ArticleMolecular and cellular biochemistry2024
Exosome-transmitted FOSL1 from cancer-associated fibroblasts drives colorectal cancer stemness and chemo-resistance through transcriptionally activating ITGB4.
Article in Molecular and cellular biochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Axitinib promotes stemness and vasculogenic mimicry in triple-negative breast cancer by disrupting THBS1-CD47 axis-mediated endothelial-tumor cell communication.Apoptosis : an international journal on programmed cell death · 2026Article
- Exosome-Transferred STAT3 from Cancer-Associated Fibroblasts Expedites Thymic Carcinoma Malignant Progression and M2 Macrophage Polarization Through Transcriptionally Activating KLHL5.Applied biochemistry and biotechnology · 2026Article
- Repression of FOSL1 augments ferroptosis to overcome oxaliplatin resistance in colorectal cancer by acting on SRSF2.Molecular biology reports · 2026Article
- Inhibition of FOS-Like Antigen 1 Reduces Chemoresistance to Temozolomide Through Stemness Reprogramming via IL-6/STAT3MedComm · 2026Article
- Exosomal FOSL1 From Cancer-associated Fibroblasts Drives the Progression and Pro-tumorigenic M2 Macrophage Polarization of Hepatocellular Carcinoma By Activating PLAU Transcription.Applied biochemistry and biotechnology · 2026Article
- The TCN1 Paradox: Unraveling the Dual Role of Transcobalamin I in Colorectal Cancer-From Metabolic Regulation to Oncogenic Signaling.Cancer management and research · 2026Review
- Exosomal circRNAs: Deciphering the novel drug resistance roles in cancer therapy.Journal of pharmaceutical analysis · 2025Review
- Cancer-associated Fibroblasts Confer Osimertinib Resistance in Non-small Cell Lung Cancer Cells via NRG1-mediated HER3/AKT Signaling.Journal of Cancer · 2025Article
- RNA Sequencing Identifies Novel Signaling Pathways and Potential Drug Target Genes Induced by FOSL1 in Glioma Progression and Stemness.Biologics : targets & therapy · 2025Article
- Exosomes: their role and therapeutic potential in overcoming drug resistance of gastrointestinal cancers.Frontiers in oncology · 2025Review
- Current perspectives and trends in colorectal cancer and cancer-associated fibroblasts: a review and bibliometric analysis.Frontiers in immunology · 2025Review
- Cancer therapy resistance mediated by cancer-associated fibroblast-derived extracellular vesicles: biological mechanisms to clinical significance and implications.Molecular cancer · 2024Review
- Interaction of NF-κB and FOSL1 drives glioma stemness.Cellular and molecular life sciences : CMLS · 2024Article
- Identification of the biological functions and chemo-therapeutic responses of ITGB superfamily in ovarian cancer.Discover oncology · 2024Article
- FOSL1's Oncogene Roles in Glioma/Glioma Stem Cells and Tumorigenesis: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Tumorigenic and tumoricidal properties of exosomes in cancers; a forward look.Cell communication and signaling : CCS · 2024Review
- Article
- Intercellular crosstalk between cancer cells and cancer-associated fibroblasts via exosomes in gastrointestinal tumors.Frontiers in oncology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer-associated fibroblasts (CAFs) have been proved to facilitate colorectal cancer (CRC) development, either with boosting chemo-resistance by communicating with CRC cells in the tumor microenvironment. However, the underlying molecular mechanisms remain largely unclear. Relative expressions of FOSL1 and ITGB4, either with their correlations in CRC tissues, were assessed using qRT-PCR analysis. Also, Kaplan-Meier survival analysis was employed for evaluating the prognosis. Identification of CAFs was determined by the detection of specific makers (α-SMA, FAP, and FSP1) using western blot and immunofluorescence staining. Cell proliferation, self-renewal capacity, and cell apoptosis were estimated by CCK-8, sphere-formation, and flow cytometry assays. Transcriptional regulation of FOSL1 on integrin β4 (ITGB4) was confirmed using ChIP and dual-luciferase reporter assays. Increased FOSL1 and ITGB4 in CRC tissues were both positively correlated with the poor prognosis of CRC patients. Interestingly, FOSL1 was enriched in the CAFs isolated from CRC stroma, instead of ITGB4. CRC cells under a co-culture system with CAFs-conditioned medium (CAFs-CM) exhibited increased FOSL1, promotive cell proliferation, and reduced apoptosis, while these effects could be blocked by exosome inhibitor (GW4869). Moreover, CAFs-derived exosomal FOSL1 was validated to enhance proliferative ability and oxaliplatin resistance of CRC cells. Our results uncovered that CAFs-derived exosomes could transfer FOSL1 to CRC cells, thereby promoting CRC cell proliferation, stemness, and oxaliplatin resistance by transcriptionally activating ITGB4.
Indexed as
Identifiers
What OpenQuestion holds
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.