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Article ; Online: Targeting chemoresistant senescent pancreatic cancer cells improves conventional treatment efficacy.

Jaber, Sara / Warnier, Marine / Leers, Christopher / Vernier, Mathieu / Goehrig, Delphine / Médard, Jean-Jacques / Vindrieux, David / Ziegler, Dorian V / Bernard, David

Molecular biomedicine

2023 Volume 4, Issue 1, Page(s) 4

Abstract: Pancreatic cancer is one of the deadliest cancers owing to its late diagnosis and of the strong resistance to available treatments. Despite a better understanding of the disease in the last two decades, no significant improvement in patient care has been ...

Abstract	Pancreatic cancer is one of the deadliest cancers owing to its late diagnosis and of the strong resistance to available treatments. Despite a better understanding of the disease in the last two decades, no significant improvement in patient care has been made. Senescent cells are characterized by a stable proliferation arrest and some resistance to cell death. Increasing evidence suggests that multiple lines of antitumor therapy can induce a senescent-like phenotype in cancer cells, which may participate in treatment resistance. In this study, we describe that gemcitabine, a clinically-used drug against pancreatic cancer, induces a senescent-like phenotype in highly chemoresistant pancreatic cancer cells in vitro and in xenografted tumors in vivo. The use of ABT-263, a well-described senolytic compound targeting Bcl2 anti-apoptotic proteins, killed pancreatic gemcitabine-treated senescent-like cancer cells in vitro. In vivo, the combination of gemcitabine and ABT-263 decreased tumor growth, whereas their individual administration had no effect. Together these data highlight the possibility of improving the efficacy of conventional chemotherapies against pancreatic cancer by eliminating senescent-like cancer cells through senolytic intervention. Further studies testing different senolytics or their combination with available treatments will be necessary to optimize preclinical data in mouse models before transferring these findings to clinical trials.
Language	English
Publishing date	2023-02-05
Publishing country	Singapore
Document type	Journal Article
ISSN	2662-8651
ISSN (online)	2662-8651
DOI	10.1186/s43556-023-00116-4
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Article ; Online: Transformed cells after senescence give rise to more severe tumor phenotypes than transformed non-senescent cells.

Palazzo, Alberta / Hernandez-Vargas, Hector / Goehrig, Delphine / Médard, Jean-Jacques / Vindrieux, David / Flaman, Jean-Michel / Bernard, David

Cancer letters

2022 Volume 546, Page(s) 215850

Abstract: Oncogenic stress-induced senescence initially inhibits tumor initiation by blocking proliferation and by attracting immune cells to clear potentially harmful cells. If these cells are not eliminated they may resume proliferation upon loss-of-tumor ... ...

Abstract	Oncogenic stress-induced senescence initially inhibits tumor initiation by blocking proliferation and by attracting immune cells to clear potentially harmful cells. If these cells are not eliminated they may resume proliferation upon loss-of-tumor suppressors, and be at risk of transformation. During tumor formation, depending on the sequence of events of gain-of-oncogenes and/or loss-of-tumor suppressors, cancer cells may emerge from senescent cells. Here, we show that these transformed cells after senescence (TS) display more aggressive tumorigenic features, with a greater capacity to migrate and a higher resistance to anti-tumoral drugs than cells having undergone transformation without senescence. Bulk transcriptomic analysis and single cell RNA sequencing revealed a signature unique to TS cells. A score of this signature was then generated and a high score was correlated with decreased survival of patients with lung adenocarcinoma, head-neck squamous cell carcinoma, adrenocortical carcinoma, liver hepatocellular carcinoma, skin cutaneous melanoma and low-grade glioma. Together, these findings strongly support that cancer cells arising from senescent cells are more dangerous, and that a molecular signature of these cells may be of prognostic value for some human cancers. It also raises questions about modeling human tumors, using cells or mice, without regards to the sequence of events leading to transformation.
MeSH term(s)	Animals ; Carcinoma, Hepatocellular ; Cellular Senescence ; Humans ; Liver Neoplasms ; Lung Neoplasms ; Melanoma ; Mice ; Phenotype ; Skin Neoplasms ; Tumor Suppressor Protein p53 ; Melanoma, Cutaneous Malignant
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2022-08-01
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2022.215850
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Article ; Online: Targeting chemoresistant senescent pancreatic cancer cells improves conventional treatment efficacy

Sara Jaber / Marine Warnier / Christopher Leers / Mathieu Vernier / Delphine Goehrig / Jean-Jacques Médard / David Vindrieux / Dorian V. Ziegler / David Bernard

Molecular Biomedicine, Vol 4, Iss 1, Pp 1-

2023 Volume 12

Abstract: Abstract Pancreatic cancer is one of the deadliest cancers owing to its late diagnosis and of the strong resistance to available treatments. Despite a better understanding of the disease in the last two decades, no significant improvement in patient care ...

Abstract	Abstract Pancreatic cancer is one of the deadliest cancers owing to its late diagnosis and of the strong resistance to available treatments. Despite a better understanding of the disease in the last two decades, no significant improvement in patient care has been made. Senescent cells are characterized by a stable proliferation arrest and some resistance to cell death. Increasing evidence suggests that multiple lines of antitumor therapy can induce a senescent-like phenotype in cancer cells, which may participate in treatment resistance. In this study, we describe that gemcitabine, a clinically-used drug against pancreatic cancer, induces a senescent-like phenotype in highly chemoresistant pancreatic cancer cells in vitro and in xenografted tumors in vivo. The use of ABT-263, a well-described senolytic compound targeting Bcl2 anti-apoptotic proteins, killed pancreatic gemcitabine-treated senescent-like cancer cells in vitro. In vivo, the combination of gemcitabine and ABT-263 decreased tumor growth, whereas their individual administration had no effect. Together these data highlight the possibility of improving the efficacy of conventional chemotherapies against pancreatic cancer by eliminating senescent-like cancer cells through senolytic intervention. Further studies testing different senolytics or their combination with available treatments will be necessary to optimize preclinical data in mouse models before transferring these findings to clinical trials.
Keywords	Cancer resistance ; Cellular senescence ; Senolysis ; Medicine ; R
Subject code	610
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	Springer
Document type	Article ; Online
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Article ; Online: Benidipine calcium channel blocker promotes the death of cigarette smoke-induced senescent cells and improves lung emphysema.

Palazzo, Alberta / Makulyte, Gabriela / Goerhig, Delphine / Médard, Jean-Jacques / Gros, Vincent / Trottein, François / Adnot, Serge / Vindrieux, David / Flaman, Jean-Michel / Bernard, David

Aging

2023 Volume 15, Issue 23, Page(s) 13581–13592

Abstract: Smoking is the main risk factor for many lung diseases including chronic obstructive pulmonary disease. Cigarette smoke (CS) contains carcinogenic and reactive oxygen species that favor DNA mutations and perturb the homeostasis and environment of cells. ... ...

Abstract	Smoking is the main risk factor for many lung diseases including chronic obstructive pulmonary disease. Cigarette smoke (CS) contains carcinogenic and reactive oxygen species that favor DNA mutations and perturb the homeostasis and environment of cells. CS induces lung cell senescence resulting in a stable proliferation arrest and a senescence-associated secretory phenotype. It was recently reported that senescent cell accumulation promotes several lung diseases. In this study, we performed a chemical screen, using an FDA-approved drug library, to identify compounds selectively promoting the death of CS-induced senescent lung cells. Aside from the well-known senolytic, ABT-263, we identified other potentially new senescence-eliminating compounds, including a new class of molecules, the dihydropyridine family of calcium voltage-gated channel (CaV) blockers. Among these blockers, Benidipine, decreased senescent lung cells and ameliorates lung emphysema in a mouse model. The dihydropyridine family of CaV blockers thus constitutes a new class of senolytics that could improve lung diseases. Hence, our work paves the way for further studies on the senolytic activity of CaV blockers in different senescence contexts and age-related diseases.
MeSH term(s)	Mice ; Animals ; Calcium Channel Blockers/pharmacology ; Calcium Channel Blockers/therapeutic use ; Cigarette Smoking/adverse effects ; Pulmonary Emphysema/genetics ; Lung/metabolism ; Dihydropyridines/pharmacology ; Dihydropyridines/therapeutic use ; Dihydropyridines/metabolism ; Emphysema/metabolism ; Cellular Senescence
Chemical Substances	Calcium Channel Blockers ; benidipine (4G9T91JS7E) ; Dihydropyridines
Language	English
Publishing date	2023-12-12
Publishing country	United States
Document type	Journal Article
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.205259
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: PLA2R1: expression and function in cancer.

Bernard, David / Vindrieux, David

Biochimica et biophysica acta

2014 Volume 1846, Issue 1, Page(s) 40–44

Abstract: The phospholipase A2 receptor 1 (PLA2R1 or PLA2R) was isolated twenty years ago for its ability to bind several secretory phospholipase A2 proteins (sPLA2). Since its identification, it has attracted only a limited interest, mainly in the sPLA2 biology ... ...

Abstract	The phospholipase A2 receptor 1 (PLA2R1 or PLA2R) was isolated twenty years ago for its ability to bind several secretory phospholipase A2 proteins (sPLA2). Since its identification, it has attracted only a limited interest, mainly in the sPLA2 biology field, as it is viewed uniquely as a regulator of sPLA2 activities. Recent discoveries outline novel important functions of this gene in cancer biology. Indeed, PLA2R1 gain or loss of function experiments in vitro and in vivo shows that this receptor promotes several tumor suppressive responses including senescence, apoptosis and inhibition of transformation. Supporting a tumor suppressive role of PLA2R1, its expression decreases in numerous cancers, and known oncogenes such as HIF2α and c-MYC repress its expression. PLA2R1 promoter methylation, a classical way to repress tumor suppressive gene expression in cancer cells, is observed in leukemia, in kidney and in breast cancer cells. Mechanistically, PLA2R1 activates the kinase JAK2 and orients its activity towards a tumor suppressive one. PLA2R1 also promotes accumulation of reactive oxygen species which induce cell death and senescence. This review compiles recent data demonstrating an unexpected tumor suppressive role of PLA2R1 and outlines the future work needed to improve our knowledge of the functions of this gene in cancer.
MeSH term(s)	Animals ; Apoptosis/genetics ; Cell Transformation, Neoplastic/genetics ; Cellular Senescence/genetics ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor/physiology ; Humans ; Neoplasms/genetics ; Receptors, Phospholipase A2/genetics ; Receptors, Phospholipase A2/physiology
Chemical Substances	PLA2R1 protein, human ; Receptors, Phospholipase A2
Language	English
Publishing date	2014-03-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbcan.2014.03.003
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Uc I Zs.247: Show issues

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Article ; Online: Loss of Pla2r1 decreases cellular senescence and age-related alterations caused by aging and Western diets.

Massemin, Amélie / Goehrig, Delphine / Flaman, Jean-Michel / Jaber, Sara / Griveau, Audrey / Djebali, Sophia / Marcos, Elisabeth / Payen, Léa / Marvel, Jacqueline / Parent, Romain / Adnot, Serge / Bertolino, Philippe / Rieusset, Jennifer / Tortereau, Antonin / Vindrieux, David / Bernard, David

Aging cell

2023 Volume 22, Issue 11, Page(s) e13971

Abstract: Cellular senescence is induced by many stresses including telomere shortening, DNA damage, oxidative, or metabolic stresses. Senescent cells are stably cell cycle arrested and they secrete many factors including cytokines and chemokines. Accumulation of ... ...

Abstract	Cellular senescence is induced by many stresses including telomere shortening, DNA damage, oxidative, or metabolic stresses. Senescent cells are stably cell cycle arrested and they secrete many factors including cytokines and chemokines. Accumulation of senescent cells promotes many age-related alterations and diseases. In this study, we investigated the role of the pro-senescent phospholipase A2 receptor 1 (PLA2R1) in regulating some age-related alterations in old mice and in mice subjected to a Western diet, whereas aged wild-type mice displayed a decreased ability to regulate their glycemia during glucose and insulin tolerance tests, aged Pla2r1 knockout (KO) mice efficiently regulated their glycemia and displayed fewer signs of aging. Loss of Pla2r1 was also found protective against the deleterious effects of a Western diet. Moreover, these Pla2r1 KO mice were partially protected from diet-induced senescent cell accumulation, steatosis, and fibrosis. Together these results support that Pla2r1 drives several age-related alterations, especially in the liver, arising during aging or through a Western diet.
MeSH term(s)	Animals ; Mice ; Aging/genetics ; Cellular Senescence/genetics ; Diet, Western ; Mice, Knockout ; Telomere Shortening
Chemical Substances	Pla2r1 protein, mouse
Language	English
Publishing date	2023-09-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13971
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Article ; Online: Generation of a conditional transgenic mouse model expressing human Phospholipase A2 Receptor 1.

Jaber, Sara / Goehrig, Delphine / Bertolino, Philippe / Massemin, Amélie / Bihl, Franck / Chabry, Joëlle / Lambeau, Gérard / Vindrieux, David / Bernard, David

Scientific reports

2020 Volume 10, Issue 1, Page(s) 8190

Abstract: The Phospholipase A2 Receptor 1 (PLA2R1) was first identified for its ability to bind some secreted PLA2s (sPLA2s). It belongs to the C-type lectin superfamily and it binds different types of proteins. It is likely a multifunctional protein that plays a ... ...

Abstract	The Phospholipase A2 Receptor 1 (PLA2R1) was first identified for its ability to bind some secreted PLA2s (sPLA2s). It belongs to the C-type lectin superfamily and it binds different types of proteins. It is likely a multifunctional protein that plays a role i) in inflammation and inflammatory diseases, ii) in cellular senescence, a mechanism participating in aging and age-related diseases including cancer, and iii) in membranous nephropathy (MN), a rare autoimmune kidney disease where PLA2R1 is the major autoantigen. To help study the role of PLA2R1 in these pathophysiological conditions, we have generated a versatile NeoR-hPLA2R1 conditional transgenic mice which will allow the specific expression of human PLA2R1 (hPLA2R1) in relevant organs and cells following Cre recombinase-driven excision of the NeoR-stop cassette flanked by LoxP sites. Proof-of-concept breeding of NeoR-hPLA2R1 mice with the ubiquitous adenoviral EIIa promoter-driven Cre mouse line resulted in the expected excision of the NeoR-stop cassette and the expression of hPLA2R1 in all tested tissues. These Tg-hPLA2R1 animals breed normally, with no reproduction or apparent growth defect. These models, especially the NeoR-hPLA2R1 conditional transgenic mouse line, will facilitate the future investigation of PLA2R1 functions in relevant pathophysiological contexts, including inflammatory diseases, age-related diseases and MN.
MeSH term(s)	Animals ; Disease Models, Animal ; Gene Expression ; Genotyping Techniques ; Humans ; Mice ; Mice, Transgenic ; Organ Specificity ; Receptors, Phospholipase A2/genetics
Chemical Substances	PLA2R1 protein, human ; Receptors, Phospholipase A2
Language	English
Publishing date	2020-05-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-64863-y
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Article ; Online: NF-κB-dependent secretome of senescent cells can trigger neuroendocrine transdifferentiation of breast cancer cells.

Raynard, Clotilde / Ma, Xingjie / Huna, Anda / Tessier, Nolwenn / Massemin, Amélie / Zhu, Kexin / Flaman, Jean-Michel / Moulin, Florentin / Goehrig, Delphine / Medard, Jean-Jacques / Vindrieux, David / Treilleux, Isabelle / Hernandez-Vargas, Hector / Ducreux, Sylvie / Martin, Nadine / Bernard, David

Aging cell

2022 Volume 21, Issue 7, Page(s) e13632

Abstract: Cellular senescence is characterized by a stable proliferation arrest in response to stresses and the acquisition of a senescence-associated secretory phenotype, called SASP, composed of numerous factors including pro-inflammatory molecules, proteases, ... ...

Abstract	Cellular senescence is characterized by a stable proliferation arrest in response to stresses and the acquisition of a senescence-associated secretory phenotype, called SASP, composed of numerous factors including pro-inflammatory molecules, proteases, and growth factors. The SASP affects the environment of senescent cells, especially during aging, by inducing and modulating various phenotypes such as paracrine senescence, immune cell activity, and extracellular matrix deposition and organization, which critically impact various pathophysiological situations, including fibrosis and cancer. Here, we uncover a novel paracrine effect of the SASP: the neuroendocrine transdifferentiation (NED) of some epithelial cancer cells, evidenced both in the breast and prostate. Mechanistically, this effect is mediated by NF-κB-dependent SASP factors, and leads to an increase in intracellular Ca
MeSH term(s)	Aged ; Breast Neoplasms/metabolism ; Cell Transdifferentiation/physiology ; Cellular Senescence/genetics ; Cellular Senescence/physiology ; Humans ; Male ; NF-kappa B/metabolism ; Neuroendocrine Cells/cytology ; Neuroendocrine Cells/metabolism ; Secretome
Chemical Substances	NF-kappa B
Language	English
Publishing date	2022-06-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13632
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Zs.A 6581: Show issues

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Article ; Online: Generation of a conditional transgenic mouse model expressing human Phospholipase A2 Receptor 1

Sara Jaber / Delphine Goehrig / Philippe Bertolino / Amélie Massemin / Franck Bihl / Joëlle Chabry / Gérard Lambeau / David Vindrieux / David Bernard

Scientific Reports, Vol 10, Iss 1, Pp 1-

2020 Volume 9

Abstract: Abstract The Phospholipase A2 Receptor 1 (PLA2R1) was first identified for its ability to bind some secreted PLA2s (sPLA2s). It belongs to the C-type lectin superfamily and it binds different types of proteins. It is likely a multifunctional protein that ...

Abstract	Abstract The Phospholipase A2 Receptor 1 (PLA2R1) was first identified for its ability to bind some secreted PLA2s (sPLA2s). It belongs to the C-type lectin superfamily and it binds different types of proteins. It is likely a multifunctional protein that plays a role i) in inflammation and inflammatory diseases, ii) in cellular senescence, a mechanism participating in aging and age-related diseases including cancer, and iii) in membranous nephropathy (MN), a rare autoimmune kidney disease where PLA2R1 is the major autoantigen. To help study the role of PLA2R1 in these pathophysiological conditions, we have generated a versatile NeoR-hPLA2R1 conditional transgenic mice which will allow the specific expression of human PLA2R1 (hPLA2R1) in relevant organs and cells following Cre recombinase-driven excision of the NeoR-stop cassette flanked by LoxP sites. Proof-of-concept breeding of NeoR-hPLA2R1 mice with the ubiquitous adenoviral EIIa promoter-driven Cre mouse line resulted in the expected excision of the NeoR-stop cassette and the expression of hPLA2R1 in all tested tissues. These Tg-hPLA2R1 animals breed normally, with no reproduction or apparent growth defect. These models, especially the NeoR-hPLA2R1 conditional transgenic mouse line, will facilitate the future investigation of PLA2R1 functions in relevant pathophysiological contexts, including inflammatory diseases, age-related diseases and MN.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2020-05-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Phospholipase A2 receptor 1 promotes lung cell senescence and emphysema in obstructive lung disease.

The European respiratory journal

2021 Volume 58, Issue 2

Abstract: Background: Cell senescence is a key process in age-associated dysfunction and diseases, notably chronic obstructive pulmonary disease (COPD). We previously identified phospholipase A2 receptor 1 (PLA2R1) as a positive regulator of cell senescence ... ...

Abstract	Background: Cell senescence is a key process in age-associated dysfunction and diseases, notably chronic obstructive pulmonary disease (COPD). We previously identified phospholipase A2 receptor 1 (PLA2R1) as a positive regulator of cell senescence acting Methods: We assessed cell senescence in lungs and cultured lung cells from patients with COPD and controls subjected to Results: We found that Conclusions: Our data support a major role for PLA2R1 activation in driving lung cell senescence and lung alterations in COPD. Targeting JAK1/2 may represent a promising therapeutic approach for COPD.
MeSH term(s)	Animals ; Cellular Senescence ; Emphysema ; Humans ; Lung ; Mice ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Emphysema ; Receptors, Phospholipase A2
Chemical Substances	PLA2R1 protein, human ; Receptors, Phospholipase A2
Language	English
Publishing date	2021-08-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.00752-2020
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