Results 101 to 110 of about 281,298 (260)
ABSTRACT Memory T cells exhibit long‐term persistence, a defining feature that underpins durable clinical responses to adoptive immunotherapies. The mechanisms that integrate metabolic cues with transcriptional control of memory fate remain undetermined. Here, we identify HS1‐binding protein 3 (HS1BP3) is preferentially expressed in memory CD8+ T cells.
Siyang Wang +13 more
wiley +1 more source
As engineered nanomaterials gain prominence in cancer imaging and therapy, understanding their impact on tumor progression becomes increasingly critical. We demonstrate that gold and silica‐coated gold nanomaterials can either suppress or enhance breast cancer metastasis through distinct tumor microenvironment interactions, while identifying ...
Kiana Buttiens +11 more
wiley +1 more source
Steven Ridwan, Ali Budi Harsono, Dodi Suardi, Andi Kurniadi, Kemala Isnainiasih Mantilidewi, Yudi Mulyana Hidayat Department of Obstetrics and Gynecology, Faculty of Medicine, Universitas Padjadjaran–Dr.
Ridwan S +5 more
doaj
Design and Application of Nanozymes: Current Trends and Cutting‐Edge Breakthroughs
Advanced Science, EarlyView.
Kelong Fan, Hui Wei, Xiyun Yan
wiley +1 more source
Chemotherapy leverages tumor‐cell autophagy to reshape the colorectal cancer immune microenvironment. Autophagy degrades FBXW2 to promote C/EBPβ‐mediated TIMP‐2 transcription and MMP‐9 suppression, driving intra‐tumoral CD8+ T‐cell infiltration. Targeting MMP‐2/9 or restoring TIMP‐2 overcomes chemo‐resistance in autophagy‐deficient tumors. ABSTRACT The
Bing Cheng +12 more
wiley +1 more source
Corynoxine exerts potent broad‐spectrum anticancer activity by directly targeting NQO1. This interaction dissociates the oncogenic NQO1‐PTPA complex, releasing PTPA to robustly activate the tumor suppressor PP2A. Consequently, downstream Raf/MEK/ERK and PI3K/AKT signaling pathways are suppressed, downregulating c‐Myc and driving tumor regression ...
Guoqing Hou +6 more
wiley +1 more source
This review elucidates how cancer cell metabolic reprogramming—across glucose, lipid, amino acid, and nucleotide pathways—remodels the tumor microenvironment to suppress anti‐tumor immunity and promote immune escape. Targeting these metabolic axes offers promising strategies to overcome immunotherapy resistance and enhance cancer treatment.
Guoqing Xiang +5 more
wiley +1 more source
BNC2 exhibits context‐dependent opposing functions across multiple cancer types. This study reveals BNC2 as an oncogenic driver of melanoma proliferation and metastasis through transcriptional activation of PIK3CA. The natural compound TSN simultaneously degrades BNC2 and its oncogenic partner SMAD3 via CRBN‐dependent ubiquitination.
Hui Dai +7 more
wiley +1 more source
CAF‐derived exosomes deliver circFAD104 into TNBC cells, where it acts as a molecular scaffold that bridges the E3 ligase MARCHF8 and PGM1, promoting MARCHF8‐mediated K48‐linked ubiquitination and proteasomal degradation of PGM1. Loss of PGM1 redirects glucose‐phosphate flux from glycogen synthesis toward glycolysis, thereby driving stemness, EMT, and ...
Lei Wang +16 more
wiley +1 more source
AMT‐676 is a novel antibody‐drug conjugate targeting CDH17, an adhesion molecule uniquely exposed on gastrointestinal tumor surfaces. Engineered with an optimized exatecan payload, it demonstrates profound tumor regression and a robust bystander effect across diverse preclinical models.
Ying‐nan Wang +21 more
wiley +1 more source

