<p>miR-26a-5p Inhibit Gastric Cancer Cell Proliferation and Invasion Through Mediated Wnt5a</p>

Abstract

Gastric cancer (GC) is a malignant disease of digestive tract. Clinically, radiation therapy is widely applied in treating GC, while with undesirable outcome due to tumor reproliferation and recurrence and metastasis after radiation. Therefore, it is crucial to explore potential molecular mechanisms to develop therapeutic strategies. The present study found that miR-26a-5p has low expression in GC patients and could regulate Wnt5a to inhibit tumor growth, which was a potential therapeutic target for GC. To explore the expression and related mechanism of miR-26a-5p and Wnt5a in GC. Patients and Methods: MiR-26a-5p and Wnt5a were extracted from the transcriptome data of GC downloaded from TCGA database for analysis. The expression levels of miR-26a-5p and Wnt5a in patients' tissues and serum were detected by qRT-PCR, and their correlation with patients' pathological data and survival was analyzed. In addition, miR-26a-5p and Wnt5a overexpression and inhibition vectors were transfected into cells to observe the effects on the proliferation, invasion and apoptosis of GC cells. The relationship between miR-26a-5p and Wnt5a was analyzed by dual luciferase report. Results: The database and clinical samples showed that miR-26a-5p level was low while Wnt5a was high in GC. MiR-26a-5p level decreased in patients with stage III+IV, lymphatic metastasis and tumor ≥3cm, and Wnt5a was contrary to that of the miR-26a-5p, with diagnostic value. Overexpressed miR-26a-5p and inhibited Wnt5a enhanced apoptosis, decreased proliferation and invasion, reduced Bcl-2 and β-catenin proteins, and elevated Caspase 3, E-cadherin and Bax proteins, while inhibited miR-26a-5p and over-expressed Wnt5a showed the opposite results. Dual luciferase report confirmed that miR-26a-5p targeted to regulate Wnt5a, and rescue experiments found that these effects could be counteracted by reducing miR-26a-5p level. Conclusion: Overexpressed miR-26a-5p can inhibit Wnt5a expression, promote cell apoptosis, and suppress cell proliferation and invasion in GC.

Silencing the lncRNA NORAD inhibits EMT of head and neck squamous cell carcinoma stem cells via miR‑26a‑5p

“…The latest report revealed that miR-26a overexpression inhibited cell migration via PAK1 and suppressed tumor formation in tongue squamous cell carcinoma ( 36 ). The present study demonstrated that miR-26a-5p silencing promoted cell viability, invasion and migration, which is in line with previous results ( 37 ). Unlike the previous study, however, the present study found that the upstream target gene of miR-26a-5p may be lncRNA NORAD, according to the prediction of bioinformatics, suggesting that NORAD mediates the stemness of HNSCC stem cells via miR-26a-5p.…”

MicroRNA‑26a inhibits cell proliferation and invasion by targeting FAM98A in breast cancer

“…Previous studies have revealed that miR-26a exerted antitumor effects in other malignancies. For example, Li et al ( 26 ) revealed that the increase in miR-26a expression induced cell apoptosis and inhibited cell proliferation and invasion by downregulating the expression level of Wnt5a. It was also found that F-box protein 11 (FBXO11) was a downstream target regulator of miR-26a and was upregulated in hepatocellular carcinoma (HCC) cells.…”

Learning from Embryogenesis—A Comparative Expression Analysis in Melanoblast Differentiation and Tumorigenesis Reveals miRNAs Driving Melanoma Development

“…Focusing on those miRNAs that are significantly downregulated in melanoma vs. MBrCs and NHEMs yields in miRNAs that have already been described as implicated in melanoma development or have described functional roles in other cancers (see Figure 2, e.g., [51][52][53][54]). Interestingly, our analysis discovered many miRNAs of the so-called miR-506-514 cluster (miR-506, miR-508, miR-509, miR-513, and miR-514) as strongly and significantly downregulated in melanoma cells compared to MBrCs and NHEMs.…”