The interplay of cellular senescence and reprogramming shapes the biological landscape of aging and cancer revealing novel therapeutic avenues DOI Creative Commons
Fuping Ding, Ying Yu, Jiangqi Zhao

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: April 28, 2025

Cellular senescence and cellular reprogramming represent two fundamentally intertwined processes that profoundly influence aging cancer. This paper explores how the permanent cell-cycle arrest of senescent cells identity-resetting capacity jointly shape biological outcomes in later life tumor development. We synthesize recent findings to show cells, while halting proliferation damaged can paradoxically promote tissue dysfunction malignancy via their secretory phenotype. Conversely, induced somatic cells—exemplified by Yamanaka factors—resets age epigenetic marks, offering a potential rejuvenate aged cells. Key highlight shared mechanisms (e.g., DNA damage responses remodeling) bidirectional crosstalk between these processes: signals facilitate neighboring cell plasticity, whereas attempts trigger intrinsic programs as barrier. In tissues, transient (partial) has been shown erase markers restore function without inducing tumorigenesis, underlining novel strategy combat age-related degeneration. cancer, we discuss therapy-induced may induce stem-cell-like traits some drive relapse, revealing delicate balance suppression promotion. Understanding interplay is crucial for developing innovative therapies. By targeting senescence–reprogramming axis–for instance, senolytic drugs, SASP inhibitors, or safe techniques–there significant therapeutic ameliorate aging-related diseases improve cancer treatment. Our underscore carefully modulating rejuvenation could pave way regenerative anti-cancer strategies.

Language: Английский

The interplay of p16INK4a and non-coding RNAs: bridging cellular senescence, aging, and cancer DOI
Ashok Kumar Balaraman, Muhammad Afzal, Ehssan Moglad

et al.

Biogerontology, Journal Year: 2025, Volume and Issue: 26(2)

Published: Feb. 5, 2025

Language: Английский

Citations

0
Spatio-temporal model of combining ADT and chemotherapy with senolytic treatment in metastatic prostate cancer DOI
Teddy Lazebnik, Avner Friedman

Journal of Theoretical Biology, Journal Year: 2025, Volume and Issue: 602-603, P. 112069 - 112069

Published: Feb. 18, 2025

Language: Английский

Citations

0
Cellular senescence in metastatic prostate cancer: A therapeutic opportunity or challenge (Review) DOI

Cen Jin,

Shujuan Liao, Guo‐Liang Lu

et al.

Molecular Medicine Reports, Journal Year: 2024, Volume and Issue: 30(3)

Published: July 8, 2024

The treatment of patients with metastatic prostate cancer (PCa) is considered to be a long‑standing challenge. Conventional treatments for PCa, such as radical prostatectomy, radiotherapy and androgen receptor‑targeted therapy, induce senescence PCa cells certain extent. While senescent can impede tumor growth through the restriction cell proliferation increasing immune clearance, microenvironment may concurrently stimulate secretion senescence‑associated secretory phenotype diminish function, which promotes recurrence metastasis. Resistance established therapies primary obstacle in treating it lead progression towards an incurable state disease. Therefore, understanding molecular mechanisms that underly crucial development novel therapeutic approaches. present study reviews phenomenon treatment‑induced dual role Furthermore, review discusses potential strategies target aforementioned processes aim providing insights into evolving landscape PCa.

Language: Английский

Citations

3
The interplay of cellular senescence and reprogramming shapes the biological landscape of aging and cancer revealing novel therapeutic avenues DOI Creative Commons
Fuping Ding, Ying Yu, Jiangqi Zhao

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: April 28, 2025

Cellular senescence and cellular reprogramming represent two fundamentally intertwined processes that profoundly influence aging cancer. This paper explores how the permanent cell-cycle arrest of senescent cells identity-resetting capacity jointly shape biological outcomes in later life tumor development. We synthesize recent findings to show cells, while halting proliferation damaged can paradoxically promote tissue dysfunction malignancy via their secretory phenotype. Conversely, induced somatic cells—exemplified by Yamanaka factors—resets age epigenetic marks, offering a potential rejuvenate aged cells. Key highlight shared mechanisms (e.g., DNA damage responses remodeling) bidirectional crosstalk between these processes: signals facilitate neighboring cell plasticity, whereas attempts trigger intrinsic programs as barrier. In tissues, transient (partial) has been shown erase markers restore function without inducing tumorigenesis, underlining novel strategy combat age-related degeneration. cancer, we discuss therapy-induced may induce stem-cell-like traits some drive relapse, revealing delicate balance suppression promotion. Understanding interplay is crucial for developing innovative therapies. By targeting senescence–reprogramming axis–for instance, senolytic drugs, SASP inhibitors, or safe techniques–there significant therapeutic ameliorate aging-related diseases improve cancer treatment. Our underscore carefully modulating rejuvenation could pave way regenerative anti-cancer strategies.

Language: Английский

Citations

0