Decreased MicroRNA-26a expression causes cisplatin resistance in human non-small cell lung cancer

Yang, Yong; Zhang, Peng; Zhao, Yanfeng; Yang, Jie; Jiang, Gening; Fan, Jie

doi:10.1080/15384047.2015.1095405

Cited by 37 publications

(30 citation statements)

References 62 publications

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“…Recent studies have reported that ncRNAs play significant rules in cDDP resistance in lung cancer [61–63]. For instance, microRNA-26a is reported to cause cDDP resistance in NSCLC by inhibiting E2F1, diminishing Akt phosphorylation and down-regulating Bcl2 expression [61].…”

Section: Discussionmentioning

confidence: 99%

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NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

et al. 2016

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Platinum-based drugs are the firstline of treatment for non-small cell lung cancer (NSCLC), but resistance to these drugs is a major obstacle to effective chemotherapy. Our previous study revealed that the green tea polyphenol, EGCG, induced cisplatin transporter CTR1 (copper transporter 1) and enhanced cisplatin sensitivity in ovarian cancer. In this study, we found that EGCG upregulated CTR1 and increased platinum accumulation in NSCLC (A549, H460 and H1299) cells, cDDP-resistant A549 cells and a nude mouse xenograft model. Cisplatin-induced inhibition of cell growth was enhanced by EGCG treatment in vitro and in vivo. MicroRNA hsa-mir-98-5p appears to suppress CTR1 gene expression, while long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) appears to enhance it. Bioinformatics analysis showed that hsa-mir-98-5p has specific complementary binding sites for NEAT1. In addition, hsa-mir-98-5p was predicted to be a putative CTR1 target. NEAT1 may act as a competing endogenous lncRNA to upregulate EGCG-induced CTR1 by sponging hsa-mir-98-5p in NSCLC. Our findings reveal a novel mechanism how NEAT1 upregulates EGCG-induced CTR1 and enhances cisplatin sensitivity in vitro and in vivo, and suggest EGCG could serve as an effective adjuvant chemotherapeutic in lung cancer treatment.

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Section: Discussionmentioning

confidence: 99%

“…For instance, microRNA-26a is reported to cause cDDP resistance in NSCLC by inhibiting E2F1, diminishing Akt phosphorylation and down-regulating Bcl2 expression [61]. In lung cancer, miR-15b regulates cDDP resistance by targeting PEBP4 [62], while lncRNA MEG3 regulates resistance by controlling p53 and Bcl-xl [63].…”

Section: Discussionmentioning

confidence: 99%

NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

et al. 2016

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“…To determine the miRNA levels of miRNA‐26a, qRT‐PCR was performed as described previously . Bulge‐loop miRNA qRT‐PCR Primer Sets specific for miRNA‐26a were designed by RiboBio (Guangzhou, China).…”

Section: Methodsmentioning

confidence: 99%

MicroRNA‐26a inhibits multiple myeloma cell growth by suppressing cyclin‐dependent kinase 6 expression

Song

Huang

et al. 2019

The Kaohsiung J of Med Scie

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MicroRNA‐26a (miR‐26a) has been reported to be involved in the tumorigenesis of several tumors, but its biological function and molecular mechanism in multiple myeloma (MM) are still unknown. In this study, we found that overexpression of miR‐26a obviously inhibited MM cell growth, and delayed tumor growth in xenografts. Further studies showed that overexpression of miR‐26a induced cell cycle arrest at G0/G1 phase in MM cells. MiR‐26a mimic down‐regulated the expression levels of CDK6 and E2F1, but up‐regulated p53 and p21 expression. In contrast, overexpression of CDK6 decreased the effect of miR‐26a mimic on MM cell survival. Moreover, miR‐26a targeted CDK6 mRNA and thus suppressed CDK6 protein expression. Overexpression of miR‐26a also enhanced the cytotoxic action of doxorubicin against MM. These results demonstrated that miR‐26a was involved in the development of MM through regulating CDK6 signaling pathway, and indicated that miR‐26a could be as a novel target for anti‐tumor therapy in clinic as a single strategy or in combination with other anti‐tumor drugs in MM.

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“…In 2014, Jiang DS et.al demonstrated that miR-26 is involved in the TLR9-mediated growth and migration of lung cancer through PI3K/Akt signaling pathway [13]. Additional, in 2016, Yang Y et.al revealed that decreased miR-26a expression could lead to cisplatin resistance in human non-small cells lung cancer through regulating HMGA1-mediated E2F1-Akt pathway [14]. Given the function of miR-26a reported in lung cancer, we hypothesis that miR-26a might be involved in the malignant phenotype acquisition of docetaxel-resistant LAD cells.…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNA-26a is commonly dysregulation in diverse cancers, and involves in various biological processes, including proliferation, migration, invasion, angiogenesis and metabolism, via targeting multiple mRNAs. Besides, it has been revealed that decreased miR-26a expression could cause cisplatin resistance and promote growth and migration in human lung cancer [13, 14]. Thus, miR-26a might be involved in the malignant phenotype acquisition of docetaxel-resistant LAD cells.…”

Section: Introductionmentioning

confidence: 99%

MiRNA-26a Contributes to the Acquisition of Malignant Behaviors of Doctaxel-Resistant Lung Adenocarcinoma Cells through Targeting EZH2

Chen

Tao

et al. 2017

Cell Physiol Biochem

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Background/Aims: Accumulating evidence revealed that microRNAs (miRNAs) have been demonstrated as critical molecules in tumor development and progression. MiR-26a, located in a fragile chromosomal region associated with various human cancer, has been reported to be involved in regulating various cellular process, such as proliferation, apoptosis and invasion through targeting multiple oncogene. Docetaxel-mediated chemotherapy has been applied in improving the survival and prognosis of patients with advanced lung adenocarcinoma (LAD). However, chemoresistance remains a major impediment to clinical application of this agent. It has been presented that decreased miR-26a expression lead to cisplatin resistance and promoted growth and migration in human lung cancer. Enhancer of zeste homolog 2 (EZH2) is the target of miR-26a. The present study aimed to investigate the function of miR-26a/EZH2 in the acquisition of malignant behaviors of LAD. Methods: MiR-26a and EZH2 expression levels in the dcetaxel-insensitive groups (n = 19) and the docetaxel-sensitive groups (n = 18) were assessed by qRT-PCR. Colony formation assay, flow cytometric analysis, wound healing assay, cell transwell assays and western blotting were performed to assess the effects of miR-26a on proliferation, apoptosis and epithelial-to-mesenchymal (EMT) phenotypes in docetaxel resistant LAD cells in vitro. Xenograft transplantation, immunohistochemistry, tunel assays and western blotting assays were employed to demonstrate the role of miR-26a in docetaxel resistant LAD cells in vivo. The expression level of EZH2 in docetaxel-resistant LAD cells and corresponding parental cells was detected by qRT-PCR and western blotting. The relationship between miR-26a and EZH2 was confirmed by luciferase reporter assay. And rescue assays were performed to further confirm that miRNA-26a contributes to the acquisition of malignant behaviors of docetaxel-resistant LAD cells through targeting EZH2. Results: MiR-26a was significantly down-regulated in the dcetaxel-insensitive groups (n = 19) compared with the docetaxel-sensitive groups (n = 18) assessed by qRT-PCR. MiR-26a decreased the proliferation, increased the apoptosis rate and reversed EMT to MET of docetaxel-resistant LAD cells both in vivo and vitro. EZH2 was confirmed as target of miR-26a. Rescue assays further verified that the function of miR-26a exerts in docetaxel-resistant LAD cells is through targeting EZH2. Conclusions: Our data revealed that overexpression of miR-26a in docetaxel-resistant LAD cells could decrease the proliferation, increase the apoptosis rate and reverse EMT to MET of docetaxel-resistant LAD cells both in vivo and vitro and such function is partially exerted via downregulating EZH2. MiR-26a/EZH2 signal pathway makes contribute to the malignant phenotype of docetaxel-resistant of LAD cells which indicated that miR-26a exerts pivotal functions in the molecular etiology of chemoresistant lung adenocarcinoma.

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Decreased MicroRNA-26a expression causes cisplatin resistance in human non-small cell lung cancer

Cited by 37 publications

References 62 publications

NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

MicroRNA‐26a inhibits multiple myeloma cell growth by suppressing cyclin‐dependent kinase 6 expression

MiRNA-26a Contributes to the Acquisition of Malignant Behaviors of Doctaxel-Resistant Lung Adenocarcinoma Cells through Targeting EZH2

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