Modulation of STAT3 signaling, cell redox defenses and cell cycle checkpoints by β-caryophyllene in cholangiocarcinoma cells: possible mechanisms accounting for doxorubicin chemosensitization and chemoprevention [PDF]
Cholangiocarcinoma (CCA) is an aggressive group of biliary tract cancers, characterized by late diagnosis, low effective chemotherapies, multidrug resistance, and poor outcomes.
Di Giacomo, Silvia +8 more
core +1 more source
Engineering Oncolytic Virus‐Armed Macrophages for Enhanced Cancer Immunotherapy
ZIFOA‐M is engineered by conjugating oncolytic adenovirus‐loaded ZIF‐8 nanoparticles onto macrophage surfaces via bioorthogonal chemistry. Upon tumor infiltration, the platform releases OA to downregulate CD47/CD24 on tumor cells, restoring macrophage phagocytosis.
Jilong Wang +10 more
wiley +1 more source
Cell cycle checkpoints, activated by stressful events, halt the cell cycle progression, and prevent the transmission of damaged DNA. These checkpoints prompt cell repair but also trigger cell death if damage persists.
Verónica Rivas +6 more
doaj +1 more source
MutY-Homolog (MYH) inhibition reduces pancreatic cancer cell growth and increases chemosensitivity [PDF]
Patients with pancreatic ductal adenocarcinoma (PC) have a poor prognosis due to metastases and chemoresistance. PC is characterized by extensive fibrosis, which creates a hypoxic microenvironment, and leads to increased chemoresistance and intracellular
Biankin, Andrew +8 more
core +1 more source
SDPR–STK38 axis controls the proliferation–differentiation balance in alveolar type II cells
The present study identifies SDPR as a pivotal regulator orchestrating the balance between proliferation and differentiation in alveolar type II (AT2) cells. In SDPR+/+ cells, SDPR binds to and inhibits STK38 activity, thereby sustaining GSK‐3β signaling functionality to promote cyclin D1 degradation and maintain cell cycle homeostasis.
Jie Wang +6 more
wiley +1 more source
Mitotic death: a mechanism of survival? A review
Mitotic death is a delayed response of p53 mutant tumours that are resistant to genotoxic damage. Questions surround why this response is so delayed and how its mechanisms serve a survival function.
Cragg M S, Erenpreisa Jekaterina
doaj +1 more source
Axitinib induces DNA damage response leading to senescence, mitotic catastrophe, and increased NK cell recognition in human renal carcinoma cells. [PDF]
Tyrosine kinase inhibitors (TKIs) including axitinib have been introduced in the treatment of renal cell carcinoma (RCC) because of their anti-angiogenic properties.
Amantini, C +6 more
core +1 more source
Redox responsive mesoporous silica nanoparticles (MSNs) were engineered to deliver gemcitabine (Gem) and cisplatin (cisPt) at defined ratios to overcome chemoresistance in pancreatic ductal adenocarcinoma (PDAC). Optimized Gem MSNs and Gem cisPt MSNs enhanced cytotoxicity in murine and human Gem resistant models, with select formulations inducing ...
Tamanna Binte Huq +5 more
wiley +1 more source
Nuclear translocation of Cyclin B1 marks the restriction point for terminal cell cycle exit in G2 phase [PDF]
Upon DNA damage, cell cycle progression is temporally blocked to avoid propagation of mutations. While transformed cells largely maintain the competence to recover from a cell cycle arrest, untransformed cells past the G1/S transition lose mitotic ...
Cascales, H.S. +4 more
core +4 more sources
Abstract Hepatocellular carcinoma (HCC), ranking as the third leading cause of cancer‐related mortality globally, continues to pose significant therapeutic challenges. Here, we developed an innovative nanosystem, Phl@PT, based on Pt‐TiO2 nanoparticles for the co‐delivery of Phlorezin, presenting a novel approach for HCC treatment through sonodynamic ...
Kairui Liu +13 more
wiley +1 more source

