MicroRNA-141 confers resistance to cisplatin-induced apoptosis by targeting YAP1 in human esophageal squamous cell carcinoma

Imanaka, Yukako; Tsuchiya, Soken; Sato, Fumiaki; Shimada, Yutaka; Shimizu, Kazuharu; Tsujimoto, Gozoh

doi:10.1038/jhg.2011.1

Cited by 94 publications

(66 citation statements)

References 41 publications

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“…Recently, a study showed that downregulated miR-141 may confer cisplatin resistance in esophageal squamous cell carcinoma (19). Moreover, miR-141 modulates cisplatin sensivitity in ovarian cancer cells (20 The present study is the first to report that increased miR-141 expression was associated with acquired docetaxel resistance in vitro and changes in miR-141 expression modulated response to docetaxel in BC cells, at least in part by targeting the eukaryotic translation initiation factor 4E (EIF4E).…”

Section: Introductionmentioning

confidence: 61%

“…All the above research reported that miR-141 not only to acts as a tumor suppressor, but also as an oncogene. Equally important, Imanaka et al highlighted an important regulatory role for miR-141 in the development of cisplatin resistance in esophageal squamous cell carcinoma (19). Furthermore, the miR-141-mediated regulation of kEAP1 has a crucial role in the cellular response to cisplatin in ovarian cancer cells (20).…”

Section: Discussionmentioning

confidence: 99%

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miR-141 confers docetaxel chemoresistance of breast cancer cells via regulation of EIF4E expression

et al. 2015

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Abstract. Resistance to docetaxel, a chemotherapy drug for breast cancer (BC) treatment, occurs in ~50% of patients, and the underlying molecular mechanisms of drug resistance are not fully understood. Gene regulation through miR-141 has been proven to play an important role in cancer drug resistance. The present study investigated the role of miR-141 expression in BC cells of acquired docetaxel resistance. Inhibition of miR-141 enhanced the response to docetaxel in docetaxel-resistant cells (MCF-7/DTX and MDA-MB-231/DTX, respectively), whereas overexpression of miR-141 confered resistance in docetaxelsensitive cells (MCF-7 and MDA-MB-231, respectively). By directly targeting the eukaryotic translation initiation factor 4E (EIF4E) mRNA, miR-141 acts on genes that are necessary for drug induced apoptosis rendering the cells drug resistant. Modulation of miR-141 expression was correlated with EIF4E expression changes and a direct interaction of miR-141 with EIF4E was shown by a luciferase assay. Thus, the present study is the first to show an increased expression of miR-141 in an acquired model of docetaxel resistance in BC. This serves as a mechanism of acquired docetaxel resistance in BC cells, possibly through direct interactions with EIF4E, therefore presenting a potential therapeutic target for the treatment of docetaxel resistant BC.

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Section: Introductionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 99%

miR-141 confers docetaxel chemoresistance of breast cancer cells via regulation of EIF4E expression

et al. 2015

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“…Again, some researchers reported that miR-451 regulates P-gp expression in doxorubicin-resistant MCF-7 cells (Kovalchuk et al, 2008). There is other evidence on miRNA and anticancer agents, such as tamoxifen (Cittelly et al, 2010), cisplatin (Bian et al, 2011;Imanaka et al, 2011), 5-fluorouracil (Shah et al, 2011;Valeri et al, 2010) and other anticancer drugs (Giovannetti et al, 2011).…”

Section: Mirna Expression and Drugsmentioning

confidence: 99%

Beyond Pharmacogenetics

Canaparo¹

2012

Clinical Applications of Pharmacogenetics

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“…miR-141 was the most highly expressed in the cisplatin-resistant ESCC cell lines and the cell viability was significantly increased following cisplatin treatment. The target of miR-141 is YAP1, which is an apoptosis-inducing gene in DNA-damaging agents (85). miR-296 and miR-27a were overexpressed in EC and the knockdown of miR-296 and miR-27a was capable of increasing sensitivity to both P-glycoproteinrelated and P-glycoprotein-non-related drugs, in turn promoting ADR-induced apoptosis in EC cells (86,87).…”

Section: The Role Of Mirnas In Treatment Of Ecmentioning

confidence: 99%

microRNAs in esophageal cancer (Review)

Yin

Wang

et al. 2012

Mol Med Report

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Abstract. Esophageal cancer (EC) is one of the most common malignant tumors worldwide. EC is usually diagnosed at a locally advanced stage or at a stage with involvement of lymph nodes. Despite aggressive treatment, the overall five-year survival rate remains poor. microRNAs (miRNAs) are small, non-coding endogenous RNAs that negatively regulate gene expression at the post-transcriptional and/or translational level. Accumulating evidence suggests that the deregulation of miRNAs not only results in cancer progression, but also directly promotes tumor initiation. Previous studies found that miRNAs are frequently deregulated in EC, indicating that miRNAs are important in tumorigenesis. In this review, we summarize therecently recognized miRNA expression and its impact on the biology of EC and the potential applications for EC. Contents1. Introduction 2. miRNA synthesis and biological properties 3. miRNAs as tumor suppressor genes 4. miRNAs as oncogenes 5. miRNAs in EC 6. miRNAs serving as diagnostic and prognostic biomarkers in EC 7. The role of miRNAs in invasion and metastasis of EC 8. The role of miRNAs in the growth of EC 9. Single nucleotide polymorphisms of miRNAs in EC 10. The roles of epigenetic regulation of miRNAs in EC 11. The role of miRNAs in treatment of EC 12. Conclusion IntroductionThe incidence and mortality of esophageal cancer (EC) are high, and rank eighth and sixth, respectively, out of all types of cancer, affecting more males than females (1). Esophageal squamous cell carcinoma (ESCC) and adenocarcinoma (EAC) are the two main subtypes of EC in terms of pathological characteristics. ESCC remains the dominant subtype of EC. EC is usually diagnosed at an advanced stage or with lymph node metastases. Due to the potential characteristics of invasion and metastasis in esophageal carcinoma cells, which are important prognostic factors, the overall 5-year survival rate is poor despite advanced treatment (1,2). Improved understanding of the biological behavior in EC is important for the development of new therapeutic strategies and diagnostic methods. microRNAs (miRNAs) are non-coding single-stranded, endogenous RNA molecules, approximately 21-25 ribonucleotides in length and highly conserved in evolution, which negatively regulate gene expression at the post-transcriptional and/or translational level. miRNAs are important in diverse biological processes including development, cell differentiation, proliferation, apoptosis, hormone secretion, tumor formation and drug resistance (3-5). Experimental evidence revealed that the majority of human miRNA genes are located at fragile sites and genomic regions involved in cancer, functioning as oncogenes or tumor suppressor genes (6-8). In this review, we aim to summarize the recognized miRNAs that play roles in the development of EC and the mechanism by which miRNAs are involved in EC. miRNA synthesis and biological propertiesmiRNAs form clusters transcribed as polycistronic transcripts by RNA polymerase II and/or III, which undergo sequential steps of matura...

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MicroRNA-141 confers resistance to cisplatin-induced apoptosis by targeting YAP1 in human esophageal squamous cell carcinoma

Cited by 94 publications

References 41 publications

miR-141 confers docetaxel chemoresistance of breast cancer cells via regulation of EIF4E expression

miR-141 confers docetaxel chemoresistance of breast cancer cells via regulation of EIF4E expression

Beyond Pharmacogenetics

microRNAs in esophageal cancer (Review)

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