TL;DR
Findings prove that SYVN1 could promote the malignant characteristics of A549 cells by modulating the GATA3/NRP1 axis and that targeting SYVN1 could represent a promising therapeutic approach for treating lung cancer.
It is demonstrated that EZH2 promotes NSCLC progression through activation of the JAK2/STAT3 signaling pathway, identifying the EZH2-JAK2/STAT3 axis as a potential therapeutic vulnerability in this malignancy.
These findings establish RNF126 as a critical contributor to cisplatin resistance in ovarian cancer via regulation of the Numb/Notch1 pathway and highlight its potential as a therapeutic target to counteract chemoresistance.
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.
A potential mechanism by which HOXC9 contributes to ESCC progression via AKT/mTOR-mediated inhibition of mitochondria-dependent apoptosis and promotion of cell proliferation is identified.
It is identified that MAGI3, as a suppressor in NSCLC progression, repressed the Wnt pathway‑including TAZ degradation, impaired β‑catenin nuclear translocation, and diminished TCF/LEF transcription‑thereby restraining tumorigenesis and metastasis of NSCLC.
KIAA1429 knockdown may suppress OS progression by inhibiting m6A-dependent SLC7A11 expression, thereby promoting ferroptosis and targeting the KIAA1429/SLC7A11 axis may represent a promising therapeutic strategy for OS.
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