Results 251 to 260 of about 1,172,272 (355)
CBP/p300, a promising therapeutic target for prostate cancer. [PDF]
Xu H +7 more
europepmc +1 more source
The authors find that by targeting intratumoral copper, they can enhance p62‐mediated ubiquitination of EZH2 at the Ub‐K63 site by suppressing copper binding to SMURF2, an E3 ligase of EZH2, leading to its autophagic degradation. This mechanism suppressed OSCC progression and potentiated anti‐PD‐1 immunotherapy, highlighting a potential new therapeutic
Xiaohu Lin +9 more
wiley +1 more source
Nrf2 isn't just a protector—it's a driver of cancer stemness. The study uncovers how arsenic‐activated Nrf2 directly upregulates KLF4, a key pluripotency factor, fueling oncogenic reprogramming. Through enhancer activation and self‐reinforcing loop, Nrf2 and KLF4 co‐opt gene networks linked to epithelial‐to‐mesenchymal transition and tumor growth ...
Ziwei Wang +9 more
wiley +1 more source
Understanding prostate cancer care: recent progress and future direction. [PDF]
Stewart KT, Choudhury A.
europepmc +1 more source
Cadmium, a carcinogenic heavy metal, drives breast cancer progression via metabolic reprogramming and autophagic flux disruption. Multi‐omics revealed cadmium‐induced 5'‐methylthioadenosine depletion activates DOT1L‐mediated H3K79me1 at PAK2 promoter, upregulating PAK2 to block autophagy and driving malignancy. Clinically, 5'‐methylthioadenosine levels
Jingdian Li +24 more
wiley +1 more source
Anti-tumor activity of CDYL2b in prostate cancer. [PDF]
Gu R +4 more
europepmc +1 more source
Advanced Microfluidics for Single Cell‐Based Cancer Research
Cutting‐edge microfluidic platforms are transforming single‐cell cancer research. This review highlights advanced technologies, from droplet microfluidics to tumour‐chips, that enable functional and spatial single‐cell analyses. By integrating biosensing, immune components, and patient‐derived materials, these systems offer new insights into tumour ...
Adriana Carneiro +10 more
wiley +1 more source
During the progression of CRC, MDM2, as an E3 ubiquitin ligase, promotes the degradation of the LLGL2 protein. Reduced expression of the LLGL2 protein leads to the loss of support for the CNOT1 protein, decreasing the degradation of THBS3 mRNA. The increased THBS3 further activates the PI3K‐Akt pathway, promoting the proliferation and metastasis of CRC.
Jiayan Huang +8 more
wiley +1 more source

