miR-137 downregulates c-kit expression in acute myeloid leukemia

Hu, Yanping; Dong, Xinxin; Chu, Guoming; Lai, Guangrui; Zhang, Bijun; Wang, Leitong; Zhao, Yanyan

doi:10.1016/j.leukres.2017.01.028

Cited by 14 publications

(5 citation statements)

References 32 publications

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“…When c-Kit activates PI3K/AKT, the latter kinase phosphorylates Bad, preventing pore formation in the mitochondrion and inhibiting apoptosis [19]. Additionally, inhibition of c-Kit with miR-137 promotes apoptosis in AML [31]. These data indicate that c-Kit/PI3K promote the inhibition of apoptosis, which is consistent with our results.…”

Section: Discussionsupporting

confidence: 91%

Cell proliferation and inhibition of apoptosis are related to c-Kit activation in leukaemic lymphoblasts

et al. 2018

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Section: Discussionsupporting

confidence: 91%

Cell proliferation and inhibition of apoptosis are related to c-Kit activation in leukaemic lymphoblasts

et al. 2018

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“…Moreover, CXCL12 might serve as an effective novel supplementary diagnostic marker for PTC [36]. As a comparison, it has been proved that miR-137 could downregulate KIT or CXCL12 in other cancers such as small cell lung cancer [37], acute myeloid leukemia [38], and glioblastoma [39]. However, recent research has shown that miR-137 was downregulated in thyroid cancer and inhibits proliferation and invasion by targeting EGFR [40], and it could act as a tumor suppressor in papillary thyroid carcinoma [41].…”

Section: Discussionmentioning

confidence: 99%

In Silico Integration Approach Reveals Key MicroRNAs and Their Target Genes in Follicular Thyroid Carcinoma

Liao

Zheng

et al. 2019

BioMed Research International

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To better understand the molecular mechanism for the pathogenesis of follicular thyroid carcinoma (FTC), this study aimed at identifying key miRNAs and their target genes associated with FTC, as well as analyzing their interactions. Based on the gene microarray data GSE82208 and microRNA dataset GSE62054, the differentially expressed genes (DEGs) and microRNAs (DEMs) were obtained using R and SAM software. The common DEMs from R and SAM were fed to three different bioinformatic tools, TargetScan, miRDB, and miRTarBase, respectively, to predict their biological targets. With DEGs intersected with target genes of DEMs, the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed through the DAVID database. Then a protein-protein interaction (PPI) network was constructed by STRING. Finally, the module analysis for PPI network was performed by MCODE and BiNGO. A total of nine DEMs were identified, and their function might work through regulating hub genes in the PPI network especially KIT and EGFR. KEGG analysis showed that intersection genes were enriched in the PI3K-Akt signaling pathway and microRNAs in cancer. In conclusion, the study of miRNA-mRNA network would offer molecular support for differential diagnosis between malignant FTC and benign FTA, providing new insights into the potential targets for follicular thyroid carcinoma diagnosis and treatment.

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“… 11 As a receptor tyrosine kinase, KIT functions in regulation processes of cell proliferation, migration, stem cell maintenance, differentiation as well as the occurrence of several cancers, such as leukemia, 12 melanoma, 13 breast cancer 14 and thyroid carcinoma, 15 suggesting KIT might be an important tumor-promoting factor that associated with metastasis and overall poor prognosis. It is reported that binding between KIT and corresponding target mRNAs, such as miR-137, 16 miR-221 17 and miR-155 18 would result in the suppression of growth and metastasis in various cancers. However, whether binding between KIT and miR-508-5p participates in progression of melanoma is still unclear.…”

Section: Introductionmentioning

confidence: 99%

A Potential Tumor Suppressor Gene Named miR-508-5p Inhibited the Proliferation and Invasion of Human Melanoma Cells by Targeting KIT

Lin

Wang

Shi

et al. 2020

Technol Cancer Res Treat

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Melanoma is the main death cause of human skin cancer. Increasing evidences demonstrate that microRNAs act as key roles in mediating tumor occurrence and progression. MiR-508-5p has proved to participate in the development of various types of human malignancies. However, the role of miR-508-5p in melanoma remained unclear. In in vitro study, miR-508-5p level in peripheral blood samples of patients with melanoma and human melanoma A375 cells was downregulated compared to that in normal peripheral blood samples or normal human epidermal melanocytes (MHEM). MiR-508-5p overexpression significantly inhibited the cell proliferation, migration and invasion in A375 cells, and thus inhibiting KIT expression at both gene and protein levels. Furthermore, western blot analysis showed miR-508-5p reduced cell proliferation by targeting KIT to modulate RAS/RAF/MEK/ERK pathway. Taken together, we speculated that miR-508-5p functioned as an important suppressor in human melanoma by targeting KIT, suggesting miR-508-5p might be a promising tumor suppressor gene for further target therapies from bench to clinic.

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miR-137 downregulates c-kit expression in acute myeloid leukemia

Cited by 14 publications

References 32 publications

Cell proliferation and inhibition of apoptosis are related to c-Kit activation in leukaemic lymphoblasts

Cell proliferation and inhibition of apoptosis are related to c-Kit activation in leukaemic lymphoblasts

In Silico Integration Approach Reveals Key MicroRNAs and Their Target Genes in Follicular Thyroid Carcinoma

A Potential Tumor Suppressor Gene Named miR-508-5p Inhibited the Proliferation and Invasion of Human Melanoma Cells by Targeting KIT

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