Overall, miR‑205‑5p functions as a tumor suppressor in RCC by targeting VEGFA and the PI3K/Akt signaling pathway, providing a potential therapeutic target for the treatment of ccRCC.
Second, through a series of assays, we concluded that SNHG5 acts as a sponge for miR-205, which inhibits tumour growth in glioma by targeting E2F transcription factor 3 (E2F3).
Our study illustrated that miR-205 was a tumor suppressor in TNBC, which attenuated the viability and the acquisition of the epithelial-to-mesenchymal transition phenotype TNBC cells at least partially exerted through targeting of HMGB1-RAGE signaling pathway.
Based on the collective findings, we propose that miR-205-5ps as important negative mediators of resistance in radiotherapy could serve as useful potential targets of concurrently applied genetic therapy aimed to inhibit tumor aggressiveness and enhance the efficiency of radiotherapy in cancer patients.
Although miR-205 is not required for normal prostate development and homeostasis, genetic deletion of miR-205 in a Pten null tumor model significantly compromises tumor progression and does not promote metastasis.
<b>Conclusion:</b> These findings demonstrate an exosome-dependent mechanism by which miR-205 derived from cancer cells regulates tumour angiogenesis and implicate exosomal miR-205 as a potential therapeutic target for OC.
The miR-205-3p expression in tumor tissues of breast cancer patients was significantly higher than that in para-carcinoma tissue, but Ezrin, LaminA/C, and cleaved caspase-3 expressions in tumor tissues were remarkably declined (P < 0.01), while the Bcl-2/Bax ratio was remarkably increased (P < 0.01).
Therefore, this study explores the action of microRNA-205 (miR-205) in the invasion, migration, and angiogenesis of CC through binding to tumor suppressor lung cancer 1 (TSLC1).
The two primary classification models consisted of four miRNAs for lung cancer diagnosis and subtyping. hsa-miR-183 and hsa-miR-135b were used to distinguish lung tumors from normal samples taken from tissues adjacent to the tumor site, and hsa-miR-944 and hsa-miR-205 to further classify the tumors into LUAD and LUSC major subtypes.
The expression level of miR-205 was associated with tumor-node-metastasis (TNM) staging and lymph node metastasis, while the expression level of miR-506 was associated with lymph node metastasis.
Taken together, our findings provide new insight into the critical role of miR-205 in regulating tumor growth, invasion, and EMT of HCC, suggesting miR-205 may serve as a promising therapeutic target and novel prognostic indicator for patients with HCC.-Lu, J., Lin, Y., Li, F., Ye, H., Zhou, R., Jin, Y., Li, B., Xiong, X., Cheng, N. MiR-205 suppresses tumor growth, invasion and epithelial-mesenchymal transition by targeting SEMA4C in hepatocellular carcinoma.
The results of the present study suggested that the tumor suppressive functions of miR‑205 via targeting YAP1 could be a novel target for the treatment of thyroid cancer.
The expression of miR-205 was closely related to the infiltration and recurrence of tumors (p < 0.01), but was not correlated with a pathological grade or clinical stage (p > 0.05).
The miRNA, miR-205-5p, has been reported to suppress the growth of various types of tumor; however, its functional contribution to oral squamous cell carcinoma (OSCC) is not yet clear.
MicroRNA205 (miR-205), as a significant tumor biomarker, is of vital importance for diagnosis of lung cancer and its overexpression patterns have been extensively studied.