<i>miR‐370</i> modulates insulin receptor substrate‐1 expression and inhibits the tumor phenotypes of oral carcinoma

Chang, Kuo Wei; Chu, Ting; Gong, Nan-Ling; Chiang, Wei Fan; Yang, Cheng Chieh; Liu, C. J.; Wu, Cheng Hsien; Lin, Shu Chun

doi:10.1111/odi.12046

Cited by 41 publications

(36 citation statements)

References 33 publications

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“…Among these were a number of miRNAs previously characterized in HNSCC, notably miR-29b-1, -2 [33], miR-370 [34], miR-126 [35], miR-337 [36] , miR-30e [37], and miR-106b [9]. Taken together, these findings suggest a substantial role for our identified ncRNAs in key oncogenic pathways and molecular signatures.…”

Section: Resultssupporting

confidence: 54%

The non-coding landscape of head and neck squamous cell carcinoma

et al. 2016

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Head and neck squamous cell carcinoma (HNSCC) is an aggressive disease marked by frequent recurrence and metastasis and stagnant survival rates. To enhance molecular knowledge of HNSCC and define a non-coding RNA (ncRNA) landscape of the disease, we profiled the transcriptome-wide dysregulation of long non-coding RNA (lncRNA), microRNA (miRNA), and PIWI-interacting RNA (piRNA) using RNA-sequencing data from 422 HNSCC patients in The Cancer Genome Atlas (TCGA). 307 non-coding transcripts differentially expressed in HNSCC were significantly correlated with patient survival, and associated with mutations in TP53, CDKN2A, CASP8, PRDM9, and FBXW7 and copy number variations in chromosomes 3, 5, 7, and 18. We also observed widespread ncRNA correlation to concurrent TP53 and chromosome 3p loss, a compelling predictor of poor prognosis in HNSCCs. Three selected ncRNAs were additionally associated with tumor stage, HPV status, and other clinical characteristics, and modulation of their expression in vitro reveals differential regulation of genes involved in epithelial-mesenchymal transition and apoptotic response. This comprehensive characterization of the HNSCC non-coding transcriptome introduces new layers of understanding for the disease, and nominates a novel panel of transcripts with potential utility as prognostic markers or therapeutic targets.

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Section: Resultssupporting

confidence: 54%

The non-coding landscape of head and neck squamous cell carcinoma

et al. 2016

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“…Many studies have shown that miR-370 is commonly deregulated in multiple human tumors and implicated in various aspects of tumors, including growth, metastasis and senescence [18-22]. Our group found that miR-370 is involved in AML and Helicobacter pylori -induced gastric carcinogenesis by directly targeting FoxM1 [17,20].…”

Section: Discussionmentioning

confidence: 99%

“…Increasing evidence has shown that miR-370 regulates a number of target genes, including Wilms tumor gene on the X chromosome [25], insulin receptor substrate 1 [22], Forkhead box protein O1 [26] and FoxM1 in AML by our group [20]. FoxM1 is the master positive regulator of the cell cycle and is related to cell proliferation, cell cycle progression and apoptosis [27-34].…”

Section: Discussionmentioning

confidence: 99%

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MiR-370 sensitizes chronic myeloid leukemia K562 cells to homoharringtonine by targeting Forkhead box M1

et al. 2013

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BackgroundHomoharringtonine (HHT) is a kind of cephalotaxus alkaloid used in traditional Chinese medicine. Although HHT has been successfully used as a therapeutic agent for leukemia, the drug resistance and toxicity are major concerns. MicroRNAs (miRNAs) have been identified to modulate cellular sensitivity to anticancer drugs. We examined the synergistic action between miR-370 and HHT in vitro and in vivo.MethodsThe synergistic action between miR-370 and HHT was examined by flow cytometry. The effect of HHT on miR-370 expression was determined by quantitative RT-PCR (qRT-PCR). The expression of miR-370 and Forkhead box M1 (FoxM1) in 23 patients with newly diagnosed chronic-phase chronic myeloid leukemia (CML-CP) and 10 patients with blast-crisis CML (CML-BP) as well as miR-370–targeted FoxM1 was determined by qRT-PCR and western blot analysis.ResultsEctopic expression of miR-370 sensitized the CML K562 cell line to HHT by targeting FoxM1, the major regulator in cell proliferation and apoptosis. miR-370 significantly promoted HHT-mediated cell apoptosis and miR-370 and HHT cooperated in affecting FoxM1 expression. As well, miR-370 was moderately upregulated after HHT treatment in K562 cells. In addition, the expression of miR-370 was significantly reduced in CML patients as compared with healthy controls. Furthermore, the expression of miR-370 was lower in CML-BP than CML-CP patients.ConclusionsMiR-370 sensitized K562 cells to HHT by inducing apoptosis in part by downregulation of FoxM1 expression. These findings may provide further information for CML treatment with HHT.

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“…Several studies revealed that miR-370 acts as tumor promoter in gastric cancer, prostate cancer, and AML; whereas other studies reported miR-370 as a tumor suppressor in leukemia and oral squamous carcinoma 206-210 . Xu et al 167 observed that the down-regulation of miR-370 was associated with HCC development in rats and correlated with poor survival in HCC patients, indicating that miR-370 serves as a tumor suppressor in HCC.…”

Section: Mirnas Are a Novel Class Of Molecules Linking Inflammation Amentioning

confidence: 99%

Role of microRNAs in inflammation-associated liver cancer

Huan

Liang

2016

Cancer Biology & Medicine

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Liver cancer, primarily hepatocellular carcinoma (HCC), is a major cause of cancer-related death worldwide. HCC is a suitable model of inflammation-induced cancer because more than 90% of HCC cases are caused by liver damage and chronic inflammation. Several inflammatory response pathways, such as NF-κB and JAK/STAT3 signaling pathways, play roles in the crosstalk between inflammation and HCC. MicroRNAs (miRNAs) are evolutionarily conserved, short endogenous, non-coding single-stranded RNAs that are involved in various biological and pathological processes by regulating gene expression and protein translation. Evidence showed that miRNAs play a pivotal role in hepatitis virus infection and serve as promoters or inhibitors of inflammatory response. Aberrant miRNA was observed during liver inflammation and HCC. Many dysregulated miRNAs modulate the initiation and progression of inflammation-induced HCC. This review summarizes the role and functions of miRNAs in inflammation-associated HCC, as well as the designed therapeutics targeting miRNAs to treat liver inflammation and HCC.

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miR‐370 modulates insulin receptor substrate‐1 expression and inhibits the tumor phenotypes of oral carcinoma

Abstract: This study concludes that miR-370 is able to target IRS-1 for oral tumorigenesis.

Cited by 41 publications

References 33 publications

The non-coding landscape of head and neck squamous cell carcinoma

The non-coding landscape of head and neck squamous cell carcinoma

MiR-370 sensitizes chronic myeloid leukemia K562 cells to homoharringtonine by targeting Forkhead box M1

Role of microRNAs in inflammation-associated liver cancer

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