hsa-miR-191 Is a Candidate Oncogene Target for Hepatocellular Carcinoma Therapy

Elyakim, Eran; Sitbon, Einat; Faerman, Alexander; Tabak, Sarit; Montia, Eve; Belanis, Liron; Dov, Avital; Marcusson, Eric G.; Bennett, C. Frank; Chajut, Ayelet; Cohen, Dalia; Yerushalmi, Noga

doi:10.1158/0008-5472.can-10-1313

Cited by 145 publications

(125 citation statements)

References 47 publications

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“…The evidence of cancer xenograft models in our study has already been shown, but studies to date have shown only changes in tumor size when cells were transfected by miR-338-3p and control vector, and then injected to produce the tumor model. Such studies were also performed for prostate cancer (37), hepatocellular carcinoma (38), and pancreatic cancer (39). These results also confirmed the tumor-suppressive role of miR-338-3p in gastric cancer.…”

Section: Discussionsupporting

confidence: 70%

miR-338-3p Suppresses Gastric Cancer Progression through a PTEN-AKT Axis by Targeting P-REX2a

Guo

Liu

Yao

et al. 2014

Molecular Cancer Research

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Results from recent studies suggest that aberrant microRNA expression is common in numerous cancers. Although miR-338-3p has been implicated in hepatocellular carcinoma, its role in gastric cancer is unknown. To this end, we report that miR-338-3p is downregulated in both gastric cancer tissue and cell lines. Forced expression of miR-338-3p inhibited cell proliferation and clonogenicity and induced a G 1 -S arrest as well as apoptosis in gastric cancer cells. Furthermore, P-Rex2a (PREX2) was identified as a direct target of miR-338-3p, and silencing P-Rex2a resulted in the same biologic effects of miR-338-3p expression in gastric cancer cells. Furthermore, both enforced expression of miR-338-3p or silencing of P-Rex2a resulted in activation of PTEN, leading to a decline in AKT phosphorylation. Also, miR-338-3p markedly inhibited the in vivo tumorigenicity in a nude mouse xenograft model system. These results demonstrate that miR-338-3p affects gastric cancer progression through PTEN-AKT signaling by targeting P-Rex2a in gastric cancer cells, which posits miR-338-3p as a novel strategy for gastric cancer treatment.

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Section: Discussionsupporting

confidence: 70%

miR-338-3p Suppresses Gastric Cancer Progression through a PTEN-AKT Axis by Targeting P-REX2a

Guo

Liu

Yao

et al. 2014

Molecular Cancer Research

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“…Elyakim et al (42) reported that miR-191-5p inhibition has great potential in the treatment of hepatocellular carcinoma patients. In addition, miR-191-5p is a potential target in treating radiation-resistant lung cancer according to the study by Liu and Huang (43).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑191‑5p exerts a tumor suppressive role in renal cell carcinoma

et al. 2017

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Abstract. Renal cell carcinoma (RCC) is a common tumor of the urinary system. Previously, miR-191-5p has been reported to be associated with various types of cancer; however, its specific functions in RCC have not been investigated to date. In the present study, the expression of miR-191-5p in the 786-O and ACHN cell lines was detected in vitro by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results of RT-qPCR revealed that miR-191-5p was significantly downregulated in the two cell lines compared with the 293T cell line. miR-191-5p was also significantly downregulated in RCC tissue compared with paired normal tissue. In addition, the effects of miR-191-5p on cell proliferation, migration, invasion and apoptosis were examined by CCK-8, MTT, wound scratch, Transwell and flow cytometry assays. Downregulation of miR-191-5p was observed to promote cell proliferation, migration and invasion, as well as to repress the cell apoptosis of 786-O and ACHN cells. Therefore, the current study suggests that miR-191-5p functions as a tumor suppressor in RCC. Further studies are required to uncover the underlying signaling pathway of miR-191-5p and its potential role as a biomarker for early detection and prognosis prediction, and as a therapeutic target of RCC.

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“…1A) were amplified in breast cancer compared with normal breast tissues. miR-191 has been validated to be amplified and is viewed as a candidate oncogenic miRNA in liver (38), stomach (39), and pancreas (40). LOH comprises not only monosomy, caused by loss of 1 allele, but also homozygous disomy and homozygous polysomies, caused by the concurrent loss of 1 allele and endomultiplication of the other allele (41).…”

Section: Discussionmentioning

confidence: 99%

Loss of SNAIL Regulated miR-128-2 on Chromosome 3p22.3 Targets Multiple Stem Cell Factors to Promote Transformation of Mammary Epithelial Cells

Qian

Banerjee

et al. 2012

Cancer Research

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A discontinuous pattern of LOH at chromosome 3p has been reported in 87% of primary breast cancers. Despite the identification of several tumor suppressor genes in this region, there has yet to be a detailed analysis of noncoding RNAs including miRNAs in this region. In this study, we identified 16 aberrant miRNAs in this region and determined several that are frequently lost or amplified in breast cancer. miR-128-2 was the most commonly deleted miRNA. Embedded in the intron of the ARPP21 gene at chromosome 3p22.3, miR-128-2 was frequently downregulated along with ARPP21 in breast cancer, where it was negatively associated with clinicopathologic characteristics and survival outcome. Forced expression of miR-128 impeded several oncogenic traits of mammary carcinoma cells, whereas depleting miR-128-2 expression was sufficient for oncogenic transformation and stem cell-like behaviors in immortalized nontumorigenic mammary epithelial cells, both in vitro and in vivo. miR-128-2 silencing enabled transforming capacity partly by derepressing a cohort of direct targets (BMI1, CSF1, KLF4, LIN28A, NANOG, and SNAIL), which together acted to stimulate the PI3K/AKT and STAT3 signaling pathways. We also found that miR-128-2 was directly downregulated by SNAIL and repressed by TGF-b signaling, adding 2 additional negative feedback loops to this network. In summary, we have identified a novel TGF-b/SNAIL/miR-128 axis that provides a new avenue to understand the basis for oncogenic transformation of mammary epithelial cells. Cancer Res; 72(22); 6036-50. Ó2012 AACR.

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hsa-miR-191 Is a Candidate Oncogene Target for Hepatocellular Carcinoma Therapy

Cited by 145 publications

References 47 publications

miR-338-3p Suppresses Gastric Cancer Progression through a PTEN-AKT Axis by Targeting P-REX2a

miR-338-3p Suppresses Gastric Cancer Progression through a PTEN-AKT Axis by Targeting P-REX2a

MicroRNA‑191‑5p exerts a tumor suppressive role in renal cell carcinoma

Loss of SNAIL Regulated miR-128-2 on Chromosome 3p22.3 Targets Multiple Stem Cell Factors to Promote Transformation of Mammary Epithelial Cells

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