Article3 Biotech2021
MiR-192-5p regulates the proliferation and apoptosis of cholangiocarcinoma cells by activating MEK/ERK pathway.
Article in 3 Biotech, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Exploring the Role of Extracellular Vesicles in Pancreatic and Hepatobiliary Cancers: Advances Through Artificial Intelligence.International journal of molecular sciences · 2026Review
- ERK1/2 Signaling in Intrahepatic Cholangiocarcinoma: From Preclinical Advances to Therapeutic Strategies.Biology · 2025Review
- Molecular mechanisms of miR-192 in cancer: a biomarker and therapeutic target.Cancer cell international · 2025Review
- Overexpression of microRNA-205-5p promotes cholangiocarcinoma growth by reducing expression of homeodomain-interacting protein kinase 3.Scientific reports · 2023Article
- Long non-coding RNA WAC antisense RNA 1 mediates hepatitis B virus replication <em>in vitro</em> by reinforcing miR-192-5p/ATG7-induced autophagy.European journal of histochemistry : EJH · 2022Article
- MiR-192/NKRF axis confers lung cancer cell chemoresistance to cisplatin via the NF-κB pathway.Thoracic cancer · 2022Article
- MiR-192-5p Alleviated Fibrosis and Inflammatory Responses of Tendon Cells by Targeting NFAT5.Computational and mathematical methods in medicine · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCholangiocarcinoma (CCA) is the second most common liver cancer, characterized by late diagnosis and fatal outcome. Although miR-192-5p has been shown to have a vital role in various cancers, its role in CCA is unknown. Here, we investigated the role of miR-192-5p in CCA cell proliferation and apoptosis, and elucidated its potential mechanism of action.
methodsThe miR-192-5p expression in CCA tissues and cell lines was detected by real-time quantitative reverse transcription-polymerase chain reaction. Cell proliferation was analyzed using the cell counting Kit-8 and 5-bromodeoxyuridine staining assays, while apoptosis was examined by flow cytometry and the terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling assay. Western blot analysis was used to measure the expression of cell proliferation and apoptosis-related proteins, as well as MEK/ERK signaling pathway-related proteins.
resultsMiR-192-5p was highly expressed in CCA tissues and cell lines. Overexpression of miR-192-5p significantly promoted CCA proliferation, and inhibited apoptosis. The MEK inhibitor, PD98059, reversed these miR-192-5p-induced effects on MEK/ERK signaling-associated protein expression, proliferation promotion, and apoptosis inhibition in TFK-1 cells.
conclusionMiR-192-5p promotes proliferation and suppressed apoptosis of CCA cells via the MEK/ERK pathway, which may be a potential therapeutic strategy for CCA treatment.
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