Differential expression of miRNAs in esophageal cancer tissue

Liu, Shangguo; Qin, Xiuguang; Zhao, Baosheng; Qi, Bo; Yao, Wenjian; Wang, Tianyun; Li, Hanchen; Wu, Xiangnan

doi:10.3892/ol.2013.1251

Cited by 124 publications

(79 citation statements)

References 15 publications

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“…By contrast, it was suggested that miR-194 served a role in the promotion and progression of breast cancer (9) and pancreatic ductal adenocarcinoma (40). These studies indicated that miR-194 had various target genes (31)(32)(33)(34)(35)(36)(37)(38)(39)(40). Previous studies have demonstrated that miR-194 inhibited cell migration and invasion, which may have contributed to the anti-tumor activity of trastuzumab on HER2-overexpressing breast cancer cells (41,42).…”

Section: Discussionmentioning

confidence: 89%

Promotional effect of microRNA-194 on breast cancer cells via targeting F-box/WD repeat-containing protein 7

et al. 2018

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Abstract. Breast cancer is the most common type of malignant cancer in females. An increasing number of studies have revealed that microRNAs (miR), which belong to a class of small non-coding RNAs, serve an important role in a number of human cancer subtypes. In the present study, the role of miR-194 in breast cancer cells and its underlying mechanisms were investigated. The results demonstrated that the serum levels of miR-194 were significantly higher in patients of the poorly differentiated and well-differentiated groups, compared with in healthy adults. Additionally, the serum level of miR-194 was significantly higher in the poorly differentiated group compared with in the well-differentiated group. In order to further investigate the role of miR-194 in breast cancer cells, the present study transfected two breast cancer cell lines, MCF-7 and MDA-MB-231, with an empty vector (control), miR-194 (overexpression), antagomiR-194 (inhibitor, functional knock down) or antagomiR-194 and miR-194. An MTT assay was performed in order to detect the proliferation of breast cancer cells in the various groups. The results revealed that the overexpression of miR-194 significantly accelerated cell proliferation, whereas the inhibition of miR-194 significantly decelerated the proliferation of MCF-7 and MDA-MB-231 cells. Furthermore, the expression levels of cyclin D and cyclin E were significantly upregulated in miR-194 overexpressing cells, and the expression levels of cyclin D and cyclin E were significantly downregulated in miR-194 inhibited cells, as compared with in control cells. No significant change was observed in the level of proliferation of cells co-transfected with miR-194 and antagomiR-194, compared with in the control cells. According to the hypothesis suggesting possible target genes of miR-194, the present study proposed that F-box/WD repeat-containing protein 7 (Fbxw-7) may be a direct target of miR-194, which was confirmed by a luciferase reporter assay. The present study suggested that miR-194 expression promoted the proliferation of breast cancer cells by targeting Fbxw-7, and may serve as a biomarker and a novel target for breast cancer therapy.

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Section: Discussionmentioning

confidence: 89%

Promotional effect of microRNA-194 on breast cancer cells via targeting F-box/WD repeat-containing protein 7

et al. 2018

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“…Deregulated miR-28 expression has been observed in several types of cancer, including up-regulation in esophageal, cervical, and renal cancer, and in myeloproliferative malignancies and down-regulation in colorectal cancer and nasal-type natural killer/T-cell lymphoma (10)(11)(12)(13)(14)(15)(16). These apparently inconsistent observations are not surprising because it is well established that miRNAs can act both as tumor suppressors and oncogenes depending on the cell context (29).…”

Section: Mir-28 As a Candidate Tumor Suppressor In Gc-derived Lymphomasmentioning

confidence: 88%

“…miR-28 has been shown to be deregulated in several cancer types. Although increased levels of miR-28 expression have been observed in esophageal, cervical, renal cancer, as well as in the platelets of a fraction of myeloproliferative neoplasm patients (10)(11)(12)(13), miR-28 is down-regulated in colorectal cancer cells and nasal-type natural killer/T-cell lymphoma. In both these latter cell types, reexpression of miR-28 leads to reduced proliferation in cell lines (14)(15)(16).…”

mentioning

confidence: 99%

microRNA 28 controls cell proliferation and is down-regulated in B-cell lymphomas

Schneider

Setty

Holmes

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Burkitt lymphoma (BL) is a highly aggressive B-cell non-Hodgkin lymphoma (B-NHL), which originates from germinal center (GC) B cells and harbors translocations deregulating v-myc avian myelocytomatosis viral oncogene homolog (MYC). A comparative analysis of microRNAs expressed in normal and malignant GC B cells identified microRNA 28 (miR-28) as significantly down-regulated in BL, as well as in other GC-derived B-NHL. We show that reexpression of miR-28 impairs cell proliferation and clonogenic properties of BL cells by modulating several targets including MAD2 mitotic arrest deficientlike 1, MAD2L1, a component of the spindle checkpoint whose downregulation is essential in mediating miR-28-induced proliferation arrest, and BCL2-associated athanogene, BAG1, an activator of the ERK pathway. We identify the oncogene MYC as a negative regulator of miR-28 expression, suggesting that its deregulation by chromosomal translocation in BL leads to miR-28 suppression. In addition, we show that miR-28 can inhibit MYC-induced transformation by directly targeting genes up-regulated by MYC. Overall, our data suggest that miR-28 acts as a tumor suppressor in BL and that its repression by MYC contributes to B-cell lymphomagenesis.

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“…In addition, miR-452 decreased cyclin-dependent kinase inhibitor 1B (CDKN1B) mRNA and protein expression by directly targeting the 3'UTR of CDKN1B; the knockdown of CDKN1B resembled the phenotype resulting from overexpression of miR-452 expression (18). miR-452 was also demonstrated to be an oncogene in esophageal cancer (26) and urothelial carcinoma (27). These conflicting studies indicated that the expression and functions of miR-452 in human cancers have tissue specificity.…”

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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Differential expression of miRNAs in esophageal cancer tissue

Cited by 124 publications

References 15 publications

Promotional effect of microRNA-194 on breast cancer cells via targeting F-box/WD repeat-containing protein 7

Promotional effect of microRNA-194 on breast cancer cells via targeting F-box/WD repeat-containing protein 7

microRNA 28 controls cell proliferation and is down-regulated in B-cell lymphomas

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

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