Results 101 to 110 of about 2,092,635 (263)

Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer

open access: yesMolecular Oncology, EarlyView.
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni   +11 more
wiley   +1 more source

E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov   +3 more
wiley   +1 more source

KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer

open access: yesMolecular Oncology, EarlyView.
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan   +16 more
wiley   +1 more source

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

open access: yesMolecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu   +10 more
wiley   +1 more source

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

open access: yesMolecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Overview of molecular signatures of senescence and associated resources: pros and cons

open access: yesFEBS Open Bio, EarlyView.
Cells can enter a stress response state termed cellular senescence that is involved in various diseases and aging. Detecting these cells is challenging due to the lack of universal biomarkers. This review presents the current state of senescence identification, from biomarkers to molecular signatures, compares tools and approaches, and highlights ...
Orestis A. Ntintas   +6 more
wiley   +1 more source

Down‐regulation of Shh in the hair follicles of mice during chemotherapy‐induced hair loss is mediated by the JAK/STAT1 signaling pathway

open access: yesFEBS Open Bio, EarlyView.
We found that during chemotherapy‐induced alopecia (CIA), Sonic hedgehog (Shh) expression significantly decreased in hair follicle Shh+ cells, whereas the Janus‐activated kinase/signal transducer and activator of transcription 1 (JAK/STAT1) signaling pathway was markedly activated.
Ruifang Fan   +6 more
wiley   +1 more source

SIRT4 positively regulates autophagy via ULK1, but independently of HDAC6 and OPA1

open access: yesFEBS Open Bio, EarlyView.
Cells expressing SIRT4 (H161Y), a catalytically inactive mutant of the sirtuin SIRT4, fail to upregulate LC3B‐II and exhibit a reduced autophagic flux under stress conditions. Interestingly, SIRT4(H161Y) promotes phosphorylation of ULK1 at S638 and S758 that are associated with inhibition of autophagy initiation.
Isabell Lehmkuhl   +13 more
wiley   +1 more source

Metformin promotes mitochondrial integrity through AMPK‐signaling in Leber's hereditary optic neuropathy

open access: yesFEBS Open Bio, EarlyView.
Metformin mediates mitochondrial quality control in Leber's hereditary optic neuropathy (LHON) fibroblasts carrying mtDNA mutations. At therapeutic levels, metformin activates AMPK signaling to restore mitochondrial dynamics by promoting fusion and restraining fission, while preserving mitochondrial mass, enhancing autophagy/mitophagy and biogenesis ...
Chatnapa Panusatid   +3 more
wiley   +1 more source

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