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Article ; Online: Living Beyond Restriction: LBR promotes cellular immortalization by suppressing genomic instability and senescence.

Choi, Haebeen / Kang, Chanhee

2024

Abstract: Cellular immortalization is a complex process that requires multiple genetic alterations to overcome restricting barriers, including senescence. Not surprisingly, many of these alterations are associated with cancer; two tumor suppressor pathways, the ... ...

Abstract	Cellular immortalization is a complex process that requires multiple genetic alterations to overcome restricting barriers, including senescence. Not surprisingly, many of these alterations are associated with cancer; two tumor suppressor pathways, the cellular tumor antigen p53 and p16-Retinoblastoma (RB) pathways, are the best-characterized examples, but their mutations alone are known to be insufficient to drive full immortalization. En et al. identified a role for the lamin B receptor (LBR) in promoting cellular proliferation and immortalization in p53- and RB-deficient cells by maintaining their genome integrity and suppressing senescence. Thus, modulation of LBR could be exploited to treat cancer and potentially also to promote cell rejuvenation.
Language	English
Publishing date	2024-04-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.17141
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Article ; Online: Senolytics and Senostatics: A Two-Pronged Approach to Target Cellular Senescence for Delaying Aging and Age-Related Diseases.

Kang, Chanhee

Molecules and cells

2019 Volume 42, Issue 12, Page(s) 821–827

Abstract: Aging is the most important single risk factor for many chronic diseases such as cancer, metabolic syndrome, and neurodegenerative disorders. Targeting aging itself might, therefore, be a better strategy than targeting each chronic disease individually ... ...

Abstract	Aging is the most important single risk factor for many chronic diseases such as cancer, metabolic syndrome, and neurodegenerative disorders. Targeting aging itself might, therefore, be a better strategy than targeting each chronic disease individually for enhancing human health. Although much should be achieved for completely understanding the biological basis of aging, cellular senescence is now believed to mainly contribute to organismal aging via two independent, yet not mutually exclusive mechanisms: on the one hand, senescence of stem cells leads to exhaustion of stem cells and thus decreases tissue regeneration. On the other hand, senescent cells secrete many proinflammatory cytokines, chemokines, growth factors, and proteases, collectively termed as the senescence-associated secretory phenotype (SASP), which causes chronic inflammation and tissue dysfunction. Much effort has been recently made to therapeutically target detrimental effects of cellular senescence including selectively eliminating senescent cells (senolytics) and modulating a proinflammatory senescent secretome (senostatics). Here, we discuss current progress and limitations in understanding molecular mechanisms of senolytics and senostatics and therapeutic strategies for applying them. Furthermore, we propose how these novel interventions for aging treatment could be improved, based on lessons learned from cancer treatment.
MeSH term(s)	Aging/drug effects ; Aging/genetics ; Aging/pathology ; Cellular Senescence/drug effects ; Cytokines/metabolism ; Healthy Aging ; Humans ; Inflammation/metabolism ; Neoplasms/drug therapy ; Neoplasms/pathology ; Neoplasms/prevention & control ; Phenotype
Chemical Substances	Cytokines
Language	English
Publishing date	2019-07-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1148964-9
ISSN	0219-1032 ; 1016-8478
ISSN (online)	0219-1032
ISSN	1016-8478
DOI	10.14348/molcells.2019.0298
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Zs.A 4713: Show issues

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Article ; Online: Metabolic remodeling in cancer and senescence and its therapeutic implications.

Kim, Yeonju / Jang, Yeji / Kim, Mi-Sung / Kang, Chanhee

Trends in endocrinology and metabolism: TEM

2024

Abstract: Cellular metabolism is a flexible and plastic network that often dictates physiological and pathological states of the cell, including differentiation, cancer, and aging. Recent advances in cancer metabolism represent a tremendous opportunity to treat ... ...

Abstract	Cellular metabolism is a flexible and plastic network that often dictates physiological and pathological states of the cell, including differentiation, cancer, and aging. Recent advances in cancer metabolism represent a tremendous opportunity to treat cancer by targeting its altered metabolism. Interestingly, despite their stable growth arrest, senescent cells - a critical component of the aging process - undergo metabolic changes similar to cancer metabolism. A deeper understanding of the similarities and differences between these disparate pathological conditions will help identify which metabolic reprogramming is most relevant to the therapeutic liabilities of senescence. Here, we compare and contrast cancer and senescence metabolism and discuss how metabolic therapies can be established as a new modality of senotherapy for healthy aging.
Language	English
Publishing date	2024-03-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2024.02.008
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Zs.A 2999: Show issues

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Article ; Online: Where should siRNAs go: applicable organs for siRNA drugs.

Ahn, Insook / Kang, Chanhee S / Han, Jinju

Experimental & molecular medicine

2023 Volume 55, Issue 7, Page(s) 1283–1292

Abstract: RNA interference mediated by small interfering RNAs (siRNAs) has been exploited for the development of therapeutics. siRNAs can be a powerful therapeutic tool because the working mechanisms of siRNAs are straightforward. siRNAs determine targets based on ...

Abstract	RNA interference mediated by small interfering RNAs (siRNAs) has been exploited for the development of therapeutics. siRNAs can be a powerful therapeutic tool because the working mechanisms of siRNAs are straightforward. siRNAs determine targets based on their sequence and specifically regulate the gene expression of the target gene. However, efficient delivery of siRNAs to the target organ has long been an issue that needs to be solved. Tremendous efforts regarding siRNA delivery have led to significant progress in siRNA drug development, and from 2018 to 2022, a total of five siRNA drugs were approved for the treatment of patients. Although all FDA-approved siRNA drugs target the hepatocytes of the liver, siRNA-based drugs targeting different organs are in clinical trials. In this review, we introduce siRNA drugs in the market and siRNA drug candidates in clinical trials that target cells in multiple organs. The liver, eye, and skin are the preferred organs targeted by siRNAs. Three or more siRNA drug candidates are in phase 2 or 3 clinical trials to suppress gene expression in these preferred organs. On the other hand, the lungs, kidneys, and brain are challenging organs with relatively few clinical trials. We discuss the characteristics of each organ related to the advantages and disadvantages of siRNA drug targeting and strategies to overcome the barriers in delivering siRNAs based on organ-specific siRNA drugs that have progressed to clinical trials.
MeSH term(s)	Humans ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Pharmaceutical Preparations/metabolism ; RNA Interference ; Lung/metabolism ; Liver/metabolism
Chemical Substances	RNA, Small Interfering ; Pharmaceutical Preparations
Language	English
Publishing date	2023-07-10
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/s12276-023-00998-y
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Zs.A 4775: Show issues

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Article ; Online: The FMRFamide Neuropeptide FLP-20 Acts as a Systemic Signal for Starvation Responses in

Kang, Chanhee / Avery, Leon

Molecules and cells

2021 Volume 44, Issue 7, Page(s) 529–537

Abstract: Most animals face frequent periods of starvation throughout their entire life and thus need to appropriately adjust their behavior and metabolism during starvation for their survival. Such adaptive responses are regulated by a complex set of systemic ... ...

Abstract	Most animals face frequent periods of starvation throughout their entire life and thus need to appropriately adjust their behavior and metabolism during starvation for their survival. Such adaptive responses are regulated by a complex set of systemic signals, including hormones and neuropeptides. While much progress has been made in identifying pathways that regulate nutrient-excessive states, it is still incompletely understood how animals systemically signal their nutrient-deficient states. Here, we showed that the FMRFamide neuropeptide FLP-20 modulates a systemic starvation response in
MeSH term(s)	Animals ; Caenorhabditis elegans ; FMRFamide/metabolism ; Neuropeptides/genetics
Chemical Substances	Neuropeptides ; FMRFamide (64190-70-1)
Language	English
Publishing date	2021-06-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	1148964-9
ISSN	0219-1032 ; 1016-8478
ISSN (online)	0219-1032
ISSN	1016-8478
DOI	10.14348/molcells.2021.0051
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Article ; Online: A focused natural compound screen reveals senolytic and senostatic effects of Isatis tinctoria

Kim, Eun-jung / Woo, Jieun / Shin, Seoungwoo / Choi, HaeBeen / Kim, Youngseok / Kim, Junoh / Kang, Chanhee

Animal Cells and Systems. 2022 Nov. 02, v. 26, no. 6 p.310-317

2022

Abstract: Natural products and their derivatives historically represent alternatives to conventional synthetic molecules for pharmacotherapy, ranging from cancer chemotherapeutics to cosmetic ingredients that exert anti-aging activities. Cellular senescence is ... ...

Abstract	Natural products and their derivatives historically represent alternatives to conventional synthetic molecules for pharmacotherapy, ranging from cancer chemotherapeutics to cosmetic ingredients that exert anti-aging activities. Cellular senescence is considered a main driver of skin aging, yet natural products that target skin senescence in a specific manner are not thoroughly explored. Here, we performed a focused compound screen to identify natural products that exert anti-senescence effects. We found that Isatis tinctoria, woad extracts, displayed a senolytic effect on senescent human skin fibroblasts. Furthermore, treatment with woad extracts attenuated the expression of pro-inflammatory senescence-associated secretory phenotype (SASP), showing a senostatic activity. Intriguingly, woad extracts displayed only a marginal cytotoxic effect toward senescent human lung fibroblasts. Thus, our results reveal the potential activities of woad extracts for targeting skin senescence and suggest that woad extracts could be an attractive ingredient for cosmetics to prevent skin aging.
Keywords	Isatis tinctoria ; cell senescence ; cosmetics ; cytotoxicity ; drug therapy ; fibroblasts ; humans ; ingredients ; lungs ; phenotype ; skin (animal) ; Cellular senescence ; senolytics ; senostatics ; I. tinctoria ; skin aging
Language	English
Dates of publication	2022-1102
Size	p. 310-317.
Publishing place	Taylor & Francis
Document type	Article ; Online
ZDB-ID	2562988-8
ISSN	2151-2485 ; 1976-8354
ISSN (online)	2151-2485
ISSN	1976-8354
DOI	10.1080/19768354.2022.2143895
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: How autophagy both activates and inhibits cellular senescence.

Kang, Chanhee / Elledge, Stephen J

Autophagy

2016 Volume 12, Issue 5, Page(s) 898–899

Abstract: Autophagy and cellular senescence are stress responses essential for homeostasis. While recent studies indicate a genetic relationship between autophagy and senescence, whether autophagy acts positively or negatively on senescence is still subject to ... ...

Abstract	Autophagy and cellular senescence are stress responses essential for homeostasis. While recent studies indicate a genetic relationship between autophagy and senescence, whether autophagy acts positively or negatively on senescence is still subject to debate. Although autophagy was originally recognized as a nonspecific lysosomal degradation pathway (general autophagy), increasing evidence supports a selective form of autophagy that mediates the degradation of specific targets (selective autophagy). Our recent study revealed distinctive roles of selective autophagy and general autophagy in the regulation of senescence, at least in part resolving apparently contradictory reports regarding the relationship between these 2 important homeostatic stress responses.
Language	English
Publishing date	2016-05-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2015.1121361
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Article ; Online: A flow-cytometry-based assessment of global protein synthesis in human senescent cells.

Lee, Yeonghyeon / Kim, Jaejin / Jeon, Taerang / Roh, Kyeonghwan / Kim, Mi-Sung / Kang, Chanhee

STAR protocols

2021 Volume 2, Issue 3, Page(s) 100809

Abstract: Senescent cells constantly experience stressful conditions and restrain their protein translation to cope with it. Here, we present a detailed protocol to measure the rate of global protein synthesis using L-azidohomoalanine (L-AHA)-based click chemistry ...

Abstract	Senescent cells constantly experience stressful conditions and restrain their protein translation to cope with it. Here, we present a detailed protocol to measure the rate of global protein synthesis using L-azidohomoalanine (L-AHA)-based click chemistry in human senescent fibroblasts. We optimized several aspects of the procedure, including senescence induction, a flow cytometry analysis of senescent cells, and the duration of L-AHA incorporation. This protocol uses senescent human fibroblasts but can be applied to other types of cells or circumstances. For complete details on the use and execution of this protocol, please refer to Lee et al. (2021).
MeSH term(s)	Alanine/analogs & derivatives ; Alanine/analysis ; Alanine/metabolism ; Animals ; Cell Line ; Cellular Senescence/physiology ; Click Chemistry ; Fibroblasts/cytology ; Fibroblasts/metabolism ; Flow Cytometry/methods ; HEK293 Cells ; Humans ; Mice ; Protein Biosynthesis/physiology ; Proteins/analysis ; Proteins/chemistry ; Proteins/metabolism
Chemical Substances	Proteins ; azidohomoalanine ; Alanine (OF5P57N2ZX)
Language	English
Publishing date	2021-09-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2021.100809
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Article ; Online: Targeting the stress support network regulated by autophagy and senescence for cancer treatment.

Kim, Jaejin / Lee, Yeonghyeon / Roh, Kyeonghwan / Kim, Mi-Sung / Kang, Chanhee

Advances in cancer research

2021 Volume 150, Page(s) 75–112

Abstract: Autophagy and cellular senescence are two potent tumor suppressive mechanisms activated by various cellular stresses, including the expression of activated oncogenes. However, emerging evidence has also indicated their pro-tumorigenic activities, ... ...

Abstract	Autophagy and cellular senescence are two potent tumor suppressive mechanisms activated by various cellular stresses, including the expression of activated oncogenes. However, emerging evidence has also indicated their pro-tumorigenic activities, strengthening the case for the complexity of tumorigenesis. More specifically, tumorigenesis is a systemic process emanating from the combined accumulation of changes in the tumor support pathways, many of which cannot cause cancer on their own but might still provide excellent therapeutic targets for cancer treatment. In this review, we discuss the dual roles of autophagy and senescence during tumorigenesis, with a specific focus on the stress support networks in cancer cells modulated by these processes. A deeper understanding of such context-dependent roles may help to enhance the effectiveness of cancer therapies targeting autophagy and senescence, while limiting their potential side effects. This will steer and accelerate the pace of research and drug development for cancer treatment.
MeSH term(s)	Autophagy/physiology ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Cellular Senescence/physiology ; DNA Damage/physiology ; Gene Regulatory Networks/physiology ; Humans ; Metabolic Networks and Pathways/genetics ; Metabolic Networks and Pathways/physiology ; Molecular Targeted Therapy/methods ; Molecular Targeted Therapy/trends ; Neoplasms/genetics ; Neoplasms/pathology ; Neoplasms/therapy ; Stress, Physiological/physiology
Language	English
Publishing date	2021-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	127-2
ISSN	2162-5557 ; 0065-230X
ISSN (online)	2162-5557
ISSN	0065-230X
DOI	10.1016/bs.acr.2021.01.003
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Article ; Online: All cells are created equal in the sight of autophagy: selective autophagy maintains homeostasis in senescent cells.

Kim, Jaejin / Lee, Yeonghyeon / Jeon, Taerang / Kim, Mi-Sung / Kang, Chanhee

Autophagy

2021 Volume 17, Issue 10, Page(s) 3260–3261

Abstract: Macroautophagy/autophagy is a sophisticated quality control program that limits cellular damage and maintains homeostasis, being an essential part of several lifespan-promoting interventions. However, autophagy is also necessary for full establishment of ...

Abstract	Macroautophagy/autophagy is a sophisticated quality control program that limits cellular damage and maintains homeostasis, being an essential part of several lifespan-promoting interventions. However, autophagy is also necessary for full establishment of cellular senescence, a causal factor for many age-related diseases and aging. What lies ahead of us to unravel such a paradoxical role of autophagy in senescence is to identify specific targets degraded by autophagy during senescence and determine their importance in the senescence regulatory network. Recently, we developed the "
MeSH term(s)	Autophagy ; Cellular Senescence ; Homeostasis ; Macroautophagy
Language	English
Publishing date	2021-07-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2021.1953848
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