Friend or foe: the role of microRNA in chemotherapy resistance

Li, Haoran; Yang, Burton B.

doi:10.1038/aps.2013.35

Cited by 106 publications

(69 citation statements)

References 109 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, understanding the mechanism underlying erlotinib resistance may help to overcome this problem. Recent evidence suggests that dys-regulation of miRNAs plays a vital role in regulating the drug response of tumor cells [8,[30][31][32]. For instance, miR-133a and miR-326 are involved in adriamycin resistance in HepG2 cells through altering expression of multidrug resistance-associated protein 1 (ABCC1) [33].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

miR-17-5p down-regulation contributes to erlotinib resistance in non-small cell lung cancer cells

Zhang

Lin

Wang

et al. 2016

Journal of Drug Targeting

View full text Add to dashboard Cite

Non-small cell lung cancer (NSCLC) is the major cause of lung cancer-related deaths. Erlotinib is an effective drug for NSCLC patients, but its effect in advanced NSCLC is compromised because of the drug resistance. The mechanism of erlotinib resistance in NSCLC is largely unknown. In the current study, we found that erlotinib treatment down-regulated miR-17-5p level in A549 cells and miR-17-5p was lower in acquired erlotinib-resistant A549 cells (A549-ER) compared with erlotinib-sensitive A549 cells. Consistently, miR-17-5p was down-regulated in the tumor tissues and the plasma of erlotinib-resistant NSCLC patients in comparison to those who are sensitive to erlotinib. Moreover, miR-17-5p mimic increased the sensitivity of A549 and A549-ER to erlotinib. In contrast, miR-17-5p inhibitor decreased the cell death of A549 and A549-ER induced by erlotinib. In addition, we also demonstrated that miR-17-5p could inhibit the mRNA and protein levels of enhancer of zeste homolog (EZH) 1, a member of the EZH family that contributes to drug resistance in several types of cancer. The luciferase assay of 3 0 -untranslated region (UTR) demonstrates that EZH1 is a direct target of miR-17-5p and EZH1 RNAi recapitulates the effect of miR-17-5p overexpression on erlotinib resistance. Further, mutation in seed sequence of miR-17-5p could totally abolish the sensitization of A549-ER to erlotinib induced by miR-17-5p overexpression. Our results indicate that miR-17-5p down-regulation contributes to erlotinib resistance of NSCLC by modulating its target genes such as EZH1 and plasma miR-17-5p might be a potential biomarker of erlotinib response in NSCLC patients. ARTICLE HISTORY

show abstract

Section: Discussionmentioning

confidence: 99%

“…Chemotherapeutic drug resistance could occur at the genetic and epigenetic levels, leading to abnormal expression of drug resistance-related genes, alteration of drug targets, and more survival of tumor cell [8]. But the mechanism of abnormal expression of drug resistance-related genes is unclear.…”

Section: Introductionmentioning

confidence: 99%

miR-17-5p down-regulation contributes to erlotinib resistance in non-small cell lung cancer cells

Zhang

Lin

Wang

et al. 2016

Journal of Drug Targeting

View full text Add to dashboard Cite

show abstract

“…In addition, mir-25 was found to be downregulated in cisplatin-resistant cervical cancer cells and overexpression of mir-25 reversed the EMT phenotype of the cisplatin-resistant cervical cancer cells [37]. MiRNAs can influence drug resistance not only in a drug-specific manner but also in a cell-specific manner [38]. Perhaps the opposing roles for mir-25 observed in these studies relative to our observations may be due to cell-specific and/or drug-specific effects.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Profiling of Oxaliplatin-Resistant HCT116 Colorectal Cancer Cells

Kosmo¹,

Lee²,

Masroni³

et al. 2017

Oncomedicine

View full text Add to dashboard Cite

Aim: To investigate the impact of oxaliplatin resistance on the cellular characteristics and miRNA expression pattern in colorectal cancer cells. Methods: A stable oxaliplatin-resistant colorectal cancer HCT116 cell line was established by exposure to increasing doses of oxaliplatin. Alterations in cytotoxicity, migration, invasion and tumorsphere formation were assessed by MTS assay, modified Boyden chamber assay, and colonosphere assay respectively. The miRNAome of the oxaliplatin-resistant HCT116 cells was analyzed using the TaqMan PCR Human miRNA array. Upregulated miRNAs from the PCR array were validated by real-time reverse transcription-quantitative PCR (RT-qPCR). Results: Oxaliplatin-resistant HCT116 cells exhibited higher migration, invasion and tumorsphere formation compared to parental oxaliplatin-sensitive HCT116 cells. The oxaliplatin-resistant cells showed a distinct miRNA expression profile compared to the parental cells. The expression of miR-601, miR-222, miR-202 and miR-25 were verified by RT-qPCR to be increased in resistant cells. Bioinformatics analyses were used to identify potential target mRNAs of these 4 miRNAs. Conclusion: Results presented in this study provide evidence that oxaliplatin-resistance induces phenotypic changes in colorectal cancer and alterations in miRNA expression. Functional studies on the miRNAs and their target mRNA may enable the discovery of functional pathways to chemoresistance in colorectal cancer.

show abstract

“…Drug resistance is multifactorial and leads to sustenance of tumor. It may be due to various mechanisms like the cancer cells opting a secondary salvage pathway when the primary one is shut [82], by preventing miRNA activation of tumor suppressor genes [83], by conversion of tumor cells into a more aggressive phenotype with increased plasticity by epithelial mesenchymal transition [84], fibrosis/desmoplasia in surrounding stroma leading to reduced drug penetration etc [85].…”

Section: Exosomes In Cancermentioning

confidence: 99%