Results 181 to 190 of about 511,111 (317)

Adenosine A3 receptor antagonists as anti‐tumor treatment in human prostate cancer: an in vitro study

open access: yesFEBS Open Bio, EarlyView.
The A3 adenosine receptors (A3ARs) are overexpressed in prostate cancer. AR 292 and AR 357, as A3AR antagonists, are capable of blocking proliferation, modulating the expression of drug transporter genes involved in chemoresistance, ferroptosis, and the hypoxia response, and inducing cell death.
Maria Beatrice Morelli   +15 more
wiley   +1 more source

Possible role of human ribonuclease dicer in the regulation of R loops

open access: yesFEBS Open Bio, EarlyView.
R loops play an important role in regulating key cellular processes such as replication, transcription, centromere stabilization, or control of telomere length. However, the unscheduled accumulation of R loops can cause many diseases, including cancer, and neurodegenerative or inflammatory disorders. Interestingly, accumulating data indicate a possible
Klaudia Wojcik   +2 more
wiley   +1 more source

Soman induces endoplasmic reticulum stress and apoptosis of cerebral organoids via the GRP78‐ATF6‐CHOP signaling pathway

open access: yesFEBS Open Bio, EarlyView.
Cerebral organoids were employed as a novel model to explore the neurotoxicity of soman. Soman inhibited acetylcholinesterase activity, increased cell apoptosis and upregulated endoplasmic reticulum (ER) stress markers glucose‐regulated protein 78 (GRP78), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP).
Yue Wei   +7 more
wiley   +1 more source

Downregulation of O‐GlcNAcylation enhances etoposide‐induced p53‐mediated apoptosis in HepG2 human liver cancer cells

open access: yesFEBS Open Bio, EarlyView.
Etoposide, a topoisomerase II inhibitor, reduces O‐GlcNAcylation in HepG2 liver cancer cells. Further inhibition of O‐GlcNAc transferase by OSMI‐1 enhanced etoposide‐induced apoptosis, lowering the IC50 for viability and increasing the EC50 for cytotoxicity.
Jaehoon Lee   +5 more
wiley   +1 more source

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