miR-24 promotes the proliferation and invasion of HCC cells by targeting SOX7

Ma, Ying; She, Xiaojun; Ming, Yingzi; Wan, Qiquan

doi:10.1007/s13277-014-2018-6

Cited by 51 publications

(29 citation statements)

References 24 publications

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“…The function of miR-24 as a tumor suppressor can inhibit cell proliferation, migration and invasion by regulating cMyc and E2F2 in HCC-derived HepG2 cell line, [45] and Fascin homologue 1 ( FSCN1 ) in nasopharyngeal carcinoma cell lines. [46] On the other hand, miR-24 acted as an oncogene directly repressing SOX7 (Sex Determining Region Y-Box 7), a putative tumor suppressor, [47] and overexpressed miR-24 led to inhibition of hepatocyte nuclear factor 4α and initiated hepatocellular transformation through an epigenetic positive feedback circuit in the absence of genetic alterations. [48] Tumor suppressor gene ( p16 ) [49] and pro-apoptotic protein FAF1 [50] can be negatively regulated by miR-24 in cervical carcinoma, prostate, gastric and HeLa cells.…”

Section: Discussionmentioning

confidence: 99%

Identifying microRNA panels specifically associated with hepatocellular carcinoma and its different etiologies

Shen

Siegel

Remotti

et al. 2016

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Aim Deregulation of microRNAs (miRNAs) expression has been identified in hepatocellular carcinoma (HCC), but few results are consistent. The objective of this study is to investigate “HCC tumor type specific” and “tumor common” miRNA panels Methods The authors integrate and analyze clinical, etiologic and miRNA profiles data from 9 types of solid tumors in The Cancer Genome Atlas (TCGA) and HCC data from Columbia University Medical Center (CUMC). Results Levels of 33 miRNAs were significant different between HCC tumor and paired non-tumor tissues (over 2-fold changes) after Bonferroni correction for multiple comparisons, and most (28 miRNAs) were down-regulated in HCC tumors. Using this panel, the authors well classified HCC tumor tissues with 4 misclassifications among 48 paired tissues. Validating this panel in an additional 302 HCC tumor tissues, the authors almost perfectly distinguished tumor from non-tumor tissues with only two misclassifications (99% of HCC tissues correctly classified). Evaluating miRNA profiles in 32 independent HCC paired tissues from CUMC, the authors observed 40 miRNAs significantly deregulated in HCC with over 2-fold changes; 14 overlapped with those identified in TCGA. Subgroup analyses by HCC etiology found that 4 upregulated and 8 downregulated miRNAs were significantly associated with alcohol-related HCC. There were 7 and 4 miRNAs significantly associated with hepatitis B virus- and hepatitis C virus-related HCC, respectively. Data for the first time revealed that miR-24-1, miR-130a and miR-505 were significantly down-regulated only in HCC tumors; miR-142 and miR-455 were significantly down-regulated in HCC, but up-regulated in 5 other solid tumors; suggesting their HCC “tumor type specific” characteristics. A panel of 8 miRNAs was significant in at least 5 tumor types, including HCC, and was identified as “tumor common” marker. Conclusion The authors concluded that aberrant miRNA panels have HCC “tumor type specificity” and may be affected by etiologic factors.

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Section: Discussionmentioning

confidence: 99%

Identifying microRNA panels specifically associated with hepatocellular carcinoma and its different etiologies

Shen

Siegel

Remotti

et al. 2016

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“…MiR-24 has been reported to be overexpressed in hepatocellular carcinoma and inhibition of miR-24 significantly represses cell proliferation, invasion, and migration by targeting sex-determining region Y-box 7 [31]. However, miR-24 was also found to be a tumor suppressor gene that inhibited gastric cancer progression by decreasing the gene expression of regenerating islet-derived family, member four [32].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-24 Regulates Osteogenic Differentiation via Targeting T-Cell Factor-1

Zhao

Dong

et al. 2015

IJMS

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MicroRNAs (miRNAs) have been reported to have diverse biological roles in regulating many biological processes, including osteogenic differentiation. In the present study, we identified that miR-24 was a critical regulator during osteogenic differentiation. We found that overexpression of miR-24 significantly inhibited osteogenic differentiation, which decreased alkaline phosphatase activity, matrix mineralization and the expression of osteogenic differentiation markers. In contrast, inhibition of miR-24 exhibited an opposite effect. Furthermore, we delineated that miR-24 regulates post-transcriptionals of T-cell factor-1 (Tcf-1) via targeting the 3'-untranslated region (UTR) of Tcf-1 mRNA. MiR-24 was further found to regulate the protein expression of Tcf-1 in the murine osteoprogenitors cells and bone mesenchymal stem cells. Additionally, the positive effect of miR-24 suppression on osteoblast differentiation was apparently abrogated by Tcf-1 silencing. Taken together, our data suggest that miR-24 participates in osteogenic differentiation by targeting and regulating Tcf-1 expression in osteoblastic cells.

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“…miRNA-mediated control is one of the posttranscriptional mechanisms that suppress protein translation by matching to the 3′-untranslated region (UTR, 3′-UTR) of the target gene [22,23]. Computational estimations suggest that one third of protein-coding genes are regulated by miRNAs [24,25].…”

Section: Introductionmentioning

confidence: 99%

MiR-30a regulates the proliferation, migration, and invasion of human osteosarcoma by targeting Runx2

et al. 2015

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Osteosarcoma (OS) is the most common primary malignant bone tumor in young patients. However, treatment paradigms and survival rates have not improved in decades. MicroRNAs have been shown to be critical regulators of physiological homeostasis and pathological process, including bone disease. Nearly half of the microRNA (miRNA) genes are located at genomic regions and fragile sites known to be frequently deleted or amplified in various kinds of cancers. In this study, we investigated the role miR-30a in OS. A negative correlation between miR-30a expression and malignant grade was observed in OS cell lines. The overexpression of miR-30a reduced proliferation, migration, and invasion in 143B cells and the inhibitor of miR-30a increased proliferation, migration, and invasion in Saos2 cells. Further studies revealed that runt-related transcription factors 2 (Runx2) was a regulative target gene of miR-30a. Rescue assay significantly reversed the effects of overexpressing or inhibiting miR-30a. miR-30a also suppressed tumor formation and pulmonary metastasis in vivo. All the results suggest a critical role of miR-30a in suppressing proliferation, migration, and invasion of OS by targeting Runx2.

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miR-24 promotes the proliferation and invasion of HCC cells by targeting SOX7

Cited by 51 publications

References 24 publications

Identifying microRNA panels specifically associated with hepatocellular carcinoma and its different etiologies

Identifying microRNA panels specifically associated with hepatocellular carcinoma and its different etiologies

MicroRNA-24 Regulates Osteogenic Differentiation via Targeting T-Cell Factor-1

MiR-30a regulates the proliferation, migration, and invasion of human osteosarcoma by targeting Runx2

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