Results 151 to 160 of about 18,641,062 (303)
Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu +13 more
wiley +1 more source
Drug resistance limits treatment success in a subset of lung cancers driven by ROS1 gene alterations. Using patient‐derived cells and computer simulations, we studied three key mutations and how they affect five targeted drugs. The mutations reduced drug effectiveness in different ways by altering protein structure and behavior.
Farhan Ul Haq +8 more
wiley +1 more source
Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer
Estrogen therapy elicits clinical benefit in ~ 30% of patients with endocrine‐resistant estrogen receptor (ER)‐positive breast cancer. Based on findings that ER transcriptional activation underlies response to estrogen therapy, we tested the effects of epigenetic dysregulation via pharmacological inhibition of histone deacetylases (HDACi).
Anneka L. Johnson Thomas +16 more
wiley +1 more source
PANoptosis in the pathogenesis of myelodysplastic syndromes
PANoptosis, a combination of three types of programmed cell death, is mediated by a large protein complex called a PANoptosome. In healthy bone marrow hematopoietic cells, PANoptosis is restricted by inhibitory signaling. In MDS, bone marrow cells become sensitive to the PANoptotic stimuli due to the aberrant inactivation of inhibitory signaling or ...
Rohit Thalla +4 more
wiley +1 more source
This study integrates publicly available transcriptomic datasets to identify molecular signatures associated with response to neoadjuvant chemoradiotherapy in locally advanced rectal cancer. By analyzing a combination of multiple cohorts with bioinformatics approaches, we reveal biological pathways and immune‐related features that may improve ...
Aleksandra Stanojevic +10 more
wiley +1 more source
The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad +2 more
wiley +1 more source
Loss of eIF5A rewires thapsigargin‐mediated endoplasmic reticulum stress responses in multiple myeloma cells by selective translation of mRNA transcripts, consequently dampening thapsigargin‐induced unfolded protein response (UPR) activation and shifting the balance from induction of apoptosis toward cell survival and proliferation.
Demi Both +7 more
wiley +1 more source
Homeostatic Regulation of Lung Dendritic Cells at Steady State. [PDF]
Park SH, Bae YS.
europepmc +1 more source
Loss of NAPRT promotes lung tumor initiation and growth through a noncanonical mechanism, independent of its role in NAD+ biosynthesis. Mechanistically, NAPRT depletion activates the mTORC2‐driven AKT/β‐catenin signaling axis to enhance clonogenic and invasive phenotypes. Furthermore, lung‐specific Naprt deletion significantly increases tumor burden in
Myung Joon Oh +11 more
wiley +1 more source
Clinical and Haematologic Correlates of Soluble VCAM-1 in Adults With Steady-State Sickle Cell Disease. [PDF]
Ghunney WK +7 more
europepmc +1 more source

