Exosomal miR-6126 plays a pivotal role in sorafenib resistance and tumorigenesis, highlighting its potential as a novel therapeutic target for overcoming drug resistance in HCC.
It was suggested that suppressed miR-126-5p or overexpressed ADAM9 induced cell proliferation and restricted cell apoptosis in ccRCC cells based on si-circ_0061140 (p < 0.01). Altogether, this study highlights that circ_0061140 plays an oncogenic role in ccRCC through modulation of the miR-126-5p/ADAM9 axis.
Overall, our study suggests that miR-126 might play a tumor suppressor role in ER+ BC. miR-126 and SLC7A5 might also be considered potential prognostic biomarkers in ER+ BC.
almost 4 years ago
Journal
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ER (Estrogen receptor) • SLC7A5 (Solute Carrier Family 7 Member 5) • MIR126 (MicroRNA 126) • PLK2 (Polo Like Kinase 2)
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ER positive • miR-126 overexpression • miR-126-3p overexpression
Taken together, the key finding of the study indicated that over-expressed BMSCs-derived exosomal miR-126-3p can suppress the progression of NSCLC through negatively regulating PTPN9.
We identified CT10 regulator of kinase (CRK), an adaptor protein dysregulated in several human malignancies, as a candidate target gene. Indeed, CRK protein levels were markedly reduced by the miR-126 restoration.