ArticleTranslational cancer research2020
MiR-449a-5p regulates the proliferation of esophageal carcinoma cell by targeting B-cell lymphoma 2.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed, 5 citations in OpenAlex.
- MicroRNAs: A novel signature in the metastasis of esophageal squamous cell carcinoma.World journal of gastroenterology · 2024Review
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEsophageal cancer (EC) is a common malignancy that claims millions of lives globally each year. Impairment of esophageal carcinoma cell proliferation could provide a therapeutic approach to treating EC. MiR-449a-5p has been put forward as a crucial tumor suppressor in multiple cancers. In this study, we aimed to determine the mechanism underlying the regulating effect of miR-449a-5p on EC cell proliferation.
methodsThe level of miR-449a-5p in esophageal squamous cell carcinoma (ESCC) tissues and adjacent normal esophageal squamous tissues was detected using real-time polymerase chain reaction. The protein level of B-cell lymphoma 2 (Bcl-2) was measured by western blot. MTT and colony formation assays were carried out to assess Eca-109 cell proliferation.
resultsThe level of miR-449a-5p in ESCC tissues was reduced in comparison with that in adjacent normal tissues. Down-regulation of miR-449a-5p promoted the proliferation of ESCC cells. Bcl-2 was established as a target gene of miR-449a-5p, and its silencing resulted in the reversal of the effects of miR-449a-5p inhibitor on the proliferation of Eca-109 cells.
conclusionOverexpression of miR-449a-5p inhibited the proliferation of Eca-109 cells via negative regulation of Bcl-2.
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