MiR-222 modulates multidrug resistance in human colorectal carcinoma by down-regulating ADAM-17

Xu, Ke; Liang, Xin; Shen, Ke; Sun, Liankun; Cui, Daling; Zhao, Yijiao; Tian, Jie; Ni, Lei; Liu, Jianwen

doi:10.1016/j.yexcr.2012.04.014

Cited by 68 publications

(34 citation statements)

References 31 publications

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“…Yang et al suggested that SIRT1 plays a suppressive role against the tumor promoting action of miR-221 and miR-222 (37). In addition, ADAM17, ARHI and HECTD2 were identified as the target genes of miR-221 and miR-222 (22,38,39). These findings suggest that miR-221 and miR-222 are a therapeutic target.…”

Section: Discussionmentioning

confidence: 97%

“…Accumulating evidence has demonstrated that microRNA-222 (miR-222) plays a crucial role in cell growth, oncogenesis, invasion, migration and drug resistance in tumor cells (17,18), and overexpression of miR-222 has been found in several types of cancers, such as breast cancer, colorectal carcinoma, glioblastoma, colorectal carcinoma, as well as liver cancer (19)(20)(21)(22)(23). In particular, several studies demonstrated that miR-222 is involved in resistance to several chemotherapeutic drugs.…”

Section: Introductionmentioning

confidence: 99%

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miR-222 regulates sorafenib resistance and enhance tumorigenicity in hepatocellular carcinoma

Liu

Zhang

et al. 2014

International Journal of Oncology

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Abstract. The miR-222 cluster has been demonstrated to function as oncomiR in human hepatocellular carcinoma (HCC). miR-222 confers chemotherapy drug resistance in various cancers, including HCC. However, the effects and mechanisms by which miR-222 regulates liver tumorigenicity and confers sorafenib (SOR) resistance remain unclear. Here we first investigated the miR-222 effect on proliferation, cell cycle, apoptosis, migration and invasion of HCC. Our results demonstrated that miRNA inhibitors specially targeting miR-222 significantly suppressed cellular proliferation, migration, invasion and G1/S transition of the cell cycle, and induced cell apoptosis in HepG2 cells. In addition, we investigated whether miR-222 confers SOR resistance in HepG2 cells to explore it roles in acquisition of drug resistance. The results showed that miR-222 inhibitors induced sensitivity to the antitumor effect of sorafenib in human HepG2 cells. Importantly, our study also showed that miR-222 could regulate the expression of phosphorylation PI3K and AKT, which might contribute to miR-222 conferred SOR resistance in HepG2 cells. In conclusion, this study demonstrates that miR-222 can promote cell proliferation, migration and invasion, and decrease cell apoptosis, as well as enhance the resistance of HCC cells to sorafenib miR-222 through activating the PI3K/AKT signaling pathway.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

miR-222 regulates sorafenib resistance and enhance tumorigenicity in hepatocellular carcinoma

Liu

Zhang

et al. 2014

International Journal of Oncology

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“…20 Additionally, miR-222 modulates the ADAM-17, a new MDR-related gene, in human colorectal carcinoma cells. 18 In the current study, we identified that ABCB1 was a direct target gene for miR-223, and miR-223 regulated the HCC cells' response to doxorubicin and paclitaxel mediated by ABCB1.…”

Section: Inhibition Of Mir-223 Resulted In the Hcc Cell Resistance Tomentioning

confidence: 71%

MiR-223 modulates multidrug resistance via downregulation of ABCB1 in hepatocellular carcinoma cells

Yang

Zheng

Li³

et al. 2013

Exp Biol Med (Maywood)

107

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Multidrug resistance (MDR) has become a major impediment to a successful treatment for liver cancer patients, and one of the common reasons for MDR is the activation of ABCB1 gene, leading to the over-expression of P-glycoprotein (P-gp), which conferred cancer cells be resistant to a broad range of anticancer drugs. MicroRNAs (miRNAs) are a class of short, non-coding RNA moleculars that can regulate gene expression at the post-transcriptional level. In the current study, the aim is to explore whether miRNA participates in the regulation of MDR mediated by ABCB1. We found that the expression of ABCB1 was correlated with the doxorubicin IC50 dose in eight hepatocellular carcinoma (HCC) cell lines: Hep3B, HCC3, LM-6, SMMC7721, Huh-7, SK-Hep-1, HepG2 and BEL-7402. Using the bioinformatics, we discovered that there were several miRNAs that can bind to the 3'UTR of ABCB1 gene. Among these candidate miRNAs, miR-223 was chosen for further study. Then, EGFP reporter assay, real-time PCR and Western blot were performed to verify that miR-223 targeted ABCB1 3'UTR directly, and miR-223 downregulated ABCB1 at both mRNA and protein levels. Finally, we found that the over-expression of miR-223 increased the HCC cell sensitivity to anticancer drugs, and the inhibition of miR-223 had the opposite effect. Importantly, the over-expression or silencing of ABCB1 can rescue the cell response to the anticancer drugs mediated by miR-223 over-expression or inhibition, respectively. In conclusion, our findings indicated that miR-223 played an important role in the regulation of MDR mediated by ABCB1, and it suggests that miR-223 may be considered as a therapeutic biomarker for HCC patients who had MDR problems induced by high expression of ABCB1.

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“…The knockdown of miR-140 expression in CRC stem cells restored their chemosensitivity to 5-FU, indicating that miRNAs and their inhibitors can be potential candidates for adjuvant therapy in addition to chemotherapy. MiR-222 has been found involved in multidrug resistance of CRC (Xu et al 2012a ). ADAM-17 is a predicted target of miR-222, which was down-regulated in multidrug-resistant CRC cells.…”

Section: Micrornas and Colorectal Cancersmentioning

confidence: 99%

MicroRNAs in Solid Tumors

Leva

Garofalo

2014

MicroRNAs: Key Regulators of Oncogenesis

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MicroRNAs (miRNAs) are a class of non-coding RNAs that hybridize to mRNAs inducing either translation repression or mRNA cleavage. MiRNAs regulate a variety of biological processes in the cell, including development, cell differentiation, proliferation, apoptosis and their abnormal expression levels are closely associated with pathogenesis of cancers. In this scenario, several high-throughput technologies studies have revealed miRNA roles in classifying tumors and predicting patient outcome with high accuracy. Because of their ability to concurrently target multiple pathways miRNA-based anticancer therapies are being developed, either alone or in combination with current targeted therapies, with the goal to improve the response and increase cure rates. Here, we highlight recent advances on the use of miRNAs as a potential approach for diagnosis and prognosis of solid cancer.

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MiR-222 modulates multidrug resistance in human colorectal carcinoma by down-regulating ADAM-17

Cited by 68 publications

References 31 publications

miR-222 regulates sorafenib resistance and enhance tumorigenicity in hepatocellular carcinoma

miR-222 regulates sorafenib resistance and enhance tumorigenicity in hepatocellular carcinoma

MiR-223 modulates multidrug resistance via downregulation of ABCB1 in hepatocellular carcinoma cells

MicroRNAs in Solid Tumors

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