MicroRNA-137-mediated Src oncogenic signaling promotes cancer progression.
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TLDR
In this paper, the authors examined whether microRNA-mediated c-Src upregulation promotes cancer progression, and they found that miR-137 targets AKT2 and paxillin also and miR137-mediated regulation of cSrc /AKT2 is crucial for controlling tumor growth, whereas that of c- Src/paxillin contributes to malignancy.Abstract:
The tyrosine kinase c-Src is frequently overexpressed and activated in a wide variety of human cancers. However, the molecular mechanisms responsible for the upregulation of c-Src remain elusive. To examine whether microRNA-mediated c-Src upregulation promotes cancer progression, we screened miRNAs with complementarity to the 3'-UTR of c-Src mRNA. Among these miRNAs, down-regulation of miR-137 was tightly associated with c-Src-mediated tumor progression of human colon cancer cells/tissues. Re-expression of miR-137 in human colon cancer cells suppressed tumor growth and caused the disruption of focal contacts, suppression of cell adhesion, and invasion, although restoration of c-Src in miR-137-treated cells could not fully rescue the tumor-suppressive effect of miR-137. We found that miR-137 targets AKT2 and paxillin also and miR-137-mediated regulation of c-Src /AKT2 is crucial for controlling tumor growth, whereas that of c-Src/paxillin contributes to malignancy. miR-137 suppressed Src-related oncogenic signaling and changed the expression of miRNAs that are regulated by Src activation. miR-137 controls the expression of c-Src/AKT2/paxillin and synergistically suppresses Src oncogenic signaling evoked from focal adhesions. In various human cancers that harbor c-Src upregulation, the dysfunction of this novel mechanism would serve as a critical trigger for tumor progression.read more
Citations
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Journal ArticleDOI
Regulation of Src Family Kinases during Colorectal Cancer Development and Its Clinical Implications
TL;DR: An overview of the current understanding of the correlations between Src and CRC progression is provided, with a special focus on cancer cell proliferation, invasion, metastasis and chemoresistance, and formation of CSCs.
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miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke.
TL;DR: It is suggested that, in mice, miR-137 confers neuroprotective effects against ischemic stroke via attenuation of oxidative, apoptotic, and inflammatory pathways through inhibiting Src-dependent MAPK signaling pathway.
Journal ArticleDOI
c-Src promotes tumor progression through downregulation of microRNA-129-1-3p.
Daisuke Okuzaki,Tomoe Yamauchi,Fumie Mitani,Mamiko Miyata,Yuichi Ninomiya,Risayo Watanabe,Hiroki Akamatsu,Chitose Oneyama +7 more
TL;DR: C‐SRC‐miR‐129‐1‐3p circuits serve as critical triggers for tumor progression in many human cancers that harbor upregulation of c‐Src.
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The Differential DNA Hypermethylation Patterns of microRNA-137 and microRNA-342 Locus in Early Colorectal Lesions and Tumours.
Elham Kashani,Elham Kashani,Mahrooyeh Hadizadeh,Vahid Chaleshi,Reza Mirfakhraie,Christopher N. J. Young,Sanaz Savabkar,Shiva Irani,Hamid Asadzadeh Aghdaei,Maziar Ashrafian Bonab +9 more
TL;DR: Methylation status of mi RNA-137 and miRNA-342 has both diagnostic and prognostic value in CRC prediction and prevention and was significantly higher in tumour lesions compared to normal adjacent mucosa.
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The full recovery of mice (Mus Musculus C57BL/6 strain) from virus-induced sarcoma after treatment with a complex of DDMC delivery system and sncRNAs.
Oxana V. Klimenko,Alexey Sidorov +1 more
TL;DR: Treatment of virus-induced sarcoma of mice with a-miR-155, piR-30074, and miR-125b as active component of anti-cancer complex and DDMC vector as delivery system due to epigenetic-regulated transformation of cancer cells into cells with non-cancerous physiology and morphology and full recovery of disease.
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