ArticlePloS one2018
CXCL1 induces senescence of cancer-associated fibroblasts via autocrine loops in oral squamous cell carcinoma.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026Review
- An integrated single-cell lung cancer atlas reveals distinct fibroblast phenotypes between adenocarcinoma and squamous cell carcinomas.NPJ precision oncology · 2026Article
- Senescence-circadian interplay stratifies patient prognosis and reveals immune remodeling heterogeneity in colorectal cancer.Frontiers in immunology · 2026Article
- Identification of senescence-related biomarkers for osteoporosis based on microarray analysis, Mendelian randomization, and experimental validation.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- C-X-C motif chemokine ligand 1 derived from oral squamous cell carcinoma promotes cancer-associated fibroblast differentiation and tumor growth.Molecular biomedicine · 2025Article
- A comprehensive transcriptome based meta-analysis to unveil the aggression nexus of oral squamous cell carcinoma.Biochemistry and biophysics reports · 2025Article
- Chemokines and their receptors in oral squamous cell carcinoma: mechanisms, clinical significance, and therapeutic implications.Frontiers in immunology · 2025Review
- Cellular senescence and metabolic reprogramming: Unraveling the intricate crosstalk in the immunosuppressive tumor microenvironment.Cancer communications (London, England) · 2024Review
- Non-pituitary growth hormone enables colon cell senescence evasion.Aging cell · 2024Article
- Prognostic Function and Immunologic Landscape of a Predictive Model Based on Five Senescence-Related Genes in IPF Bronchoalveolar Lavage Fluid.Biomedicines · 2024Article
- Integrative Analysis and Validation of a Cancer-associated Fibroblasts Senescence-related Signature for Risk Stratification and Therapeutic Prediction in Esophageal Squamous Cell Carcinoma.Journal of Cancer · 2024Article
- Tumor cell-induced macrophage senescence plays a pivotal role in tumor initiation followed by stable growth in immunocompetent condition.Journal for immunotherapy of cancer · 2023Article
- Oral squamous cell carcinomas: state of the field and emerging directions.International journal of oral science · 2023Review
- A natural variation-based screen in mouse cells reveals USF2 as a regulator of the DNA damage response and cellular senescence.G3 (Bethesda, Md.) · 2023Article
- Review
- Review
- Paracrine Signals in Calcified Conditioned Media Elicited Differential Responses in Primary Aortic Vascular Smooth Muscle Cells and in Adventitial Fibroblasts.International journal of molecular sciences · 2023Article
- Cellular Senescence as a Brake or Accelerator for Oncogenic Transformation and Role in Lymphatic Metastasis.International journal of molecular sciences · 2023Review
- What is the Potential Interplay between Microbiome and Tumor Microenvironment in Oral Squamous Cell Carcinomas?Asian Pacific journal of cancer prevention : APJCP · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-associated fibroblasts (CAFs) have emerged as one of the main factors related to cancer progression, however, the conversion mechanism of normal fibroblasts (NOFs) to CAFs has not been well elucidated. The aim of this study was to investigate the underlying mechanism of CAF transformation from NOFs in oral squamous cell carcinoma (OSCC). This study found that NOFs exposed to OSCC cells transformed to senescent cells. The cytokine antibody array showed the highest secretion levels of IL-6 and CXCL1 in NOFs co-cultured with OSCC cells. Despite that both IL-6 and CXCL1 induced the senescent phenotype of CAFs, CXCL1 secretion showed a cancer-specific response to transform NOFs into CAFs in OSCC, whereas IL-6 secretion was eventuated by common co-culture condition. Further, CXCL1 was released from NOFs co-cultured with OSCC cells, however, CXCL1 was undetectable in mono-cultured NOFs or co-cultured OSCC cells with NOFs. Taken together, this study demonstrates that CXCL1 can transform NOFs into senescent CAFs via an autocrine mechanism. These data might contribute to further understanding of CAFs and to development of a potential therapeutic approach targeting cancer cells-CAFs interactions.
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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.