ArticleOncotarget2016
Cancer-associated S100P protein binds and inactivates p53, permits therapy-induced senescence and supports chemoresistance.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Fatty acid synthesis therapy-induced senescence (FASTIS) in cancer cells.Cell death & disease · 2026Article
- sc-rDSeq: a robust and cost-effective full-length total RNA sequencing method for single cells reveals multilayered heterogeneity in drug-resistant lung cancer cells.Nucleic acids research · 2026Article
- Development and validation of a highly accurate multigene gene expression biomarker to predict chemotherapy response in primary triple-negative breast cancer.Breast cancer research and treatment · 2026Article
- Role of S100 family proteins in colorectal cancer (CRC): an overview of their potential function as new biomarkers and therapeutic agents.Expert reviews in molecular medicine · 2025Review
- S100P is a core gene for diagnosing and predicting the prognosis of sepsis.Scientific reports · 2025Article
- The S100 protein family in bladder cancer: mechanisms, clinical value, and targeted therapeutic prospects.Frontiers in oncology · 2025Review
- Combating Methotrexate Resistance in Cancer Treatment: A Review on Navigating Pathways and Enhancing Its Efficacy With Fat-Soluble Vitamins.Scientifica · 2025Review
- S100PBP is regulated by mutated KRAS and plays a tumour suppressor role in pancreatic cancer.Oncogene · 2023Article
- S100P as a potential biomarker for immunosuppressive microenvironment in pancreatic cancer: a bioinformatics analysis and in vitro study.BMC cancer · 2023Article
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- A prognostic model of non small cell lung cancer based on TCGA and ImmPort databases.Scientific reports · 2022Article
- Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- S100P Interacts with p53 while Pentamidine Inhibits This Interaction.Biomolecules · 2021Article
- A Novel S100 Family-Based Signature Associated with Prognosis and Immune Microenvironment in Glioma.Journal of oncology · 2021Article
- CAIX-Mediated Control of LIN28/International journal of molecular sciences · 2020Article
- Calcium-Binding Protein S100P Promotes Tumor Progression but Enhances Chemosensitivity in Breast Cancer.Frontiers in oncology · 2020Article
- S100P is a molecular determinant of E-cadherin function in gastric cancer.Cell communication and signaling : CCS · 2019Article
- LncRNA NORAD is repressed by the YAP pathway and suppresses lung and breast cancer metastasis by sequestering S100P.Oncogene · 2019Article
- Expression profile and functional role of S100A14 in human cancer.Oncotarget · 2019Review
- Inhibition of FAK Signaling Elicits Lamin A/C-Associated Nuclear Deformity and Cellular Senescence.Frontiers in oncology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100P belongs to the S100 family of calcium-binding proteins regulating diverse cellular processes. Certain S100 family members (S100A4 and S100B) are associated with cancer and used as biomarkers of metastatic phenotype. Also S100P is abnormally expressed in tumors and implicated in migration-invasion, survival, and response to therapy. Here we show that S100P binds the tumor suppressor protein p53 as well as its negative regulator HDM2, and that this interaction perturbs the p53-HDM2 binding and increases the p53 level. Paradoxically, the S100P-induced p53 is unable to activate its transcriptional targets hdm2, p21WAF, and bax following the DNA damage. This appears to be related to reduced phosphorylation of serine residues in both N-terminal and C-terminal regions of the p53 molecule. Furthermore, the S100P expression results in lower levels of pro-apoptotic proteins, in reduced cell death response to cytotoxic treatments, followed by stimulation of therapy-induced senescence and increased clonogenic survival. Conversely, the S100P silencing suppresses the ability of cancer cells to survive the DNA damage and form colonies. Thus, we propose that the oncogenic role of S100P involves binding and inactivation of p53, which leads to aberrant DNA damage responses linked with senescence and escape to proliferation. Thereby, the S100P protein may contribute to the outgrowth of aggressive tumor cells resistant to cytotoxic therapy and promote cancer progression.
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