SESN2 (Sestrin 2)

Our findings demonstrate cell line - specific redox responses and identify SESN2, SESN3, and SOD1 as key players in the antioxidant defense network. These genes may serve as potential therapeutic targets in aggressive, hormone-independent endometrial cancers.

Mechanistically, we found that Sesn2 depletion downregulated the PI3K/AKT/mTOR pathway and reduced the phosphorylation of AKT and p38 MAPK. Our findings demonstrate that Sesn2 functions as an oncogene in OSCC, promoting tumor progression by modulating the PI3K/AKT/mTOR and MAPK signaling pathways, suggesting its potential as a therapeutic target for OSCC.

BC emerges as a promising therapeutic agent for TNBC by targeting SESN2 and MAP1LC3B, modulating associated signaling pathways, and inducing ferroptosis and mitophagy. These findings provide the basis for further investigation of BC's potential as a targeted therapy for TNBC.

Plantainoside D was identified as a novel KCMF1 inhibitor that exhibited potent antitumor activity in OC. Overall, KCMF1 regulates HRI ubiquitination to inhibit ISR, thereby promoting tumor growth and progression in OC.

Chemotherapy resistance in GBM, particularly to temozolomide, is driven by factors such as O6-methylguanine-DNA methyltransferase upregulation, defective mismatch repair, hypoxia-induced gene expression and activation of several signaling pathways, such as the NF-κB, Hippo and Wnt pathways...Robust patient stratification and biomarker-driven interventions are critical for tailoring therapies and improving outcomes. The present review highlights the urgent need for innovative, multidisciplinary approaches to address the complexity of GBM resistance and advance therapeutic strategies for this lethal disease.

Importantly, the lysine at residue 74 of vCyclin is crucial for its cytosolic localization, OTUB1 recruitment, and subsequent SESN2 upregulation and AMPK activation. These findings unveil a regulatory mechanism for SESN2 involving vCyclin and OTUB1, positioning them as potential therapeutic targets for diseases associated with AMPK dysregulation.

Our findings demonstrate that hypoxia promotes SS metastasis through activation of HIF-1α and related pathways. Fusion-positive SS cells appear particularly responsive to hypoxic cues, suggesting that targeting hypoxia-induced signaling could be a promising strategy to inhibit metastasis in SS. These results provide mechanistic insight into SS progression and support the integration of hypoxia-targeted therapies into future treatment strategies.

Additionally, we found that HIF1α directly regulates expression of CCN3 by binding to the promoter region of CCN3. This CCN3-HIF1α positive feedback loop may play an important role in HIF1α-induced tumorigenesis in TNBC and be involved in the metastasis of TNBC cells.

These biomarkers may enhance early diagnosis, enable personalized therapy, and improve kidney disease outcomes. Their integration into clinical practice may bridge the gap between early detection and effective intervention, potentially improving long-term outcomes in patients with kidney disease.

Our thorough bioinformatics analysis reveals significant molecular events in RILI, identifying 5 key genes and their related signaling pathways. These insights deepen our understanding of the mechanisms underlying the development and progression of RILI and suggest a practical and effective approach for treatment and early diagnosis.

P=N/A, N=300, Active, not recruiting, University of Oregon | Recruiting --> Active, not recruiting

Our study reveals SND1 overexpression in PCa, which is transcriptionally activated by SREBF1. Mechanistically, SND1 interacts with MTDH and promotes SESN2 mRNA degradation, modulating PCa progression through the AMPK/mTOR pathway.