Articles tagged with Cellular Senescence
A study published in Life Science Alliance found that the enzyme D-amino acid oxidase (DAO) promotes cellular senescence and aging by producing reactive oxygen species. By inducing DNA double-strand breaks, researchers found increased expression of DAO is dependent on p53, a cancer-suppressing protein.
Newborn naked mole rats display developmental senescence in various tissues, including hair follicles, nail beds, and skin dermis. Oncogene-induced and DNA damage-induced senescence occur in embryonic and skin fibroblasts, suggesting cellular senescence is not eliminated with evolution.
Researchers identified genes that control cellular senescence, a process that permanently arrests cell growth. These findings have potential applications for creating new anticancer drugs and developing anti-aging products.
Researchers found that eliminating p19ARF-expressing cells enhances pulmonary function in mice. Senescent cells contribute to tissue aging and impaired lung function with age.
Research highlights the intertwined pathways regulating apoptosis and cellular senescence in cancer and aging. The review suggests that harnessing benefits of both processes could lead to new combination therapies, while limiting drawbacks.
Researchers discovered how NORE1A prevents excessive cell proliferation associated with cancer. Overexpressing NORE1A induced cell senescence, whereas removing the protein enhanced cancer-promoting Ras mutations. This study highlights the critical role of NORE1A in regulating tumor growth.
Scientists have mapped the physical structure of the nuclear landscape to understand changes in genomic interactions during cell senescence and ageing. They reconciled two models of ageing, finding that SAHF domains show a dramatic loss of local interconnectivity and internal structure in senescent chromatin.
Manuel Serrano proposes a new vision of cellular senescence as a mechanism to eliminate unwanted cells and promote tissue regeneration. Recent research reveals that senescence is not intrinsically negative for the organism, but rather a protective mechanism against cell damage.
A new study found that adjuvant chemotherapy increases markers of molecular aging in the blood of BC survivors, including p16INK4a and ARF expression. These age-promoting effects may last for several years after treatment and even be permanent.
A team of investigators has identified a previously unknown mechanism regulating oncogene-induced senescence (OIS), a natural response to tumor development. Down-regulation of deoxyribonucleoside pools causes DNA damage, leading to cell cycle arrest and senescence. Restoration of depleted dNTP pools can suppress DNA damage and OIS.
Disabling the Skp2 gene after oncogenic stress induces cellular senescence in cancer cells, restricting tumor growth. Researchers believe this could lead to novel agents that suppress tumor development in common types of cancer.
Researchers enhanced a type of cellular senescence to suppress prostate tumor development and growth in mice. This novel approach uses Pten-loss-induced cellular senescence to prevent cancer progression.
A new study reveals that cellular senescence, a natural process for fighting cancer in younger persons, can actually promote cancer in older individuals by triggering the secretion of proteins that cause inflammation. This process is linked to almost every major disease associated with aging, including many cancers.
A new study identifies CUL7 E3 ubiquitin ligase as a key regulator of protein degradation linked to cellular senescence. The researchers found that the enzyme targets insulin receptor substrate 1 (IRS-1) for degradation, leading to oncogene-induced senescence.
Dr. Smith, editor of GSA's Journal of Gerontology: Biological Sciences, receives the Robert W. Kleemeier Award for his decades-long research on cellular senescence. His work focuses on chromatin structure alterations in this process.
Researchers found that MYC binds to the WRN gene promoter, activating WRN expression and promoting cellular senescence in tumor cells. This discovery suggests a potential therapeutic target for cancer treatment by inhibiting WRN in MYC-induced tumor cells.