ArticleInternational journal of oncology2018
CDCA3 mediates p21-dependent proliferation by regulating E2F1 expression in colorectal cancer.
Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 61 citations in OpenAlex.
- Article
- CDCA3-MYC positive feedback loop promotes bladder cancer progression via ENO1-mediated glycolysis.Journal of experimental & clinical cancer research : CR · 2025Article
- Integrating machine learning and bioinformatics approaches for identifying novel diagnostic gene biomarkers in colorectal cancer.Scientific reports · 2024Article
- IdentifyingTranslational andrology and urology · 2024Article
- Comprehensive bioinformatics analysis and cell line experiments revealed the important role of CDCA3 in sarcoma.Heliyon · 2024Article
- Modifications of The Human Liver Cancer Cells through microRNA-145-Mediated Targeting of CDCA3.Cell journal · 2023Article
- SNHG18 inhibits bladder cancer cell proliferation by increasing p21 transcription through destabilizing c-Myc protein.Cancer cell international · 2023Article
- Structural investigation of CDCA3-Cdh1 protein-protein interactions using in vitro studies and molecular dynamics simulation.Protein science : a publication of the Protein Society · 2023Article
- Lamin B2 contributes to the proliferation of bladder cancer cells via activating the expression of cell division cycle‑associated protein 3.International journal of molecular medicine · 2022Article
- Pan-cancer analysis identifiesTranslational cancer research · 2022Article
- Systematic study on expression and prognosis of E2Fs in human colorectal cancer.International journal of clinical oncology · 2022Article
- Suppression of CDCA3 inhibits prostate cancer progression via NF‑κB/cyclin D1 signaling inactivation and p21 accumulation.Oncology reports · 2022Article
- Cell Division Cycle-Associated Protein 3 (CDCA3) Is a Potential Biomarker for Clinical Prognosis and Immunotherapy in Pan-Cancer.BioMed research international · 2022Review
- Article
- Comprehensive analysis of differentially expressed genes reveals the promotive effects of UBE2T on colorectal cancer cell proliferation.Oncology letters · 2021Article
- CDCA1/2/3/5/7/8 as novel prognostic biomarkers and CDCA4/6 as potential targets for gastric cancer.Translational cancer research · 2021Article
- Elevating CDCA3 levels in non-small cell lung cancer enhances sensitivity to platinum-based chemotherapy.Communications biology · 2021Article
- The inhibitory effect of silencing CDCA3 on migration and proliferation in bladder urothelial carcinoma.Cancer cell international · 2021Article
- Circular RNA hsa_circ_101555 promotes hepatocellular carcinoma cell proliferation and migration by sponging miR-145-5p and regulating CDCA3 expression.Cell death & disease · 2021Article
- Comprehensive analysis of ceRNA networks reveals prognostic lncRNAs related to immune infiltration in colorectal cancer.BMC cancer · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated cell cycle progression serves a crucial role in tumor development. Cell division cycle-associated 3 (CDCA3) is considered a trigger of mitotic entry; it is an important part of the S phase kinase-associated protein 1/Cullin/F-box ubiquitin ligase complex and mediates the destruction of mitosis-inhibitory kinase wee1. However, little is known about the role of CDCA3 in cancer, particularly colorectal cancer (CRC). The present study aimed to explore the biological and clinical significance of CDCA3 in CRC growth and progression. CDCA3 expression was significantly associated with tumor progression and poor survival. Overexpression of CDCA3 increased proliferation in LoVo CRC cells, whereas CDCA3 knockdown in SW480 CRC cells led to decreased proliferation, in vitro and in vivo. Further mechanistic investigations demonstrated that reduced CDCA3 expression resulted in G1/S phase transition arrest, which was attributed to a significant accumulation of p21 in SW480 cells; conversely, increased CDCA3 expression promoted G1/S phase transition through decreased p21 accumulation in LoVo cells. It was also demonstrated that CDCA3 was able to regulate the expression of transcription factor E2F1, thereby repressing p21 expression. Taken together, these results suggested that overexpression of CDCA3 may serve a crucial role in tumor malignant potential and that CDCA3 may be used as a prognostic factor and a potential therapeutic target in CRC.
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