Results 201 to 210 of about 287,154 (333)

Oncogenic and immunological roles of NSUN2 in triple negative breast cancer. [PDF]

open access: yesSci Rep
An N   +8 more
europepmc   +1 more source

Enhanced Killing of Triple-Negative Breast Cancer Cells by Reassortant Reovirus and Topoisomerase Inhibitors [PDF]

open access: gold, 2019
Roxana M. Rodríguez Stewart   +8 more
openalex   +1 more source

Development of CAPER peptides for the treatment of triple negative breast cancer [PDF]

open access: bronze, 2020
Shannon Chilewski   +7 more
openalex   +1 more source

GLUL Confers Perivascular Cancer‐Associated Fibroblasts With Pro‐Angiogenic Capacity to Promote Glioma Progression

open access: yesAdvanced Science, EarlyView.
Schematic illustration of the proposed model. Primary CAFs are isolated from fresh human GBM specimens according to established protocols. GLUL is essential for pro‐angiogenic capacity of CAFs through its impact on the PI3K/AKT pathway. GLUL enhances the pro‐angiogenic capacity of CAFs, driving aberrant tumor vasculature that fuels tumor growth ...
Qing Zhang   +4 more
wiley   +1 more source

WDR5‐H3K4me3 Epigenetic Axis Promotes TRMT6‐Dependent tRNA M1A Modification to Facilitate Triple‐Negative Breast Cancer Progression by Suppressing Ferroptosis

open access: yesAdvanced Science, EarlyView.
Upregulated TRMT6 forms aberrant hypermethylation of a specific tRNA pool and serves as a predictor of poor prognosis in TNBC. This m1A modification in tRNAs enhances translation of FTH1 and FTL, reducing the pool of bioavailable Fe2⁺. Reduced Fe2+ availability impairs RSL3‐induced lipid peroxidation and tumor progression.
Yuqing Lei   +12 more
wiley   +1 more source

Surface‐Associated Proteins on Extracellular Vesicles Remodel the Tumor Microenvironment by Potentiating TGF‐β Signaling in a Contact‐Dependent Manner

open access: yesAdvanced Science, EarlyView.
Extracellular vesicles (EVs) released from TGF‐β‐activated CAFs are enriched with ECM proteins such as TSG6 and THBS1, which facilitate their binding to recipient cell membranes. This EV–cell interaction promotes the clustering of CD44 and TGF‐β receptors on the target cell surface, thereby potentiating TGF‐β signaling activity. This study highlights a
Chao Li   +7 more
wiley   +1 more source

Dual Targeting of Mutant p53 and SNRPD2 via Engineered Exosomes Modulates Alternative Splicing to Suppress Ovarian Cancer

open access: yesAdvanced Science, EarlyView.
Mutant p53 drives oncogenic splicing to promote the progression of ovarian cancer by partnering with the spliceosome factor SNRPD2. Therefore, it is engineered iRGD‐exosomes to co‐deliver siRNAs against both targets. This approach restored tumor‐suppressive mRNA isoforms, effectively enhanced sensitivity to cisplatin, and ultimately blocked tumor ...
Wei Zhao   +14 more
wiley   +1 more source

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