Anti-microRNA-222 (Anti-miR-222) and -181B Suppress Growth of Tamoxifen-resistant Xenografts in Mouse by Targeting TIMP3 Protein and Modulating Mitogenic Signal

Lu, Yuanzhi; Roy, Satavisha; Nuovo, Gerard J.; Ramaswamy, Bhuvaneswari; Miller, Tyler E.; Shapiro, Charles L.; Jacob, Samson T.; Majumder, Sarmila

doi:10.1074/jbc.m111.270926

Cited by 95 publications

(69 citation statements)

References 39 publications

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“…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%

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: 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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“…As a member of the miR-181 family, miR-181b also may play a role in the variation in tumorigenesis among different cancers, and its decreased expression is inversely correlated with increased protein levels of the myeloid cell leukemia sequence 1-and B-cell lymphoma 2-targeted genes (Ji et al, 2009;Chen et al, 2010). miR-181b may also contribute to drug resistance of tamoxifen in breast cancer and tumor progression of gastric carcinomas (Jiang et al, 2011;Lu et al, 2011;Visone et al, 2012). In our study, the higher expression of miR-181b in signet-ring cell carcinoma compared with that in tubular adenocarcinoma suggests a correlation with the more malignant clinical behavior of signet-ring cell carcinoma.…”

Section: Discussionsupporting

confidence: 53%

Differential microRNA expression in signet-ring cell carcinoma compared with tubular adenocarcinoma of human gastric cancer

Li¹,

Xu²,

Wu³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Gastric cancer is a disease with a heterogeneous pathology; its pathological mechanisms remain unclear because there is a poor understanding of its etiology. In this study, we identified differentially expressed microRNAs (miRNAs) among various gastric cancer subtypes. miRNA microarray analysis and bioinformatic analysis were used to compare miRNA expression between the signet-ring cell carcinoma and tubular adenocarcinoma subtypes of gastric cancer. Thirteen dysregulated miRNAs were identified in signet-ring cell carcinoma compared with tubular adenocarcinoma: miR-30a, miR-26b,

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“…Recently, it has been indicated that these miRNAs induce resistance to the selective ER downregulator, and this was caused by the activation of β-catenin and the repression of transforming growth factor-β-mediated growth inhibition. 54 Lu et al 55 demonstrated that miR-221, miR-222 and miR-181b directly target tissue inhibitor of metalloproteinases (TIMP)3, and MCF7 cells that had been subjected to TIMP3 knockdown were found to be able to Figure 2 Biogenesis and function of microRNA (miRNA). miRNA genes are transcribed by RNA polymerase II (Pol II) in the nucleus to generate primary miRNA (pri-miRNA).…”

Section: Mirna In Hormone Receptor-positive/her2-negative Breast Cancermentioning

confidence: 99%

Recent trends in microRNA research into breast cancer with particular focus on the associations between microRNAs and intrinsic subtypes

et al. 2016

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MicroRNAs (miRNAs) are short non-coding RNAs that regulate the function of target genes at the post-transcriptional phase. miRNAs are considered to have roles in the development, progression and metastasis of cancer. Recent studies have indicated that particular miRNA signatures are correlated with tumor aggressiveness, response to drug therapy and patient outcome in breast cancer. On the other hand, in routine clinical practice, the treatment regimens for breast cancer are determined based on the intrinsic subtype of the primary tumor. Previous studies have shown that miRNA expression profiles of each intrinsic subtypes of breast cancer differ. In hormone receptor-positive/human epidermal growth factor receptor 2 (HER2)-negative breast cancer, miRNA expressions are found to be correlated with endocrine therapy resistance, progesterone receptor expression and heat shock protein activity. Some miRNAs are associated with resistance to HER2-targeted therapy and HER3 expression in HER2-positive breast cancer. In triple-negative breast cancer, miRNA expressions are found to be associated with BRCA mutations, immune system, epithelial-mesenchymal transition, cancer stem cell properties and androgen receptor expression. As it has been clarified that the expression levels and functions of miRNA differ among the various subtypes of breast cancer, and it is necessary to take account of the characteristics of each breast cancer subtype during research into the roles of miRNA in breast cancer. In addition, the discovery of the roles played by miRNAs in breast cancer might provide new opportunities for the development of novel strategies for diagnosing and treating breast cancer.

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Anti-microRNA-222 (Anti-miR-222) and -181B Suppress Growth of Tamoxifen-resistant Xenografts in Mouse by Targeting TIMP3 Protein and Modulating Mitogenic Signal

Cited by 95 publications

References 39 publications

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

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

Differential microRNA expression in signet-ring cell carcinoma compared with tubular adenocarcinoma of human gastric cancer

Recent trends in microRNA research into breast cancer with particular focus on the associations between microRNAs and intrinsic subtypes

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