ArticleOncology letters2021
Cancer-associated fibroblast-derived CCL5 contributes to cisplatin resistance in A549 NSCLC cells partially through upregulation of lncRNA HOTAIR expression.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Lactate derived from CAFs mediates H3K18la in stemness gene promoters, which promotes tumor malignant phenotype formation.Molecular genetics and genomics : MGG · 2026Article
- In vitro effects of tensile strain on cancer-associated and matched normal fibroblasts derived from oral squamous cell carcinoma: an exploratory study.BMC cancer · 2026Article
- CCL5 improves radiation resistance through activation of the AMPK/mTOR pathway in adenoid cystic carcinoma.Journal of translational medicine · 2026Article
- Mechanisms and intervention strategies of microenvironment-mediated drug resistance in multiple myeloma.Cancer cell international · 2026Review
- A silence catalyst: CCL5-mediated intercellular communication in cancer.Archives of toxicology · 2025Review
- Extracellular Vesicles Secreted by Cancer-Associated Fibroblasts Drive Non-Invasive Cancer Cell Progression to Metastasis via TGF-β Signalling Hyperactivation.Journal of extracellular vesicles · 2025Article
- Breast Cancer Stem Cells Upregulate IRF6 in Stromal Fibroblasts to Induce Stromagenesis.Cells · 2024Article
- Shedding light on function of long non-coding RNAs (lncRNAs) in glioblastoma.Non-coding RNA research · 2024Review
- Cancer-associated fibroblasts promote enzalutamide resistance and PD-L1 expression in prostate cancer through CCL5-CCR5 paracrine axis.iScience · 2024Article
- Crosstalk between cancer-associated fibroblasts and regulated cell death in tumors: insights into apoptosis, autophagy, ferroptosis, and pyroptosis.Cell death discovery · 2024Review
- Long non-coding RNAs are involved in the crosstalk between cancer-associated fibroblasts and tumor cells.Frontiers in immunology · 2024Review
- Cancer-associated fibroblast cell surface markers as potential biomarkers or therapeutic targets in lung cancer.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Stromal cells in the tumor microenvironment: accomplices of tumor progression?Cell death & disease · 2023Review
- Research Progress on Therapeutic Targeting of Cancer-Associated Fibroblasts to Tackle Treatment-Resistant NSCLC.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Chemokines network in bone metastasis: Vital regulators of seeding and soiling.Seminars in cancer biology · 2022Review
- Cancer-associated fibroblasts in nonsmall cell lung cancer: From molecular mechanisms to clinical implications.International journal of cancer · 2022Review
- Article
- Tumor bud-derived CCL5 recruits fibroblasts and promotes colorectal cancer progression via CCR5-SLC25A24 signaling.Journal of experimental & clinical cancer research : CR · 2022Article
- Extracellular Vesicles Derived from Lung Cancer Cells Induce Transformation of Normal Fibroblasts into Lung Cancer-Associated Fibroblasts and Promote Metastasis of Lung Cancer by Delivering lncRNA HOTAIR.Stem cells international · 2022Article
- A promising research direction for colorectal cancer immunotherapy: The regulatory mechanism of CCL5 in colorectal cancer.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant C-C motif chemokine ligand 5 (CCL5) is associated with disease progression, poor prognosis and chemotherapy resistance in human malignancy. The tumor microenvironment (TME) contributes to chemotherapy resistance. However, the role of cancer-associated fibroblasts (CAFs)-derived CCL5 is not well documented. Hence, the present study aimed to investigate the effects of CAFs on chemotherapy resistance in A549 non-small cell lung cancer (NSCLC) cells and the underlying mechanism. Primary CAFs isolated from patients with NSCLC were found to express and secrete elevated levels of CCL5, which attenuated cisplatin (DDP)-induced apoptosis, as indicated by flow cytometry analysis. In addition, CCL5 upregulated the expression levels of long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) in the tumor cells, and silencing HOTAIR in tumor cells enhanced the cytotoxic effect of cisplatin, characterized by decreased cell viability and increased apoptotic rate. Mechanistically, HOTAIR was found to inactivate the caspase-3/BCL-2 signaling pathway in A549 NSCLC cells. Collectively, the current study demonstrated that CAFs in the TME may serve a crucial role in the higher expression levels of CCL5 in tumors and that CAF-derived CCL5 may promote cisplatin resistance via upregulating lncRNA HOTAIR expression.
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