Results 121 to 130 of about 66,124 (248)

OCIAD2 Stabilizes Integrin β1 Signaling Through SNX17‐Mediated Endosomal Recycling to Lipid Rafts and Modulates Cisplatin Response in HNSCC

open access: yesAdvanced Science, EarlyView.
This study identifies OCIAD2 as a critical regulator of cisplatin resistance in HNSCC. Mechanistically, OCIAD2 stabilizes integrin β1 through a direct physical interaction and facilitates its SNX17‐dependent endosomal recycling to lipid raft microdomains. Targeting OCIAD2 disrupts integrin β1 trafficking and significantly enhances cisplatin sensitivity,
Li Cui   +9 more
wiley   +1 more source

Decoding Triphenotypic Neutrophils in Cervical Cancer Evolution and Targeting SPP1+/GBP1+/ELOVL5+ Tumor‐Associated Neutrophils to Sensitize Immunotherapy

open access: yesAdvanced Science, EarlyView.
The functional schematic diagram of tumor associated neutrophils. Abstract Enhancing cervical cancer (CC) immunotherapy requires deciphering the heterogeneous tumor immune microenvironment (TIME), particularly neutrophil phenotypic dynamics. Here, 1) we collected 543 CC cases to find that patients with elevated neutrophil levels have a higher incidence
Xingyu Chang   +7 more
wiley   +1 more source

KLK3 in the Regulation of Angiogenesis—Tumorigenic or Not? [PDF]

open access: gold, 2021
Hannu Koistinen   +2 more
openalex   +1 more source

An Insulin‐Exosome‐TNFAIP8 Axis Drives Stromal Fibrosis and Therapeutic Resistance in Pancreatic Cancer

open access: yesAdvanced Science, EarlyView.
In pancreatic ductal adenocarcinoma (PDAC), insulin is associated with activation of PI3K/AKT–RAB3A signaling and enhanced secretion of TNFAIP8‐enriched exosomes from tumor cells. Uptake of these exosomes by fibroblasts is linked to TRIM21‐dependent STAT1 degradation and the emergence of myofibroblastic CAF–associated features, accompanied by increased
Zhenyu Li   +15 more
wiley   +1 more source

Activating Transcription Factor 5 Promotes Tumorigenic Capability in Cervical Cancer Through the Wnt/β-Catenin Signaling Pathway

open access: yesCancer Management and Research
Fengjuan Shi,1,2 Yumei Wei,2 Yingmei Huang,2 Desheng Yao1 1Department of Gynecologic Oncology, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, People’s Republic of China; 2Department of Gynecology, the Fifth Affiliated Hospital of Guangxi ...
Shi F, Wei Y, Huang Y, Yao D
doaj  

HSP90AB1‐Mediated Ubiquitin‐Proteasome Degradation of ITGBL1 Promotes Osteosarcoma Progression by Inhibiting Endoplasmic Reticulum Stress‐Induced Autophagy

open access: yesAdvanced Science, EarlyView.
This study delineates a novel HSP90AB1‐ITGBL1 signaling axis governing osteosarcoma. HSP90AB1 promotes K63‐linked ubiquitination and proteasomal degradation of ITGBL1. Restoring ITGBL1 induces reactive oxygen species‐dependent endoplasmic reticulum stress and pro‐death autophagy, suppressing tumor growth and metastasis.
Zhen Wang   +17 more
wiley   +1 more source

Disulfide‐Bridged Ru Complex–Mediated Photo‐Disulfidptosis for Colorectal Cancer Therapy

open access: yesAdvanced Science, EarlyView.
In this work, a binuclear ruthenium complex, RuSSRu was developed for efficient colorectal cancer (CRC) treatment. The synergistic interaction between disulfidptosis and lysosomal damage‐induced apoptosis induced by RuSSRu amplified tumor cell death. This innovative approach offers a potent therapeutic strategy for CRC.
Simeng He   +8 more
wiley   +1 more source

GNL3 Orchestrates AR Transcriptional Programs to Drive Castration‐Resistant Prostate Cancer and Immune Evasion

open access: yesAdvanced Science, EarlyView.
GNL3 is a novel AR coregulator with dual coactivator and corepressor functions in prostate cancer (PCa). Our study uncovers a previously unrecognized mechanism by which the AR transcriptional complex integrates oncogenic signaling and immune suppression.
Cuiting Zhang   +12 more
wiley   +1 more source

OCTN2 Activates a Non‐Canonical Carnitine Metabolic Pathway to Promote MASH‐HCC Progression and Immunotherapy Resistance

open access: yesAdvanced Science, EarlyView.
In non‐MASH‐HCC, L‐carnitine promotes tumor progression primarily through its classical role in enhancing fatty acid oxidation (FAO). However, in MASH‐HCC, where FAO is markedly suppressed, L‐carnitine shifts from this canonical function to serve instead as an intracellular acetyl group buffer.
Chuqi Xia   +11 more
wiley   +1 more source

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