Cited by 43Prostate Cancer Treatment and ResearchCancer-related Molecular PathwaysSynthesis and biological activity

Molecular interplay between cdk4 and p21 dictates G0/G1 cell cycle arrest in prostate cancer cells

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Gulappa, Thippeswamy, Reddy, Ramadevi Subramani, Suman, Suman, Nyakeriga, Alice M., Damodaran, Chendil·2013·Cancer Letters

Abstract

This study examined the effect of 3, 9-dihydroxy-2-prenylcoumestan (pso), a furanocoumarin, on PC-3 and C4-2B castration-resistant prostate cancer (CRPC) cell lines. Pso caused significant G0/G1 cell cycle arrest and inhibition of cell growth. Molecular analysis of cyclin (D1, D2, D3, and E), cyclin-dependent kinase (cdk) (cdks 2, 4, and 6), and cdk inhibitor (p21 and p27) expression suggested transcriptional regulation of the cdk inhibitors and more significant downregulation of cdk4 than of cyclins or other cdks. Overexpression of cdk4, or silencing of p21 or p27, overcame pso-induced G0/G1 arrest, suggesting that G0/G1 cell cycle arrest is a potential mechanism of growth inhibition in CRPC cells.

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Crossref · 10.1016/j.canlet.2013.05.014

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  • p21 also causes cell-cycle arrest in G0 in different settings.

    “p21 also causes cell-cycle arrest in G 0 in different settings (43,44)”

    From <i>Txnip</i> Enhances Fitness of <i>Dnmt3a</i> -Mutant Hematopoietic Stem Cells via <i>p21</i> (2022) · cites this paper as [44]

    The Results (§3.5; page unavailable) show that knocking down p21 attenuated psoralidin-induced G0/G1 arrest in PC-3 prostate cancer cells. This supports a role for p21 in arrest, but the paper does not establish arrest specifically in G0 or across the broader range of settings implied by the claim. (LLM, conf=0.86)

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1 of the 48 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. [35]Siegel R Naishadham D Jemal A Cancer statistics CA Cancer J. Clin 2012 62 2012 10 29 22237781
  2. [41]Viallard JF Lacombe F Belloc F Pellegrin JL Reiffers J Molecular mechanisms controlling the cell cycle: fundamental aspects and implications for oncology Cancer Radiother 2001 5 109 129 11355576

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Authors
Gulappa, T., Reddy, R. S., Suman, S., Nyakeriga, A. M., & Damodaran, C.
Affiliations
Texas Tech University Health Sciences Center (US)
Corresponding author
Damodaran, Chendil
Venue
Cancer Letters
Publisher
Elsevier BV
Published
2013-09
Volume
337
Issue
2
Pages
177-183
ISSN
0304-3835 (ISSN-L)
OpenAlex
W1974026054
Cited by
43
References
48
Citations by year
2026: 1 · 2024: 3 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 5 · 2019: 4 · 2018: 2 · 2017: 4 · 2016: 3 · 2015: 3 · 2014: 4 · 2013: 4
FWCI
3.80
Type
journal article
Language
en
Open access
Locations
  • Cancer Letters (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Cancer Institute (R01CA138797, R01CA140605)
  • National Center for Complementary and Integrative Health (R01AT002890)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Physical Sciences › Chemistry › Organic Chemistry › Synthesis and biological activity
Keywords
castration-resistant prostate cancer, G0/G1 cell cycle arrest, CDK4, p21, p27, cyclin-dependent kinases, cyclins, cell growth inhibition, PC-3 cells, C4-2B cells
MeSH terms
Cell Survival, Dose-Response Relationship, Drug, Humans, Male, Phosphorylation, Prostatic Neoplasms, Furocoumarins, Time Factors, Transcription, Genetic, Transfection, Signal Transduction, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Neoplastic, Retinoblastoma Protein, Resting Phase, Cell Cycle, RNA Interference, Cell Line, Tumor, E2F1 Transcription Factor, Cyclin-Dependent Kinase Inhibitor p21, Cyclin-Dependent Kinase Inhibitor p27, Cyclin-Dependent Kinase 4, G1 Phase Cell Cycle Checkpoints

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