ArticleOpen life sciences2021
Expression of CDK9 in endometrial cancer tissues and its effect on the proliferation of HEC-1B.
Article in Open life sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 4 citations in OpenAlex.
- CDK9 inhibitors for the treatment of solid tumors.Biochemical pharmacology · 2024Review
- DNMT1-mediated epigenetic suppression of FBXO32 expression promoting cyclin dependent kinase 9 (CDK9) survival and esophageal cancer cell growth.Cell cycle (Georgetown, Tex.) · 2024Article
- Drugging Hijacked Kinase Pathways in Pediatric Oncology: Opportunities and Current Scenario.Pharmaceutics · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer (EC) is one of the most common malignant tumors in the female reproductive system, which has been threatening the life and health of many women. Its incidence and mortality rate remain high, resulting in a low survival rate. In this study, the expression of cyclin-dependent kinase 9 (CDK9) in EC tissues was investigated, and its effect on the proliferation of EC cell line HEC-1B was preliminarily analyzed. RT-qPCR and Western blotting showed that CDK9 mRNA and protein were significantly reduced in the small interfering (si)RNA interference group compared with the siRNA control and blank control groups. MTT assay showed that the EC cell proliferative ability was significantly decreased, and phosphorylated-phosphatidylinositol 3 kinase (p-PI3K)/PI3K and phosphorylated-protein kinase B (p-AKT)/AKT were significantly reduced in the siRNA interference group compared with the siRNA control and blank control groups. In conclusion, the high expression of CDK9 is a factor of poor prognosis in EC, and the reduction of CDK9 can inhibit HEC-1B cell proliferation, which may be related to the inhibition on the activation of the PI3K/AKT signaling pathway.
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Registered trials
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