Senescence-associated IL-6 and IL-8 cytokines induce a self- and cross-reinforced senescence/inflammatory milieu strengthening tumorigenic capabilities in the MCF-7 breast cancer cell line
Open accessAbstract
BACKGROUND: There is compelling evidence associating senescent cells with the malignant progression of tumours. Of all senescence-related mechanisms, the so-called senescence-associated secretory phenotype (SASP) has attracted much attention. Since the pro-inflammatory cytokines IL-6 and IL-8 are consistently present in the SASP, and secreted by highly aggressive breast cancer cell lines, we aimed at elucidating their role on the less aggressive breast cancer cell line MCF-7, which does not secret these cytokines. METHODS: The MCF-7 cell line was treated with either senescence-conditioned medium (SCM), IL-6 or IL-8 and then evaluated for phenotypic (CD44 and CD24 by FACS) and functional changes associated with an EMT program (migration/invasion) and for the acquisition of stem cell properties: mammosphere-forming capacity, expression of reprogramming factors (by qRT-PCR) and multilineage differentiation potential. We also evaluated the role of IL6 and IL8 in the cytokine-secreting, highly tumorigenic cell line MDA-MB-231. RESULTS: Our results show that treatment of MCF-7 cells with IL6 and IL8, alone or together, induced the appearance of cells with fibroblastoid morphology, increased CD44 expression and migration, self-renewal and multilineage differentiation capacity, all characteristics compatible with an EMT program and stemness. These changes closely resembled those induced by a SCM. Interestingly, SCM treatments further increased IL6 and IL8 secretion by MCF-7 cells, thus suggesting the participation of an autocrine loop. Indeed, neutralizing antibodies against IL6 and IL8 reversed the effects of SCM on MCF-7, pinpointing these cytokines as major mediators of EMT and stemness-related effects associated with the senescent microenvironment. Additionally, prolonged exposure of MCF cells to IL6 or IL8 induced the appearance of senescent cells, suggesting a mechanism by which senescence and inflammation are reinforced favouring the acquisition of EMT and stem-like features at the population level, thus increasing tumour aggressiveness. Strikingly, our results also show that both IL6 and IL8 are important to maintain aggressive traits in MDA-MB-231 cells, a highly tumorigenic cell line, which appears to be devoid of stemness-related features. CONCLUSIONS: This study demonstrates that, similar to what is observed with a senescent microenvironment, purified IL6 and IL8 induce a self- and cross-reinforced senescence/inflammatory milieu responsible for the emergence of epithelial plasticity and stemness features, thus conferring more aggressive phenotypes to a luminal breast cancer cell line. On the other hand, the basal-like MDA-MB-231 cells, whose aggressiveness-related features depend on IL6 and IL8 secretion, almost completely lack mammosphere formation and differentiation capacities, suggesting that tumour aggressiveness is not always related to stemness.
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IL-6 and IL-8 are known drivers of cancer proliferation.
“IL-6 and IL-8, two well- characterized and abundant SASP factors, are known drivers of cancer proliferation 163,164 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [164]
The Background (page unavailable) says both cytokines are essential for cell growth in triple-negative breast cancer cells, supporting the claim in that setting. But the Results (page unavailable) report no major difference in proliferation between IL-6- or IL-8-treated MCF-7 cells and controls, so the paper does not support an unqualified claim that they drive cancer proliferation. (LLM, conf=0.87)
Experimental — accuracy not yet measuredSenescent cells in each pathological condition enhance the SASP autocrine loop.
“but also enhance SASP autocrine loop, as found in multiple previous studies,124,125,126,127”
From Single-cell senescence identification reveals senescence heterogeneity, trajectory, and modulators (2024) · cites this paper as [126]
The Discussion (page unavailable) reports that senescent-cell conditioned medium induced IL-6 and IL-8 secretion by MCF-7 cells, suggesting a reinforcing inflammatory loop. The study supports such a loop in this breast-cancer cell model, but not the claim that senescent cells enhance it in every pathological condition; the Background also says SASP composition varies by cell, tissue, and trigger. (LLM, conf=0.86)
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- Authors
- Ortiz-Montero, P., Londoño-Vallejo, A., & Vernot, J.-P.
- Affiliations
- Universidad Nacional de Colombia (CO)
- Corresponding author
- Vernot, Jean-Paul
- ORCID
- Vernot, Jean-Paul
- Venue
- Cell Communication and Signaling
- Published
- 2017-05-04
- Volume
- 15
- Issue
- 1
- Pages
- 17-17
- ISSN
- 1478-811X (ISSN-L)
- PMC
- PMC5418812
- OpenAlex
- W2611479744
- Cited by
- 428
- References
- 88
- Citations by year
- 2026: 58 · 2025: 87 · 2024: 57 · 2023: 35 · 2022: 47 · 2021: 63 · 2020: 37 · 2019: 20 · 2018: 21 · 2017: 3
- FWCI
- 16.40
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Cell Communication and Signaling (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Patrimonio Autónomo Fondo Nacional de Financiamiento para la Ciencia, la Tecnología y la Innovación, Francisco José de Caldas, Colciencias (Contract No RC-692–2013)
- DIEB and Faculty of Medicine, Universidad Nacional de Colombia. (30174)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- senescence-associated secretory phenotype, interleukin-6, interleukin-8, senescence, breast cancer, MCF-7 cells, MDA-MB-231 cells, epithelial-mesenchymal transition, cancer stemness, tumorigenicity, autocrine loop, inflammation, multilineage differentiation, CD44, CD24
- MeSH terms
- Breast Neoplasms, Humans, Inflammation, Phenotype, Interleukin-6, Interleukin-8, Cellular Senescence, Culture Media, Conditioned, MCF-7 Cells, Carcinogenesis
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