especially exosome‐derived miRNAs, can make this aim feasible. miRNAs signatures associated with therapeutic drug resistances in BC patients have been widely studied and identified . Although the exact mechanisms involved in BC drug‐resistance by exosomes are not still well known, there are some suggestions regarding this issue.…”

Section: Roles Of Exosomes In Breast Cancer Resistancementioning

confidence: 99%

“…As examples, miRNAs such as miRNAs 663, 25, 505, and 145 induce BC resistance against chemotherapeutic agents; miRNAs 101, 451, 214, and 873 are associated with endocrine therapy resistance in BC cells; miRNAs 21, 210, 630, and 515 induce targeted therapy drug resistance; miRNAs 7, 200, and 205 endow both chemotherapeutic and targeted therapy resistances to BC cells via different signaling pathways; and miRNAs 16, 221, and 375 are involved in endocrine and targeted therapy resistances in BC cells. Source : Adapted from Hu et al…”

Section: Exosomal Mirnas In Bc Drug Resistancementioning

confidence: 99%

Emerging roles of exosomal miRNAs in breast cancer drug resistance

Najminejad

Kalantar

Abdollahpour‐Alitappeh³

et al. 2019

IUBMB Life

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Breast cancer (BC), as a heterogeneous disease, is considered as one of the most common malignancies in women worldwide. The resistance of BC cells to therapeutic agents has remained a big challenge in the treatment of BC patients. Some factors such as cytokines, exosomes, and soluble receptors were recognized as crucial agents involved in the development of drug resistance. However, the exact mechanisms underlying the drug resistance is still unknown. There is growing evidence to support the emerging roles of exosomes, especially exosomal miRNAs, in tumor initiation, angiogenesis, proliferation, migration, invasion, metastasis, and drug resistance. Therefore, identification of BC-specific exosomal miRNAs and their underlying mechanisms would be helpful to define sensitivity to therapeutic drugs and establish an appropriate therapeutic strategy. This review focuses mainly on the roles of exosomal miRNAs and their associated mechanisms in the resistance of BC cells to therapeutic agents, as well as critically examines the potential of these macromolecules as a treatment biomarker in BC patients. K E Y W O R D Sbreast cancer, exosomes, drug resistance, therapeutics, exosomal miRNA, microRNA 1 | INTRODUCTION Breast cancer (BC), after skin cancer, was reported to be the most common malignancy in women worldwide. 1 Conversely, BC was showed to have a low incidence rate in men, approximately 1%. BC does not kill in primary stage. It was shown that the 5-year survival rates are 99%, 84%, and 23% for women with localized BC, regional stage, and

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“…Pathways such as EMT pathway, MMP/MMP2 pathway and wnt/β‐catenine are proposed to induce therapeutic resistance in cancer (Son et al, ). Interestingly, molecular studies have shown that altered miRNA expression can play a major role in the activation of drug resistance pathways (Hu et al, ). miRNA clusters contain multiple miRNA encoding genes that can target members of drug‐resistant pathways.…”

Section: Resistance To Treatment (Radio‐ and Chemoresistance)mentioning

confidence: 99%

Cluster miRNAs and cancer: Diagnostic, prognostic and therapeutic opportunities

et al. 2019

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MiRNAs are class of noncoding RNA important for gene expression regulation in many plants, animals and viruses. MiRNA clusters contain a set of two or more miRNA encoding genes, transcribed together as polycistronic miRNAs. Currently, there are approximately 159 miRNA clusters reported in the human genome consisting of miRNAs ranging from two or more miRNA genes. A large proportion of clustered miRNAs resides in and around the fragile sites or cancer associated genomic hotspots and plays an important role in carcinogenesis. Altered expression of miRNA cluster can be pro‐tumorigenic or anti‐tumorigenic and can be targeted for clinical management of cancer. Over the past few years, manipulation of miRNA clusters expression is attempted for experimental purpose as well as for diagnostic, prognostic and therapeutic applications in cancer. Re‐expression of miRNAs by epigenetic therapy, genome editing such as clustered regulatory interspaced short palindromic repeats (CRISPR) and miRNA mowers showed promising results in cancer therapy. In this review, we focused on the potential of miRNA clusters as a biomarker for diagnosis, prognosis, targeted therapy as well as strategies for modulating their expression in a therapeutic context. This article is categorized under: Regulatory RNAs/RNAi/Riboswitches > Regulatory RNAs RNA Processing > Processing of Small RNAs RNA in Disease and Development > RNA in Disease Regulatory RNAs/RNAi/Riboswitches > Biogenesis of Effector Small RNAs

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Functional miRNAs in breast cancer drug resistance

Cited by 102 publications

References 151 publications

MiR‐873 inhibition enhances gefitinib resistance in non‐small cell lung cancer cells by targeting glioma‐associated oncogene homolog 1

MiR‐873 inhibition enhances gefitinib resistance in non‐small cell lung cancer cells by targeting glioma‐associated oncogene homolog 1

Emerging roles of exosomal miRNAs in breast cancer drug resistance

Cluster miRNAs and cancer: Diagnostic, prognostic and therapeutic opportunities

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