YWHAG promotes the progression of lung adenocarcinoma through the JAK2/STAT3 pathway

Your study sheds light on the pivotal role of YWHAG (14-3-3-γ) in the pathogenesis of lung adenocarcinoma (LUAD) and its potential as both a prognostic biomarker and therapeutic target. The upregulation of YWHAG mRNA in LUAD, along with its higher protein expression levels in poorly differentiated tumors and those with lymph node metastasis, underscores its association with aggressive tumor behavior and poor prognosis. Its identification as an independent prognostic factor strengthens its clinical relevance.

The functional assays revealing that YWHAG silencing inhibits proliferation and migration, while promoting apoptosis in lung cancer cells, provide key insights into its oncogenic properties. Gene Set Enrichment Analysis (GSEA) further illustrates YWHAG’s involvement in critical pathways, including mTOR signaling, unfolded protein response, MYC targets, and notably, JAK/STAT3 signaling. The reduction in p-JAK2 and p-STAT3 expression upon YWHAG knockdown, as shown by Western blot analysis, links YWHAG directly to the JAK2/STAT3 axis, a pathway pivotal in cancer progression.

These findings emphasize the potential of targeting YWHAG to disrupt oncogenic signaling Abraxane, particularly via the JAK2/STAT3 pathway, offering a novel therapeutic strategy for LUAD. Additionally, its ability to predict responses to chemotherapeutic agents like cisplatin, paclitaxel, docetaxel, and erlotinib further enhances its utility as a biomarker in personalized medicine. This comprehensive investigation provides a strong foundation for exploring YWHAG as a key player in LUAD management, opening avenues for future research into targeted therapies.