ArticleOncogene2022
TP53 mutations upregulate RCP expression via Sp1/3 to drive lung cancer progression.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
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- Canonical BAF chromatin remodeling complex specifies stem cell fate via cell-type-specific co-factor recruitment.Nature communications · 2026Article
- Δ133p53 isoform enhances TLR4 function to promote tumor growth.Carcinogenesis · 2025Article
- Influencing factors and prediction of growth heterogeneity in solid nodule non-small cell lung cancer based on artificial intelligence: a prospective study.Translational lung cancer research · 2025Article
- miR-493-5p Silenced by DNA Methylation Promotes Angiogenesis via Exosomes and VEGF-A-Mediated Intracellular Cross-Talk Between ESCC Cells and HUVECs.International journal of nanomedicine · 2024Article
- SP3-induced Timeless transcription contributes to cell growth of lung adenocarcinoma cells.PloS one · 2024Article
- NThoracic cancer · 2023Article
- High FAAP24 expression reveals poor prognosis and an immunosuppressive microenvironment shaping in AML.Cancer cell international · 2023Article
- DEGBOE: Discrete time Evolution modeling of Gene mutation through Bayesian inference using qualitative Observation of mutation Events.Journal of biomedical informatics · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutant p53 (mtp53) can exert cancer-promoting activities via "gain-of-function", which has become a popular research target. Although lots of researchers focus on the tumor-suppressor role for p53, the regulation of mutant p53 remains unknown. Here, we report a mechanism by which mtp53 regulate the transcription of Rab coupling protein (RCP) to influence lung cancer behavior. First, we show that RCP is specifically expressed at high levels in lung cancer tissues and cells, and RCP knockout suppresses tumor growth and metastasis. Further mass spectrometry and functional analysis identify that Sp1, Sp3 and Stat3 are the transcriptional activators of RCP. Moreover, p53 is involved in modulating RCP expression in an Sp1/3 dependent manner. Mechanistically, in contrast to wild-type p53 suppression of RCP transcription by decreasing Sp1/3 proteins, TP53 mutations have changed on Sp1/3 expression via "loss-of-function". Surprisingly, the DNA contact mutants of p53 further robustly enhance their binding ability with Sp1/3 to drive RCP expression through the "gain-of-function" activity. Collectively, we reveal a mechanism by which p53 regulating the transcription of RCP to influence lung cancer progression, which provides new insights for treating p53 mutant lung cancer.
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