We injected nude mice with Bel/5-Fu cells to promote tumor growth, and found that co-treatment with a miR-205-5p antagomir and 5-Fu slowed tumor growth more than either treatment alone.
Two miRNA signatures: miR-92a/miR-410 and miR-92a/miR-205/miR-410 classified tumor tissues with higher accuracy in comparison to single miRNAs (AUC: 0.977, 95% CI: 0.927-0.996 and 0.984, 95% CI: 0.938-0.999, respectively). miRNA signature composed of miR-205 and miR-200a predicted relapse with AUC of 0.854 (95% CI: 0.691-0.951).
Transient and stable overexpression of miR-205 in A498 cells resulted in induction of G₀/G₁ cell-cycle arrest and apoptosis, as indicated by decreased levels of cyclin D1 and c-Myc, suppressed cell proliferation, colony formation, migration, and invasion in renal cancer cells. miR-205 also inhibited tumor cell growth in vivo.
These results suggest that miR-205 may play as a tumor suppressor in LSCC, probably by targeting Bcl-2 and serve as a potential target for therapeutic intervention.
Therefore, we conclude that HBx is able to inhibit tumor suppressor miR-205 to enhance hepatocarcinogenesis through inducing hypermethylation of miR-205 promoter during their interaction.
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 verification of tumor-specific miRNA expression profile, together with the observed association of miR-141 and miR-205 expression with overall survival, underline the potential of miRNAs to function as diagnostic and/or prognostic markers of bladder cancer.
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 role that miR-205 plays in tumor formation and metastasis is likely context-dependent as reports have indicated that it may function as either a tumor suppressor or an oncogene.
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 results of the present study demonstrated that miR‑205, which has been reported to function as a tumor suppressor in various types of cancer, significantly suppressed the migration and invasion of GC cells, which may be correlated with its suppressive effects on EMT.
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.
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 expression of miR-205 was reduced in four breast cancer cell lines compared to the normal-like epithelial cell line MCF10A and in tumor and metastatic tissues compared to adjacent benign breast tissue.
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.
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).