ArticleThe Journal of biological chemistry2008
CCL2 protects prostate cancer PC3 cells from autophagic death via phosphatidylinositol 3-kinase/AKT-dependent survivin up-regulation.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 167 citations in OpenAlex.
- NLRX1 Drives Prostate Cancer Progression Through Activation of AKT and ERK Signaling Pathways.International journal of biological sciences · 2026Article
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- Exosomes in Cancer Biology: Emerging Biomarkers and Therapeutic Targets.Journal of Cancer · 2026Review
- E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistance.Cell death discovery · 2025Article
- Chemokine ligand 2: beyond chemotaxis-a multifaceted role in tumor progression.Frontiers in immunology · 2025Review
- The role and therapeutic targeting of the CCL2/CCR2 signaling axis in inflammatory and fibrotic diseases.Frontiers in immunology · 2024Review
- Evaluation of Genes and Molecular Pathways Common between Diffuse Large B-cell Lymphoma (DLBCL) and Systemic Lupus Erythematosus (SLE): A Systems Biology Approach.Medical journal of the Islamic Republic of Iran · 2024Article
- CCL2 promotes lymphatic metastasis via activating RhoA and Rac1 pathway and predict prognosis to some extent in tongue cancer.Cancer biology & therapy · 2023Article
- Anti-CCL2 antibody combined with etoposide prolongs survival in a minimal residual disease mouse model of neuroblastoma.Scientific reports · 2023Article
- ESS2 controls prostate cancer progression through recruitment of chromodomain helicase DNA binding protein 1.Scientific reports · 2023Article
- Tumor-associated macrophages promote epithelial-mesenchymal transition and the cancer stem cell properties in triple-negative breast cancer through CCL2/AKT/β-catenin signaling.Cell communication and signaling : CCS · 2022Article
- Plasma Chemokine C-C Motif Ligand 2 as a Potential Biomarker for Prostate Cancer.Research and reports in urology · 2022Article
- Functional Roles of Chemokine Receptor CCR2 and Its Ligands in Liver Disease.Frontiers in immunology · 2022Review
- Role of the CCL2-CCR2 signalling axis in cancer: Mechanisms and therapeutic targeting.Cell proliferation · 2021Review
- Inhibitors of the PI3K/Akt/mTOR Pathway in Prostate Cancer Chemoprevention and Intervention.Pharmaceutics · 2021Review
- Mechanistic Insights into the Link between Obesity and Prostate Cancer.International journal of molecular sciences · 2021Review
- Targeting the CCL2/CCR2 Axis in Cancer Immunotherapy: One Stone, Three Birds?Frontiers in immunology · 2021Review
- CCL2 in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021Article
- Research trends in pharmacological modulation of tumor-associated macrophages.Clinical and translational medicine · 2021Review
- Article
37 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Resistance to cell death is a hallmark of cancer. Autophagy is a survival mechanism activated in response to nutrient deprivation; however, excessive autophagy will ultimately induce cell death in a nonapoptotic manner. The present study demonstrates that CCL2 protects prostate cancer PC3 cells from autophagic death, allowing prolonged survival in serum-free conditions. Upon serum starvation, CCL2 induced survivin up-regulation in PC3, DU 145, and C4-2B prostate cancer cells. Both cell survival and survivin expression were stunted in CCL2-stimulated PC3 cells when treated either with the phosphatidylinositol 3-kinase inhibitor LY294002 (2 microm) or the Akt-specific inhibitor-X (Akti-X; 2.5 microm). Furthermore, CCL2 significantly reduced light chain 3-II (LC3-II) in serum-starved PC3; in contrast, treatment with LY294002 or Akti-X reversed the effect of CCL2 on LC3-II levels, suggesting that CCL2 signaling limits autophagy in these cells. Upon serum deprivation, the analysis of LC3 localization by immunofluorescence revealed a remarkable reduction in LC3 punctate after CCL2 stimulation. CCL2 treatment also resulted in a higher sustained mTORC1 activity as measured by an increase in phospho-p70S6 kinase (Thr389). Rapamycin, an inducer of autophagy, both down-regulated survivin and decreased PC3 cell viability in serum-deprived conditions. Treatment with CCL2, however, allowed cells to partially resist rapamycin-induced death, which correlated with survivin protein levels. In two stable transfectants expressing survivin-specific short hairpin RNA, generated from PC3, survivin protein levels controlled both cell viability and LC3 localization in response to CCL2 treatment. Altogether, these findings indicate that CCL2 protects prostate cancer PC3 cells from autophagic death via the phosphatidylinositol 3-kinase/Akt/survivin pathway and reveal survivin as a critical molecule in this survival mechanism.
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Registered trials
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.