ArticleThe Kaohsiung journal of medical sciences2019
Increased miR-323a induces bladder cancer cell apoptosis by suppressing c-Met.
Article in The Kaohsiung journal of medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Targeting c-Met in the treatment of urologic neoplasms: Current status and challenges.Frontiers in oncology · 2023Review
- MicroRNA-323a-3p Negatively Regulates NEK6 in Colon Adenocarcinoma Cells.Journal of oncology · 2022Article
- c-Met: A Promising Therapeutic Target in Bladder Cancer.Cancer management and research · 2022Review
- MiR-483-5p downregulation contributed to cell proliferation, metastasis, and inflammation of clear cell renal cell carcinoma.The Kaohsiung journal of medical sciences · 2021Article
- Increased miR-323a induces bladder cancer cell apoptosis by suppressing c-Met.The Kaohsiung journal of medical sciences · 2019Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The current study aimed to evaluate the expression and role of miR-323a in the progression of bladder cancer (BC), thereby providing a theoretical basis and potential therapy methods for BC patients. Our data showed that miR-323a levels were significantly reduced in BC tissues compared with those of non-cancerous tissues. Meanwhile, miR-323a was significantly decreased in human BC cell lines (T24, J82, TCCSUP, RT-112) than that in human normal bladder epithelial cell line SV-HUC-1. Furthermore, inhibition of miR-323a markedly enhanced the migration and invasive capacity of T24 and TCCSUP cells. Moreover, overexpression of miR-323a significantly prompted the apoptosis of BC cells. Dual luciferase reporter assay and western blot analysis confirmed that c-Met was a target gene of miR-323a. More importantly, upregulation of c-Met significantly prompted BC cell proliferation mainly as a result of the enhanced level of phosphorylation of AKT. This effect could be abolished when c-Met was silenced in BC cells. In summary, reduced miR-323a expression in BC contributed to enhanced BC cell proliferation and migration mainly by targeting c-Met.
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Registered trials
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