Senescent cells develop a parp-1 and nuclear factor-κB-associated secretome (PNAS).
Open accessAbstract
Melanoma cells can enter the process of senescence, but whether they express a secretory phenotype, as reported for other cells, is undetermined. This is of paramount importance, because this secretome can alter the tumor microenvironment and the response to chemotherapeutic drugs. More generally, the molecular events involved in formation of the senescent-associated secretome have yet to be determined. We reveal here that melanoma cells experiencing senescence in response to diverse stimuli, including anti-melanoma drugs, produce an inflammatory secretory profile, where the chemokine ligand-2 (CCL2) acts as a critical effector. Thus, we reveal how senescence induction might be involved in therapeutic failure in melanoma. We further provide a molecular relationship between senescence induction and secretome formation by revealing that the poly(ADP-ribose) polymerase-1 (PARP-1)/nuclear factor-κB (NF-κB) signaling cascade, activated during senescence, drives the formation of a secretome endowed with protumoral and prometastatic properties. Our findings also point to the existence of the PARP-1 and NF-κB-associated secretome, termed the PNAS, in nonmelanoma cells. Most importantly, inhibition of PARP-1 or NF-κB prevents the proinvasive properties of the secretome. Collectively, identification of the PARP-1/NF-κB axis in secretome formation opens new avenues for therapeutic intervention against cancers.
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Blocking PARP-1, ATM, or NF-κB in melanoma cells prevents secretion of chemokine CCL2, thereby restricting deleterious pro-invasive properties of inflammatory SASP mediated by PNAS.
“Blocking PARP-1, ATM, or NF-κB in melanoma cells prevents the secretion of chemokine CCL2 thereby restricting the deleterious pro-invasive properties of the inflammatory SASP mediated by PNAS (Ohanna et al., 2011).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Ohanna et al., 2011
Chemotherapeutic drugs or oxidative stress induced DNA damage engage PARP-1/ATM/NF-κB signaling cascade to induce senescence in melanoma and non-melanoma cells.
“Chemotherapeutic drugs or oxidative stress induced DNA damage engage PARP-1/ATM/NF-κB signaling cascade to induce senescence in melanoma and non-melanoma cells (Ohanna et al., 2011).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Ohanna et al., 2011
These senescent cells develop a PARP-1 and NF-κB associated secretome (PNAS) containing chemokine CCL2 along with other SASP factors, thereby augmenting invasiveness of melanoma cells which might have escaped senescence.
“These senescent cells develop a PARP-1 and NF-κB associated secretome (PNAS) containing chemokine CCL2 along with other SASP factors thereby augmenting the invasiveness of melanoma cells which might have escaped senescence.”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Ohanna et al., 2011
Some tumor cells can enter senescence in response to DNA damaging therapies.
“some tumor cells can enter senescence in response to DNA damaging therapies [363,364].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [364]
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Self-citation
- Authors
- Ohanna, M., Giuliano, S., Bonet, C., Imbert, V., Hofman, V., Zangari, J., Bille, K., Robert, C., Bressac-de Paillerets, B., Hofman, P., Rocchi, S., Peyron, J.-F., Lacour, J.-P., Ballotti, R., & Bertolotto, C.
- Affiliations
- Inserm (FR)
- Institut Gustave Roussy (FR)
- Centre Hospitalier Universitaire de Nice (FR)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2011-06-06
- Volume
- 25
- Issue
- 12
- Pages
- 1245-1261
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC3127427
- OpenAlex
- W2162942873
- Cited by
- 267
- References
- 67
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 17 · 2023: 24 · 2022: 20 · 2021: 33 · 2020: 25 · 2019: 15 · 2018: 16 · 2017: 13 · 2016: 16 · 2015: 17 · 2014: 13 · 2013: 21 · 2012: 15
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Association pour la Recherche sur le Cancer
- Institut National de la Santé et de la Recherche Médicale
- Fondation de France
- Institut National Du Cancer
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- cellular senescence, senescence-associated secretome, melanoma, PARP1, NF-κB signaling, MCP-1, chemokines, tumor microenvironment, chemoresistance, metastasis, tumor invasion
- MeSH terms
- Poly (ADP-Ribose) Polymerase-1, DNA Damage, Humans, Melanoma, Neoplasm Invasiveness, Poly(ADP-ribose) Polymerases, Signal Transduction, Gene Expression Regulation, Neoplastic, NF-kappa B, Cellular Senescence, Chemokine CCL2, Gene Expression Profiling, Cell Line, Tumor
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