The miR-203 expression had close correlations with the tumor size, differentiation grade and tumor stage (p<0.01), and the 5-year survival rate of patients in low miR-203 expression group was remarkably lower than that in the high miR-203 expression group (p<0.01).
CircTADA2A functions as a tumor promoter in OS to increase malignant tumor behavior through the miR-203a-3p/CREB3 axis, which could be a novel target for OS therapy.
It is considered that miRNA de-regulation contributes to tumor progression and metastasis in various cancers, and MiR-203a has been identified as a tumor suppressor in cancers, such as glioma, gastric cancer and hepatocellular carcinoma.
PTC tissues had decreased miR-130a and miR-203 relative to adjacent normal tissues and normal thyroid tissue (both P < .05). miR-130a was in positive correlation with miR-203 (r = 0.754, P < .01). miR-130a was related with tumor infiltration and tumor stage while miR-203 was implicated in tumor stage and lymph-node metastasis.
Increased miR-203 levels in OC patients were correlated with unfavorable prognosis and higher risk for disease progression, independently of FIGO stage, tumor grade, residual tumor after surgery, chemotherapy response and age.
MicroRNA-203 is highly expressed in NSCLC, and is closely related to tumor stage, lymph node metastasis, distant metastasis and poor prognosis of NSCLC patients.
Moreover, overexpression of miR-203 decreased survival fraction, cell viability and tumor growth but promoted cell apoptosis in radiation-treated GC cells.
Taken together, these data demonstrate that miR-203 is a tumor suppressor in EC cells and its expression level could potentially be used as a prognostic indicator for EC patient outcomes.
Finally, in-vivo studies showed that overexpression of miR-203-3p, combined with the suppression of miR-21-5p, significantly co-inhibited growth of tumors.
We show that miR-203-HOTAIR interaction resulted in the inhibition of epithelial-to-mesenchymal transition (EMT) and metastatic genes as indicated by induction of key metastasis-suppressing proteins E-cadherin, claudin (epithelial markers), and PTEN along with induction of tumor suppressor genes p21 and p27.
The aim of the present study was to elucidate the molecular mechanisms underlying the tumor suppressor activity of miRNA-203 (miR-203) in YD-38 human oral cancer cells.
Tumoral miR-203 abundance correlated negatively with both plasma aldosterone level and tumor size in patients with APAs. miR-203 inhibitors increased aldosterone production and cell proliferation in HAC15 cells, and restoration of expression via miR-203 mimics showed decreased cell proliferation and aldosterone hypersecretion in APA cell cultures.
We further showed that miR-203 expression attenuated the TGFβ pathway in both SKOV3 and OVCAR3 cells. miR-203 expression also inhibited primary tumor growth in ovaries and metastatic tumors in multiple peritoneal organs including liver and spleen.
The purpose of this study was to elucidate the molecular mechanism underlying regulation of semaphorin-6A (SEMA6A) involving microRNA-203 (miR-203) as a tumor suppressor in YD-38 human oral cancer cells.
MicroRNA(miR)-203 is a tumor suppressor of HCC and may act as a positive intermediary in A20-enhanced interleukin (IL-6)/signal transducer and activator of transcription 3 (STAT3) pro-proliferative signals, which may promote liver regeneration after PH.
Chi-squared analysis showed that a significant correlation was found between low serum miR-203 expression and larger tumor size as well as lower Karnofsky Performance Scale scores.
In addition, intravenous and intratumoral injection of miR-203/F-PNDs could efficiently inhibit tumor growth through down-regulation of the expressions of oncogenes Ran and Δp63.