ArticleOncogenesis2023
Programmed cell death 11 modulates but not entirely relies on p53-HDM2 loop to facilitate G2/M transition in colorectal cancer cells.
Article in Oncogenesis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Role of microRNA-136 inWorld journal of gastrointestinal oncology · 2026Article
- Identifying the Genetic Basis of Fetal Loss in Cows and Heifers Through a Genome-Wide Association Analysis.Animals : an open access journal from MDPI · 2026Article
- Integrated proteome, phospho-proteome and malonyl-proteome revealed a molecular alteration of breast cancer.Scientific reports · 2025Article
- PDCD11 Stabilizes C-MYC Oncoprotein by Hindering C-MYC-SKP2 Negative Feedback Loop to Facilitate Progression of p53-Mutant Breast and Colon Malignancies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Protein-RNA interaction dynamics reveal key regulators of oncogenic KRAS-driven cancers.Scientific reports · 2024Article
- High expression of PDCD11 in colorectal cancer and its correlation with the prognosis and immune cell infiltration.Heliyon · 2024Article
Corrections and comments
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Authors and funding
11 authors.
Funding
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Abstract
We previously described a nucleolar protein RSL1D1 but distributed throughout the nucleus in HCT116 colorectal cancer (CRC) cells to facilitate G1/S transition by inhibiting p53 signaling. Here, we found another nucleolar protein, programmed cell death 11 (PDCD11), also with an "Extra-nucleolar" localization in CRC cells but to regulate G2/M checkpoint. This protein directly interacts with p53 and HDM2 in the nucleoplasm, thereby recruiting p53 to HDM2 for ubiquitination and degradation. The ensuing downregulation of p53 increases the CDK1 level to help the cells pass G2/M checkpoint. Upon DNA damage stress, PDCD11 gains the power to upregulate CDK1 independently of p53. Beyond these, PDCD11 also upregulates CDC25C in a p53-independent manner to dephosphorylate CDK1 to facilitate G2/M transition. Downregulation of PDCD11 greatly reduced cancer cell growth in vitro and in vivo, additionally sensitized cells to DNA damage signals, highlighting that PDCD11 is a crucial driving factor of CRC and a potential target for cancer treatment.
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Registered trials
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