Down-regulation of miRNA-452 is Associated with Adriamycin-resistance in Breast Cancer Cells

Hu, Qing; Gong, Jie; Li, Jian; Zhong, Shanliang; Chen, Weixian; Zhang, Junying; Ma, Tengfei; Jiang, Hao; Lv, Mengmeng; Zhao, Jinmin; Tang, Jinhai

doi:10.7314/apjcp.2014.15.13.5137

Cited by 57 publications

(35 citation statements)

References 23 publications

(25 reference statements)

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“…Emerging evidences have shown that microRNAs are implicated in kinds of essential tumor cellular processes, such as cell proliferation, invasion, and apoptosis (Shi et al, 2008). Recent research indicated that knock-down or restored expression of specific miRNAs by miRNA inhibitors or mimics could regulate the acquired drug resistance in cancer cells (Giovannetti et al, 2012, Hu et al, 2014. For instance, it was indicated that the enhanced sensitivity of breast cancer patients to anthracycline-based chemotherapy may associate with the deletion of chromosome 11q, a region containing miR125b gene (Wang et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

miR-340 Reverses Cisplatin Resistance of Hepatocellular Carcinoma Cell Lines by Targeting Nrf2-dependent Antioxidant Pathway

Shi

Chen²,

Wu³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Section: Introductionmentioning

confidence: 99%

miR-340 Reverses Cisplatin Resistance of Hepatocellular Carcinoma Cell Lines by Targeting Nrf2-dependent Antioxidant Pathway

Shi

Chen²,

Wu³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…miR-452 has been studied in numerous types of human cancer (15,16,25). For example, He et al (15) reported that the expression levels of miR-452 were decreased in non-small-cell lung cancer, and low expression levels of miR-452 were associated with advanced tumor stage and more extent of lymph nodes metastasis.…”

Section: Discussionmentioning

confidence: 99%

“…In breast cancer, miR-452 was downregulated in adriamycin-resistant MCF-7 cells compared with in parental MCF-7 cells. miR-452 mediated chemosensitivity to adriamycin in human breast cancer cells (16). Furthermore, bioinformatics analysis, RT-qPCR and western blot analysis have demonstrated that miR-452 may be at least in part be involved in adriamycin-resistance of breast cancer via the targeting of insulin-like growth factor-1 (16).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-452 suppresses pancreatic cancer migration and invasion by directly targeting B-cell-specific Moloney murine leukemia virus insertion site 1

Li¹,

Wu²,

Li³

2017

Oncology Letters

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Abstract. Pancreatic cancer, one of the most common cancers globally, is the fourth most common cause of cancer-associated mortality in the USA. The 5-year relative survival rate for patients with pancreatic cancer is ~5% and the median survival time is only 6 months. The poor prognosis is mainly due to early and aggressive local invasion and metastasis, as well as dissemination of the pancreatic cancer cells. The present study demonstrated that microRNA-452 (miR-452) was markedly downregulated in pancreatic cancer tissues, particularly in metastatic tumors and pancreatic cancer cell lines. Overexpression of miR-452 significantly inhibited migration and invasion in pancreatic cancer cells. In addition, the molecular mechanism underlying the inhibitory functions of miR-452 in pancreatic cancer was also investigated. The results indicated that B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI1) was a direct target gene of miR-452 in pancreatic cancer. Overexpression of miR-452 inhibited the migration and invasion of pancreatic cancer, at least partially by knockdown of BMI1 expression. The results provided novel insight with potential therapeutic applications for the treatment of metastatic pancreatic cancer.

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“…[34][35][36][37] MiR-452-5p is located in Xq28 of human being, which can target multiple genes and thus play a potentially important role in the BP of tumors through a variety of mechanisms. Hu et al 21 reported that miR-452-5p expression was downregulated in breast cancer, which may lead to adriamycin resistance by targeting the insulin analogue, insulin like growth factor 1 receptor (IGF-1R), and the docetaxel resistance of breast cancer cells by targeting the anaphase promoting complex 4 (APC4). Liu et al reported that the expression of multifunctional stem cell regulatory factors such as SRY-box 2 (SOX2) was downregulated after upregulating the expression of miR-452-5p in glioma cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have reported that miR-452-5p expressions in different neoplasms are distinct, which is upregulated in urinary tract epithelial tumors, esophageal cancer, and liver cancer, [18][19][20] but downregulated in breast cancer, prostate cancer, and glioma. [21][22][23] Currently, there have been only a few reports regarding the relationship between miR-452-5p and lung cancer. The clinical significance and possible molecular function (MF) of miR-452-5p in NSCLC was reported by Zhang et al 24 and He et al 25,26 However, clinical samples in their research were restricted by region and quantity, and the complicated mechanism of miR-452-5p in LUAD remained unclear.…”

Section: Introductionmentioning

confidence: 99%

Clinical value of miR-452-5p expression in lung adenocarcinoma: A retrospective quantitative real-time polymerase chain reaction study and verification based on The Cancer Genome Atlas and Gene Expression Omnibus databases

et al. 2017

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The role and mechanism of miR-452-5p in lung adenocarcinoma remain unclear. In this study, we performed a systematic study to investigate the clinical value of miR-452-5p expression in lung adenocarcinoma. The expression of miR-452-5p in 101 lung adenocarcinoma patients was detected by quantitative real-time polymerase chain reaction. The Cancer Genome Atlas and Gene Expression Omnibus databases were joined to verify the expression level of miR-452-5p in lung adenocarcinoma. Via several online prediction databases and bioinformatics software, pathway and network analyses of miR-452-5p target genes were performed to explore its prospective molecular mechanism. The expression of miR-452-5p in lung adenocarcinoma in house was significantly lower than that in adjacent tissues (p < 0.001). Additionally, the expression level of miR-452-5p was negatively correlated with several clinicopathological parameters including the tumor size (p = 0.014), lymph node metastasis (p = 0.032), and tumor-node-metastasis stage (p = 0.036). Data from The Cancer Genome Atlas also confirmed the low expression of miR-452 in lung adenocarcinoma (p < 0.001). Furthermore, reduced expression of miR-452-5p in lung adenocarcinoma (standard mean deviations = −0.393, 95% confidence interval: −0.774 to −0.011, p = 0.044) was validated by a meta-analysis. Five hub genes targeted by miR-452-5p, including SMAD family member 4, SMAD family member 2, cyclin-dependent kinase inhibitor 1B, tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein epsilon, and tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein beta, were significantly enriched in the cell-cycle pathway. In conclusion, low expression of miR-452-5p tends to play an essential role in lung adenocarcinoma. Bioinformatics analysis might be beneficial to reveal the potential mechanism of miR-452-5p in lung adenocarcinoma.

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Down-regulation of miRNA-452 is Associated with Adriamycin-resistance in Breast Cancer Cells

Cited by 57 publications

References 23 publications

miR-340 Reverses Cisplatin Resistance of Hepatocellular Carcinoma Cell Lines by Targeting Nrf2-dependent Antioxidant Pathway

miR-340 Reverses Cisplatin Resistance of Hepatocellular Carcinoma Cell Lines by Targeting Nrf2-dependent Antioxidant Pathway

MicroRNA-452 suppresses pancreatic cancer migration and invasion by directly targeting B-cell-specific Moloney murine leukemia virus insertion site 1

Clinical value of miR-452-5p expression in lung adenocarcinoma: A retrospective quantitative real-time polymerase chain reaction study and verification based on The Cancer Genome Atlas and Gene Expression Omnibus databases

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