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senescence associated secretory phenotype

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https://www.readbyqxmd.com/read/28217839/targeting-the-sasp-to-combat-ageing-mitochondria-as-possible-intracellular-allies
#1
Jodie Birch, João F Passos
Anti-senescence therapies, such as drugs that specifically kill senescent cells, to stave off ageing are currently under investigation. While these interventions show promise, their potential pitfalls are discussed herein. We have shown that the mitochondria are essential for development of senescence and many of the associated phenotypes, including the often detrimental senescence-associated secretory phenotype (SASP). Here, we disentangle many ways in which the mitochondria may influence senescence and development of the SASP and focus on possible pathways that could be exploited for future generation of anti-senescence therapies with a clear aim; to specifically eliminate the problematic features of senescent cells, while maintaining their beneficial characteristics...
February 20, 2017: BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology
https://www.readbyqxmd.com/read/28217805/-induction-of-robust-senescence-associated-secretory-phenotype-in-mouse-nih-3t3-cells-by-mitomycin-c
#2
Wei-Xing Huang, Xiao-Xuan Guo, Zhong-Zhi Peng, Chun-Liang Weng, Chun-Yan Huang, Ben-Yan Shi, Jie Yang, Xiao-Xin Liao, Xiao-Yi Li, Hui-Ling Zheng, Xin-Guang Liu, Xue-Rong Sun
Senescence-associated secretory phenotype (SASP) is often a concomitant result of cell senescence, embodied by the enhanced function of secretion. The SASP factors secreted by senescent cells include cytokines, proteases and chemokines, etc, which can exert great influence on local as well as systemic environment and participate in the process of cell senescence, immunoregulation, angiogenesis, cell proliferation and tumor invasion, etc. Relative to the abundance of SASP models in human cells, the in vitro SASP model derived from mouse cells is scarce at present...
February 25, 2017: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/28202625/gut-microbiota-promotes-obesity-associated-liver-cancer-through-pge2-mediated-suppression-of-antitumor-immunity
#3
Tze Mun Loo, Fumitaka Kamachi, Yoshihiro Watanabe, Shin Yoshimoto, Hiroaki Kanda, Yuriko Arai, Yaeko Nakajima-Takagi, Atsushi Iwama, Tomoaki Koga, Yukihiko Sugimoto, Takayuki Ozawa, Masaru Nakamura, Miho Kumagai, Koichi Watashi, Makoto M Taketo, Tomohiro Aoki, Shuh Narumiya, Masanobu Oshima, Makoto Arita, Eiji Hara, Naoko Ohtani
Obesity increases the risk of cancers, including hepatocellular carcinomas (HCCs). However, the precise molecular mechanisms through which obesity promotes HCC development are still unclear. Recent studies have shown that gut microbiota may influence liver diseases by transferring its metabolites and components. Here, we show that the hepatic translocation of obesity-induced lipoteichoic acid (LTA), a Gram positive gut microbial component, promotes HCC development by creating a tumor-promoting microenvironment...
February 15, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/28197538/cancer-cell-cannibalism-and-the-sasp-ripples-in-the-murky-waters-of-tumor-dormancy
#4
Thomas J Bartosh
Relapse in cancer patients following an apparent cure and a prolonged latency period, known as tumor dormancy, remains an unrelenting clinical crisis. Here, I expand on our recent findings that potentially link cancer cell cannibalism of bone marrow-derived mesenchymal stem/stromal cells (BM-MSCs) to the senescence-associated secretory phenotype (SASP) and tumor dormancy.
2017: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/28185345/the-female-reproduction-and-senescence-nexus
#5
Cielo Mae D Marquez, Joyce A Ibana, Michael C Velarde
Successful pregnancy is regulated by several soluble factors that are differentially expressed throughout gestation. These factors are important to initiate and establish embryo implantation and parturition. Senescent cells, which undergo permanent cell proliferation arrest in response to stress, also produce several secreted factors, referred to as the senescence-associated secretory phenotype (SASP). Here, we review some of the secreted factors found during early and late pregnancy and compare their expression profile with those of the SASP...
February 10, 2017: American Journal of Reproductive Immunology: AJRI
https://www.readbyqxmd.com/read/28166834/downregulation-of-mir-130b-301b-cluster-is-mediated-by-aberrant-promoter-methylation-and-impairs-cellular-senescence-in-prostate-cancer
#6
João Ramalho-Carvalho, Inês Graça, Antonio Gomez, Jorge Oliveira, Rui Henrique, Manel Esteller, Carmen Jerónimo
BACKGROUND: Numerous DNA-damaging cellular stresses, including oncogene activation and DNA-damage response (DDR), may lead to cellular senescence. Previous observations linked microRNA deregulation with altered senescent patterns, prompting us to investigate whether epigenetic repression of microRNAs expression might disrupt senescence in prostate cancer (PCa) cells. METHODS: Differential methylation mapping in prostate tissues was carried using Infinium HumanMethylation450 BeadChip...
February 6, 2017: Journal of Hematology & Oncology
https://www.readbyqxmd.com/read/28165648/the-impact-of-sasp-and-its-potential-as-a-therapeutic-target-for-senescence-associated-diseases
#7
Sugiko Watanabe, Shimpei Kawamoto, Naoko Ohtani, Eiji Hara
'Cellular senescence' is a state in which cells undergo irreversible cell cycle arrest in response to a variety of cellular stresses. Once cells senesce, they are strongly resistant to any mitogens, including oncogenic stimuli. Therefore, cellular senescence has been assumed to be a potent anticancer mechanism. Although irreversible cell-cycle arrest is traditionally considered the major characteristic of senescent cells, recent studies have revealed some additional functions. Most noteworthy is the increased secretion of various secretory proteins, such as inflammatory cytokines, chemokines, growth factors, and matrix metalloproteinases, into the surrounding extracellular fluid...
February 6, 2017: Cancer Science
https://www.readbyqxmd.com/read/28143833/the-senescence-associated-secretory-phenotype-induces-cellular-plasticity-and-tissue-regeneration
#8
Birgit Ritschka, Mekayla Storer, Alba Mas, Florian Heinzmann, Mari Carmen Ortells, Jennifer P Morton, Owen J Sansom, Lars Zender, William M Keyes
Senescence is a form of cell cycle arrest induced by stress such as DNA damage and oncogenes. However, while arrested, senescent cells secrete a variety of proteins collectively known as the senescence-associated secretory phenotype (SASP), which can reinforce the arrest and induce senescence in a paracrine manner. However, the SASP has also been shown to favor embryonic development, wound healing, and even tumor growth, suggesting more complex physiological roles than currently understood. Here we uncover timely new functions of the SASP in promoting a proregenerative response through the induction of cell plasticity and stemness...
January 15, 2017: Genes & Development
https://www.readbyqxmd.com/read/28123407/reversing-multiple-age-related-pathologies-by-controlling-the-senescence-associated-secretory-phenotype-of-stem-cells
#9
Daisuke Hisamatsu, Hayato Naka-Kaneda
No abstract text is available yet for this article.
November 2016: Neural Regeneration Research
https://www.readbyqxmd.com/read/28055114/quantitative-analysis-of-cellular-senescence-in-culture-and-in-vivo
#10
Jing Zhao, Heike Fuhrmann-Stroissnigg, Aditi U Gurkar, Rafael R Flores, Akaitz Dorronsoro, Donna B Stolz, Claudette M St Croix, Laura J Niedernhofer, Paul D Robbins
Cellular senescence refers to the irreversible growth arrest of normally dividing cells in response to various types of stress. Cellular senescence is induced by telomere shortening due to repeated cell division, which causes a DNA damage response, as well as genotoxic, oxidative, and inflammatory stress. Strong mitogenic signaling, such as oncogene activation, also drives cells into a senescent state. Senescent cells express a specific subset of genes, termed the senescence-associated secretory phenotype (SASP), including pro-inflammatory factors, growth factors, and matrix metalloproteinases, which together promote non-cell autonomous, secondary senescence...
January 5, 2017: Current Protocols in Cytometry
https://www.readbyqxmd.com/read/28039358/stromal-senescence-by-prolonged-cdk4-6-inhibition-potentiates-tumor-growth
#11
Xiangnan Guan, Kyle M LaPak, Rebecca C Hennessey, Christina Y Yu, Reena Shakya, Jianying Zhang, Christin E Burd
: Senescent cells within the tumor microenvironment (TME) adopt a pro-inflammatory, senescence-associated secretory phenotype (SASP) that promotes cancer initiation, progression and therapeutic resistance. Here, exposure to Palbociclib (PD-0332991), a CDK4/6 inhibitor, induces senescence and a robust SASP in normal fibroblasts. Senescence caused by prolonged CDK4/6 inhibition is DNA damage-independent and associated with Mdm2 downregulation, whereas the SASP elicited by these cells is largely reliant upon NF-kappaB activation...
December 30, 2016: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28030837/bafilomycin-a1-triggers-proliferative-potential-of-senescent-cancer-cells-in-vitro-and-in-nod-scid-mice
#12
Halina Was, Kamila Barszcz, Joanna Czarnecka, Agata Kowalczyk, Tytus Bernas, Ewelina Uzarowska, Paulina Koza, Agata Klejman, Katarzyna Piwocka, Bozena Kaminska, Eva Sikora
Anticancer therapies that induce DNA damage tend to trigger senescence in cancer cells, a process known as therapy-induced senescence (TIS). Such cells may undergo atypical divisions, thus contributing to tumor re-growth. Accumulation of senescent cancer cells reduces survival of patients after chemotherapy. As senescence interplays with autophagy, a dynamic recycling process, we sought to study whether inhibition of autophagy interferes with divisions of TIS cells. We exposed human colon cancer HCT116 cells to repeated cycles of a chemotherapeutic agent - doxorubicin (doxo) and demonstrated induction of hallmarks of TIS (e...
February 7, 2017: Oncotarget
https://www.readbyqxmd.com/read/28017795/injury-induced-senescence-enables-in%C3%A2-vivo-reprogramming-in-skeletal-muscle
#13
Aurélie Chiche, Isabelle Le Roux, Mathieu von Joest, Hiroshi Sakai, Sabela Búa Aguín, Coralie Cazin, Rana Salam, Laurence Fiette, Olinda Alegria, Patricia Flamant, Shahragim Tajbakhsh, Han Li
In vivo reprogramming is a promising approach for tissue regeneration in response to injury. Several examples of in vivo reprogramming have been reported in a variety of lineages, but some including skeletal muscle have so far proven refractory. Here, we show that acute and chronic injury enables transcription-factor-mediated reprogramming in skeletal muscle. Lineage tracing indicates that this response frequently originates from Pax7+ muscle stem cells. Injury is associated with accumulation of senescent cells, and advanced aging or local irradiation further enhanced in vivo reprogramming, while selective elimination of senescent cells reduced reprogramming efficiency...
December 22, 2016: Cell Stem Cell
https://www.readbyqxmd.com/read/27979832/cellular-senescence-promotes-adverse-effects-of-chemotherapy-and-cancer-relapse
#14
Marco Demaria, Monique N O'Leary, Jianhui Chang, Lijian Shao, Su Liu, Fatouma Alimirah, Kristin Koenig, Catherine Le, Natalia Mitin, Allison M Deal, Shani Alston, Emmeline C Academia, Sumner Kilmarx, Alexis Valdovinos, Boshi Wang, Alain de Bruin, Brian K Kennedy, Simon Melov, Daohong Zhou, Norman E Sharpless, Hyman Muss, Judith Campisi
: Cellular senescence suppresses cancer by irreversibly arresting cell proliferation. Senescent cells acquire a proinflammatory senescence-associated secretory phenotype. Many genotoxic chemotherapies target proliferating cells nonspecifically, often with adverse reactions. In accord with prior work, we show that several chemotherapeutic drugs induce senescence of primary murine and human cells. Using a transgenic mouse that permits tracking and eliminating senescent cells, we show that therapy-induced senescent (TIS) cells persist and contribute to local and systemic inflammation...
February 2017: Cancer Discovery
https://www.readbyqxmd.com/read/27951455/relationship-of-inflammatory-profile-of-elderly-patients-serum-and-senescence-associated-secretory-phenotype-with-human-breast-cancer-cells-proliferation-role-of-il6-il8-ratio
#15
Bertha Alicia Barajas-Gómez, Oscar Rosas-Carrasco, Sandra Lisbeth Morales-Rosales, Gibrán Pedraza Vázquez, Viridiana Yazmín González-Puertos, Teresa Juárez-Cedillo, Jorge Antonio García-Álvarez, Norma Edith López-Diazguerrero, Pablo Damián-Matsumura, Mina Königsberg, Armando Luna-López
Aging is considered a systemic, chronic and low-grade inflammatory state, called "inflammaging", which has been contemplated as a risk factor for cancer development and progression in the elderly population. Cellular senescence is a multifactorial phenomenon of growth arrest and distorted function, which has been recognized as a contributor to aging. Senescent cells have an altered secretion pattern called Senescent Associated Secretory Phenotype (SASP), that comprise a complex mix of factors including cytokines, growth factors, chemokines and matrix metalloproteinases among others...
December 9, 2016: Cytokine
https://www.readbyqxmd.com/read/27931848/human-peripheral-late-exhausted-memory-b-cells-express-a-senescent-associated-secretory-phenotype-and-preferentially-utilize-metabolic-signaling-pathways
#16
Daniela Frasca, Alain Diaz, Maria Romero, Bonnie B Blomberg
The percentage of late/exhausted memory (LM) B cells increases with age and we show here that this is associated with a lower influenza vaccine response. To identify novel contributors to the phenotypic and functional changes observed in aged B cells, we sorted the major peripheral B cell subsets [naïve, IgM memory, switched memory (swIg) and late/exhausted memory (LM)] and determined their percentages in the peripheral blood as well as their level of immune activation by measuring basal levels of expression of multiple senescence-associated secretory phenotype (SASP) markers, such as pro-inflammatory cytokines (TNF-α/IL-6/IL-8), inflammatory micro-RNAs (miRs, miR-155/16/93), cell cycle regulators (p16(INK4))...
January 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/27927801/physiological-aging-links-among-adipose-tissue-dysfunction-diabetes-and-frailty
#17
REVIEW
Michael B Stout, Jamie N Justice, Barbara J Nicklas, James L Kirkland
Advancing age is associated with progressive declines in physiological function that lead to overt chronic disease, frailty, and eventual mortality. Importantly, age-related physiological changes occur in cellularity, insulin-responsiveness, secretory profiles, and inflammatory status of adipose tissue, leading to adipose tissue dysfunction. Although the mechanisms underlying adipose tissue dysfunction are multifactorial, the consequences result in secretion of proinflammatory cytokines and chemokines, immune cell infiltration, an accumulation of senescent cells, and an increase in senescence-associated secretory phenotype (SASP)...
January 2017: Physiology
https://www.readbyqxmd.com/read/27907906/senescent-fibroblast-derived-chemerin-promotes-squamous-cell-carcinoma-migration
#18
Vida Farsam, Abhijit Basu, Martina Gatzka, Nicolai Treiber, Lars A Schneider, Medhanie A Mulaw, Tanja Lucas, Stefan Kochanek, Reinhard Dummer, Mitchell P Levesque, Meinhard Wlaschek, Karin Scharffetter-Kochanek
Aging is associated with a rising incidence of cutaneous squamous cell carcinoma (cSCC), an aggressive skin cancer with the potential for local invasion and metastasis. Acquisition of a senescence-associated secretory phenotype (SASP) in dermal fibroblasts has been postulated to promote skin cancer progression in elderly individuals. The underlying molecular mechanisms are largely unexplored. We show that Chemerin, a previously unreported SASP factor released from senescent human dermal fibroblasts, promotes cSCC cell migration, a key feature driving tumor progression...
November 18, 2016: Oncotarget
https://www.readbyqxmd.com/read/27889642/redox-control-of-senescence-and-age-related-disease
#19
REVIEW
Akshaya Chandrasekaran, Maria Del Pilar Sosa Idelchik, J Andrés Melendez
The signaling networks that drive the aging process, associated functional deterioration, and pathologies has captured the scientific community's attention for decades. While many theories exist to explain the aging process, the production of reactive oxygen species (ROS) provides a signaling link between engagement of cellular senescence and several age-associated pathologies. Cellular senescence has evolved to restrict tumor progression but the accompanying senescence-associated secretory phenotype (SASP) promotes pathogenic pathways...
November 16, 2016: Redox Biology
https://www.readbyqxmd.com/read/27886850/cellular-senescence-and-autophagy-in-the-pathogenesis-of-chronic-obstructive-pulmonary-disease-copd-and-idiopathic-pulmonary-fibrosis-ipf
#20
REVIEW
Kazuyoshi Kuwano, Jun Araya, Hiromichi Hara, Shunsuke Minagawa, Naoki Takasaka, Saburo Ito, Kenji Kobayashi, Katsutoshi Nakayama
Aging is associated with impairments in homeostasis. Although aging and senescence are not equivalent, the number of senescent cells increases with aging. Cellular senescence plays important roles in tissue repair or remodeling, as well as embryonic development. Autophagy is a process of lysosomal self-degradation that maintains a homeostatic balance between the synthesis, degradation, and recycling of cellular proteins. Autophagy diminishes with aging; additionally, accelerated aging can be attributed to reduced autophagy...
November 2016: Respiratory Investigation
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