ArticleInternational journal of biological sciences2024
Diallyl disulfide induces DNA damage and growth inhibition in colorectal cancer cells by promoting POU2F1 ubiquitination.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- TRIM21 inhibition alleviates acute kidney injury by promoting INTS3-associated DNA damage repair.Apoptosis : an international journal on programmed cell death · 2026Article
- Mechanisms and functions of the TRIM protein family in digestive system cancers.Journal of translational medicine · 2026Review
- Mechanistic insights into SOCS5-related DNA damage and cellular senescence in diabetic retinopathy.Cell death discovery · 2026Article
- ABHD11-AS1 Suppresses Colorectal Cancer Progression by Disrupting EIF4E-mediated POU2F1 Ubiquitination.International journal of biological sciences · 2026Article
- Association of root-knot nematode (Frontiers in plant science · 2026Article
- Diallyl disulfide in oncotherapy: molecular mechanisms and therapeutic potentials.Apoptosis : an international journal on programmed cell death · 2025Review
- The oncogenic role of SPOCK1 in lung carcinoma by promoting immune evasion and its related mechanisms.Cytotechnology · 2025Article
- A positive feedback loop between FOSB and miR-133b controls colon cancer cell proliferation.Acta biochimica et biophysica Sinica · 2025Article
- Long non‑coding RNA ABHD11‑AS1 inhibits colorectal cancer progression through interacting with EGFR to suppress the EGFR/ERK signaling pathway.International journal of oncology · 2025Article
- The Pentose Phosphate Pathway: From Mechanisms to Implications for Gastrointestinal Cancers.International journal of molecular sciences · 2025Review
- CTHRC1: a key player in colorectal cancer progression and immune evasion.Frontiers in immunology · 2025Review
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have demonstrated that diallyl disulfide (DADS) exhibits potent anti-tumor activity. However, the pharmacological actions of DADS in inhibiting the growth of colorectal cancer (CRC) cells have not been clarified. Herein, we show that DADS treatment impairs the activation of the pentose phosphate pathway (PPP) to decrease PRPP (5-phosphate ribose-1-pyrophosphate) production, enhancing DNA damage and cell apoptosis, and inhibiting the growth of CRC cells. Mechanistically, DADS treatment promoted POU2F1 K48-linked ubiquitination and degradation by attenuating the PI3K/AKT signaling to up-regulate TRIM21 expression in CRC cells. Evidently, TRIM21 interacted with POU2F1, and induced the K272 ubiquitination of POU2F1. The effects of DADS on the enhanced K272 ubiquitination of POU2F1, the PPP flux, PRPP production, DNA damage and cell apoptosis as well as the growth of CRC tumors
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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.