TL;DR
It is confirmed that PPIB activates the PI3K-AKT signaling pathway by interacting with MET, thereby promoting the malignant progression of HNSCC.
HIST1H4L was significantly upregulated in SCLC tumors versus normal tissues and enriched in DNA transcription-related pathways and correlated with poor patient survival; critically, high HIST1H4L expression correlated with poor patient survival.
Findings identify a novel PSMA6/NEDD8/NF-κB regulatory axis that promotes NSCLC progression and suggest PSMA6 as a potential therapeutic target.
Findings reveal a potential RNF113A/SNIP1/TGF-β regulatory axis and highlight RNF113A as a potential therapeutic target in CRC, warranting further mechanistic validation.
PPIB promotes prostate cancer progression and is associated with broad transcriptional and alternative splicing alterations, with enriched pathways involving DNA repair, the cell cycle, and amino acid metabolism.
The molecular mechanism by which FAM117B promotes HCC progression via forming a bidirectional regulatory loop with NAT10 and activating the JAK-STAT3 signaling pathway through acetylation modification is revealed, providing a novel potential target and theoretical basis for targeted therapy of HCC.
This study investigates the role of mitochondrial ribosomal protein S17 in the progression of LUAD, with a specific focus on its interaction with the PI3K-AKT-mTOR signaling pathway and highlights the potential of MRPS17 as a prognostic marker and therapeutic target.
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