ArticleEvidence-based complementary and alternative medicine : eCAM2012
Retinoic Acid Induces Apoptosis of Prostate Cancer DU145 Cells through Cdk5 Overactivation.
Article in Evidence-based complementary and alternative medicine : eCAM, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 42 citations in OpenAlex.
- CDK5 targets p21Molecular medicine reports · 2025Article
- Network pharmacology, molecular docking, and in vitro study on Aspilia pluriseta against prostate cancer.BMC complementary medicine and therapies · 2024Article
- CDK5 promotes apoptosis and attenuates chemoresistance in gastric cancer via E2F1 signaling.Cancer cell international · 2023Article
- Retinoic Acid Receptor Activation Reduces Metastatic Prostate Cancer Bone Lesions by Blocking the Endothelial-to-Osteoblast Transition.Cancer research · 2022Article
- Article
- Review
- RET Regulates Human Medullary Thyroid Cancer Cell Proliferation through CDK5 and STAT3 Activation.Biomolecules · 2021Article
- Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications.International journal of molecular sciences · 2019Review
- SP1 and RARα regulate AGAP2 expression in cancer.Scientific reports · 2019Article
- Taiwanin E Induces Cell Cycle Arrest and Apoptosis in Arecoline/4-NQO-Induced Oral Cancer Cells Through Modulation of the ERK Signaling Pathway.Frontiers in oncology · 2019Article
- Combination treatment of all-trans retinoic acid (ATRA) and γ-secretase inhibitor (DAPT) cause growth inhibition and apoptosis induction in the human gastric cancer cell line.Cytotechnology · 2018Article
- Cdk5 links with DNA damage response and cancer.Molecular cancer · 2017Review
- Cyclin-dependent kinase 5 acts as a critical determinant of AKT-dependent proliferation and regulates differential gene expression by the androgen receptor in prostate cancer cells.Molecular biology of the cell · 2015Article
- Retinal Targets ALDH Positive Cancer Stem Cell and Alters the Phenotype of Highly Metastatic Osteosarcoma Cells.Sarcoma · 2015Article
- Retinoic acid and cancer treatment.BioMedicine · 2014Article
- Decitabine and SAHA-induced apoptosis is accompanied by survivin downregulation and potentiated by ATRA in p53-deficient cells.Oxidative medicine and cellular longevity · 2014Article
- Emodin and Aloe-Emodin Suppress Breast Cancer Cell Proliferation through ER α Inhibition.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Higher Levels of Tumour-Infiltrating Lymphocytes (TILs) are Associated with a Better Prognosis, While CDK5 Plays a Different Role Between Nonmetastatic and Metastatic Colonic Carcinoma.Cancer control : journal of the Moffitt Cancer CenterArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinoic acid (RA) has been believed to be an anticancer drug for a long history. However, the molecular mechanisms of RA actions on cancer cells remain diverse. In this study, the dose-dependent inhibition of RA on DU145 cell proliferation was identified. Interestingly, RA treatment triggered p35 cleavage (p25 formation) and Cdk5 overactivation, and all could be blocked by Calpain inhibitor, Calpeptin (CP). Subsequently, RA-triggered DU145 apoptosis detected by sub-G1 phase accumulation and Annexin V staining could also be blocked by CP treatment. Furthermore, RA-triggered caspase 3 activation and following Cdk5 over-activation were destroyed by treatments of both CP and Cdk5 knockdown. In conclusion, we report a new mechanism in which RA could cause apoptosis of androgen-independent prostate cancer cells through p35 cleavage and Cdk5 over-activation. This finding may contribute to constructing a clearer image of RA function and bring RA as a valuable chemoprevention agent for prostate cancer patients.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.