ArticleOncology letters2020
MicroRNA-490-3p suppresses the proliferation and invasion of hepatocellular carcinoma cells via targeting TMOD3.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Clinicopathological Characteristics, Prognosis, and Correlated Tumor Cell Function of Tropomodulin-3 in Pancreatic Adenocarcinoma.Combinatorial chemistry & high throughput screening · 2024Article
- Exploring the Study of miR-1301 Inhibiting the Proliferation and Migration of Squamous Cell Carcinoma YD-38 Cells through PI3K/AKT Pathway under Deep Learning Medical Images.Computational intelligence and neuroscience · 2022Article
- Upregulation of ubiquitin-conjugating enzyme E2T (UBE2T) predicts poor prognosis and promotes hepatocellular carcinoma progression.Bioengineered · 2021Article
- LINC00958 promotes bladder cancer carcinogenesis by targeting miR-490-3p and AURKA.BMC cancer · 2021Article
- MicroRNA-490-3p inhibits migration and chemoresistance of colorectal cancer cells via targeting TNKS2.World journal of surgical oncology · 2021Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is a primary malignancy of the liver. It has been reported that microRNAs (miRs) play important roles in the progression and development of HCC. The expression of miR-490-3p has been shown to be downregulated in HCC tissues. Therefore, the present study aimed to investigate the effects of miR-490-3p on HCC cells and the underlying mechanism. Cell Counting Kit-8, flow cytometry, and Transwell migration and invasion assays were performed to determine the viability, apoptosis, migration and invasion of HCC cells, respectively. Furthermore, a luciferase activity assay was used to verify the association between miR-490-3p and its predicted target tropomodulin 3 (TMOD3). In addition, the protein levels of Bax, Bcl-2, cleaved caspase-3, TMOD3, phosphorylated (p)-p38 and p-ERK in HCC cells were detected using western blot analysis. The results demonstrated that the overexpression of miR-490-3p via transfection with miR-490-3p mimics significantly inhibited the proliferation of Huh-7 and HEP 3B2.1-7 cells. In addition, overexpression of miR-490-3p markedly suppressed the migration and invasion abilities of Huh-7 cells. miR-490-3p mimics significantly induced liver cancer cell apoptosis via upregulating Bax and cleaved caspase-3 and downregulating anti-apoptotic protein Bcl-2. Additionally, a luciferase activity assay indicated that TMOD3 is a downstream target gene of miR-490-3p. The protein levels of TMOD3, p-p38 and p-ERK were significantly downregulated in Huh-7 cells following transfection with miR-490-3p mimics, and the overexpression of TMOD3 attenuated these effects. In conclusion, the aforementioned results suggest that the overexpression of miR-490-3p inhibited the proliferation and invasion of HCC cells by targeting TMOD3. Therefore, the miR-490-3p/TMOD3 axis may be a potent target for the treatment of HCC.
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