Oxidative stress and cellular senescence: Roles in tumor progression and therapeutic opportunities DOI Creative Commons
Ping Jin, Xudong Feng, Chongan Huang

и другие.

MedComm – Oncology, Год журнала: 2024, Номер 3(4)

Опубликована: Дек. 1, 2024

Abstract Oxidative stress results from an imbalance between the production and neutralization of reactive oxygen species. It induces oxidative damage to cellular components including proteins, lipids, nucleic acids, membranes, therefore intrinsically linking aging‐related diseases such as cancer, cardiovascular disease, neurological disorders. Emerging evidence suggests that may promote tumor development by influencing various aspects senescence, its onset, pro‐inflammatory secretion, alteration function structure. Modulating target senescence offers a novel strategy for cancer prevention treatment. However, thorough grasp specific mechanisms at play is lacking. This review will present association their regulatory role in progression treatment, with emphasis on senescence‐associated secretory phenotype, immunosenescence therapy‐induced senescence. Current agents strategies remove side effects via killing senescent cells or modulating improve antitumor efficacy be summarized. help readers better understand complex relationship also provide basis further research this area.

Язык: Английский

Exploring the Thioredoxin System as a Therapeutic Target in Cancer: Mechanisms and Implications DOI Creative Commons

Rebecca Seitz,

Deniz Tümen,

C Kunst

и другие.

Antioxidants, Год журнала: 2024, Номер 13(9), С. 1078 - 1078

Опубликована: Сен. 4, 2024

Cells constantly face the challenge of managing oxidants. In aerobic organisms, oxygen (O

Язык: Английский

Процитировано

7

Structural characterizations and antiaging activities of hydrolyzed low-molecular-weight polysaccharides from Polygoni Multiflori Radix Praeparata DOI
Xu We, Xuejian Li,

Yu-Sen Zhong

и другие.

Carbohydrate Polymers, Год журнала: 2025, Номер 356, С. 123381 - 123381

Опубликована: Фев. 14, 2025

Язык: Английский

Процитировано

0

PLK3 weakens antioxidant defense and inhibits proliferation of porcine Leydig cells under oxidative stress DOI Creative Commons
Chujie Chen, Jinyan He, Weixian Huang

и другие.

Scientific Reports, Год журнала: 2025, Номер 15(1)

Опубликована: Янв. 21, 2025

Aging is characterized by cellular degeneration and impaired physiological functions, leading to a decline in male sexual desire reproductive capacity. Oxidative stress (OS) lead testicular aging impairing the system, but potential mechanisms remain unclear. In present study, functional status of tissues from young aged boars was compared, transcriptional responses Leydig cells (LCs) hydrogen peroxide (H2O2)-induced senescence were explored, revealing role OS promoting system. 601 differentially expressed genes (DEGs) associated with OS, cell cycle regulation, intracellular processes identified. These DEGs significantly enriched critical pathways, including p53 signaling pathway, autophagy, senescence. Protein-protein interaction (PPI) network analysis unveiled 15 key related DNA replication, polo-like kinase 3 (PLK3) exhibiting increased expression under OS. vitro, PLK3 knockdown enhanced viability antioxidant capacity LCs This study deepens our understanding how respond provides new therapeutic targets for enhancing resistance oxidative damage tissue health.

Язык: Английский

Процитировано

0

Extracellular vesicles within a tumourigenic therapy-induced senescent tumour secretome are able to confer anti-cancer properties DOI Creative Commons
Matius Robert, Rekha Jakhar,

Bijin Veonice Au

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Март 29, 2024

ABSTRACT Triple-negative breast cancers (TNBC), associated with poor prognosis and high tumour recurrence, are often-treated taxanes in first-line treatment regimens. However, acquired disease resistance can often set in, hampering clinical efficacy. One avenue that could engender therapy is therapy-induced senescence (TIS), as they represent a population of residual highly secretory. Although it known TIS contribute to development via the secretome, underlying molecular mechanisms not fully understood. In this study, we sought dissect role TNBC-derived TIS-associated secretome chemoresponse. We found paclitaxel-treated cells induced mitotic slippage entered tetraploid cells. The SASP was be enriched soluble cytokines other pro-tumorigenic factors linked recurrence distant metastasis. Interestingly, senescence-associated small extracellular vesicles (sEVs) or exosomes, an underappreciated component SASP, increased genomic instability, ROS anti-tumour activity. Exosomal proteomic transcriptomic profiling further revealed DKK1, negative regulator WNT signalling, TIS-sEVs. Further investigation demonstrated DKK1-control inflammatory production confer reduced activity recipient TNBC cancer Taken together, study unexpected findings where TIS-sEVs opposing tumourigenic outcomes elicited by TIS-SASP, indicating sEVs should considered distinct entities.

Язык: Английский

Процитировано

0

Oxidative stress and cellular senescence: Roles in tumor progression and therapeutic opportunities DOI Creative Commons
Ping Jin, Xudong Feng, Chongan Huang

и другие.

MedComm – Oncology, Год журнала: 2024, Номер 3(4)

Опубликована: Дек. 1, 2024

Abstract Oxidative stress results from an imbalance between the production and neutralization of reactive oxygen species. It induces oxidative damage to cellular components including proteins, lipids, nucleic acids, membranes, therefore intrinsically linking aging‐related diseases such as cancer, cardiovascular disease, neurological disorders. Emerging evidence suggests that may promote tumor development by influencing various aspects senescence, its onset, pro‐inflammatory secretion, alteration function structure. Modulating target senescence offers a novel strategy for cancer prevention treatment. However, thorough grasp specific mechanisms at play is lacking. This review will present association their regulatory role in progression treatment, with emphasis on senescence‐associated secretory phenotype, immunosenescence therapy‐induced senescence. Current agents strategies remove side effects via killing senescent cells or modulating improve antitumor efficacy be summarized. help readers better understand complex relationship also provide basis further research this area.

Язык: Английский

Процитировано

0