Articles tagged with Cell Cycle Arrest
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Polyploidy, a state with extra genetic material, allows cancer cells to survive longer under DNA damage. This phenomenon explains why some cancers are resistant to anti-cancer drug treatments.
Researchers at Colorado State University have identified an alternate method to study changes during the DNA replication process in lab settings using genetically modified yeast. This new approach provides a less toxic and quickly reversible alternative to hydroxyurea, allowing for better insight into cell cycle arrest mechanisms.
Researchers at Osaka Metropolitan University found compounds in nucleic acids from salmon DNA and torula yeast RNA inhibit cancer cell growth. These compounds may prevent cancer by stopping cell replication.
A recent study published in Nature Aging suggests that mechanical damage to the cell membrane can induce cellular senescence, a state characterized by cell cycle arrest and tissue dysfunction. This mechanism involves calcium ion influx and the tumor suppressor gene p53, offering new insights into the aging process.
A study published in Nature Cardiovascular Research reveals that a dynamic synergy between cell types facilitates cardiac renewal, challenging existing paradigms. Targeting the microenvironment rather than specific cell types is key to healing injured hearts.
Researchers found that p21 knockout mice experienced reduced senescent cell presence, alleviated chronic lung inflammation, and improved fitness. Resident epithelial and endothelial cells played a significant role in mediating the p21-dependent inflammatory response.
Researchers found that senescence-associated exosomes (SA-EXOs) from MSCs induce fibrosis and activate invasive characteristics in neighboring cells via the TGF-β pathway. SA-EXOs play a large role in cancer-related fibrosis, and their unique miRNA content influences myofibroblast phenotypes.
Researchers explore cellular senescence's complex relationship with growth stimulation and cell cycle arrest, revealing potential anti-aging drug targets. Understanding these mechanisms is crucial for developing new treatments for age-related diseases.
A study from Tokyo Medical and Dental University reveals that the TGF-β signaling molecule can induce EMT in oral cancer cells, leading to high motility and metastatic potential. KRTAP2-3 expression is associated with poorer overall survival, suggesting its role as a prognostic biomarker.
Researchers found that mTOR inhibition is crucial for p53-mediated tumor suppression, delaying cancer and increasing lifespan. In the absence of mTOR inhibition, cancer-promoting senescent cells drive tumor growth.
The TTUHSC's C. Patrick Reynolds has received a $1.34 million CPRIT grant to investigate updating the clinical risk stratification scale for neuroblastoma and rhabdomyosarcoma, two childhood cancers in need of improved therapies.
Researchers at TTUHSC will investigate common mechanisms of resistance and sensitivity in alternate telomere lengthening (ALT) cancers, with a focus on targeting ATM kinase inhibitors for therapy. The team aims to develop clinical trials for patients with ALT+ cancers.
Researchers discovered that a transcription factor called MUTE induces a cell cycle inhibitor SMR4 to slow down the cell cycle, allowing for asymmetric division. A variant with excess SMR4 showed a longer cell cycle during symmetric division, revealing a crucial regulatory mechanism in plant stomatal development.
Researchers found that Fgr binds to Numb, activating the signalosome and promoting cell differentiation and G1/0 arrest. The study provides insights into RA resistance and suggests potential therapeutic targets.
Researchers found that roscovitine enhances nuclear enrichment of certain signaling molecules and promotes differentiation in leukemia cells treated with all-trans retinoic acid (ATRA). This novel mechanism reveals new therapeutic vulnerabilities and basic molecular features of ATRA-induced differentiation.
Researchers found that geranylgeraniol suppressed human DU145 prostate carcinoma cell viability via cell cycle arrest at the G1 phase and apoptosis initiation. The compound also down-regulated HMG CoA reductase, a key enzyme in the mevalonate pathway.
Researchers found Chrysanthemum indicum extract inhibits cancer cell proliferation and induces apoptosis in hepatocellular carcinoma cells. The extract also arrests the cell cycle by regulating key proteins, suggesting its potential as a novel cancer treatment.
Researchers identified a unique stretch of internal telomeric repeats that suppress the DNA damage checkpoint response. The arrest duration was significantly shorter than expected, indicating a potential mechanism for preventing normal telomeres from being recognized as damaged DNA.