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BIOMARKER:

miR-155 overexpression

i
Other names: MiRNA155, Hsa-Mir-155, Hsa-MiR-155-5p, MIR155 , Hsa-MiR-155-3p
Entrez ID:
Related biomarkers:
5d
LINC-PINT was negatively correlated with miR-155-5p. LINC-PINT is a potential prognostic marker of bladder cancer, and the up-regulation of Lin-PINT can inhibit the proliferation, invasion, and migration of bladder cancer cells by targeting miR-155-5p.
Journal
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MIR155 (MicroRNA 155)
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miR-155 overexpression
11d
PPF might inhibit the activation of the NF-κB pathway by downregulating miR-155 expression, thereby reducing the secretion of inflammatory cytokines. This might be the mechanism by which PPF protected the intestinal barrier of CRC surgical model mice.
Journal • IO biomarker
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MIR155 (MicroRNA 155)
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miR-155 overexpression
1m
Obviously, miR-155 overexpression is characteristic of cancer-transformed blood cells during myeloid proliferation. Conclusion The data obtained confirm the participation of miR-155 in the pathogenesis of MPN and suggest the possibility of using the miR-155 test as an additional diagnostic test for the differentiation of the clonal nature of the disease.
MIR155 (MicroRNA 155)
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miR-155 overexpression
2ms
Our findings demonstrated that targeting of SMAD5 and TGF-βR2 links miR-155 to TGF-β signaling in CML. Overexpression of miR-155 enables CD34 CML cells to evade growth-inhibitory effects of the TGF-β1 and BMP signaling, providing new perspectives for miR-155 as a therapeutic target for CML.
Journal
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MIR155 (MicroRNA 155) • CD34 (CD34 molecule) • TGFB1 (Transforming Growth Factor Beta 1)
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miR-155 overexpression
2ms
In conclusion, this work clarifies a new possible mechanism for the anti-tumorigenic effect of EPSs in cancer cells and provides insights into the biological pathways through which EPSs act. Moreover, it paves the way for new prospective cancer therapeutics as anti-miRNA.
Journal
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MIR155 (MicroRNA 155)
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miR-155 overexpression
2ms
We report the abnormal expression of the miR-155 cluster in liver cancer cells, which inhibits cancer cell proliferation and metastasis. In addition, we identified SRPK1 as a target gene of miR-155 during the process of liver cancer cell proliferation and metastasis.
Journal
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MIR155 (MicroRNA 155)
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miR-155 overexpression
3ms
The subsequent combination of the knockdown of miR-155-5p and the overexpression of TP53INP1 conferred paclitaxel sensitivity in resistant cells. These results may enhance the understanding of the molecular mechanisms underlying breast cancer progression and resistance to chemotherapy, and suggested that miR-155-5p or TP53INP1 may serve as novel therapeutic approaches to combat resistance to therapy, as well as the proliferation and evasion of apoptosis in breast cancer.
Journal
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MIR155 (MicroRNA 155)
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miR-155 overexpression
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paclitaxel
3ms
Our study indicates a pro-inflammatory role of miR-155 in diabetic kidney disease by downregulating renal expression of SOCS1. Therefore, antagonism of miR-155 may have a renoprotective effect in diabetic nephropathy through SOCS1-mediated feedback inhibition of JAK/STAT overactivation. Ongoing in vivo studies with miR-155 inhibitor in experimental diabetes will clarify its role in the development and progression of diabetic nephropathy.
IL6 (Interleukin 6) • MIR155 (MicroRNA 155) • TNFA (Tumor Necrosis Factor-Alpha) • CXCL10 (Chemokine (C-X-C motif) ligand 10) • STAT3 (Signal Transducer And Activator Of Transcription 3) • CCL2 (Chemokine (C-C motif) ligand 2) • SOCS1 (Suppressor Of Cytokine Signaling 1) • APOE (Apolipoprotein E)
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miR-155 overexpression
3ms
Xenograft models confirmed that M2 macrophage-derived exosomal miR-155-5p reduced the ZC3H12B expression to upregulate IL-6, which consequently induced immune escape and tumor formation. Collectively, our findings indicated that M2 macrophage-derived exosomal miR-155-5p can potentially promote the immune escape of colon cancer by impairing ZC3H12B-mediated IL-6 stability reduction, thereby promoting the occurrence and development of colon cancer.
Journal
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IL6 (Interleukin 6) • MIR155 (MicroRNA 155)
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miR-155 overexpression
5ms
However, the interaction between miR-155 and lncTCL6 attenuated the regulatory role of lncTCL6 on Src-mediated EMT. In conclusion, this study is the first report documenting the lncTCL6-miR155-Src/Akt/EMT network as a novel regulatory mechanism in aggressive ccRCC and a promising therapeutic target to inhibit renal cancer.
Journal
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MIR155 (MicroRNA 155)
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miR-155 overexpression
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