AKT1 (V-akt murine thymoma viral oncogene homolog 1)

Using the autophagy suppressor, 3-methyladenine (3MA, 2mM), chloroquine (CQ, 10μM), and knockdown of autophagy-related protein 4 homolog B (ATG4B) gene by siRNA, it was shown that Cr (VI)-provoked mTOR was reliant on autophagy...HMGA2 mediated this effect by transcription regulation of ATG4B. These suggested that blocking the HMGA2-autophagy-mTOR axis could serve as an effective strategy to inhibit Cr (VI)-induced cell viability.

In a xenograft model, Procyanidin B2 administration significantly suppressed tumor growth without evident toxicity, consistent with the in vitro signaling alterations. These results suggest that Procyanidin B2 exerts anti-ovarian cancer effects partly through modulating the EGFR/AKT signaling axis, supporting its potential as a complementary therapeutic candidate.

Therefore, Viscosalactone B and Withasomniferol C are promising natural candidates for further validation as potential MAPK14 inhibitors. In comparison with synthetic drugs like ralimetinib, these plant-derived compounds may offer complementary therapeutic potential with fewer adverse or off-target effects and favorable pharmacokinetic and pharmacophoric profiles.

Genipin targets TNK2 to inhibit the progression of ESCC. It provides new insights into the pathogenesis of ESCC and theoretical basis for positioning TNK2 gene as a potential therapeutic target.

The computational results reveal that kinases like AKT1, ROR1, and ROR2, and non-kinase targets like UBC, RPS6, CDH1, AR, and SMAD3, are the most promising candidates. All screened compounds showed varying strong interacting profiles, with Ellagic Acid and Erioflorin standing out as potent candidates against critical targets in metastatic breast cancer.

Further mechanism studies showed that LRRC1 enhances PDK1 stability by promoting its deubiquitination via USP7, thereby increasing AKT1 phosphorylation levels and activating the AKT/GSK3β/β-catenin/VEGFA signaling pathway, ultimately accelerating tumor angiogenesis in HCC. These findings demonstrated a novel role of LRRC1 in tumor angiogenesis, opening up new avenues for future research and treatment development.

All 7/7 sequenced tumors harbored the AKT1 c.49G>A variant with no additional oncogenic alterations identified by exome sequencing. This series is the largest series to date documenting the clinicopathologic features of paratesticular tumors, a poorly understood component of the Proteus syndrome phenotype.

This integrative molecular and phenotypic profiling of blood-derived components identified potentially distinct molecular signatures, such as overexpression of IL12, ANGPT1 downregulation and HIF1A downregulation, in the literature described as linked to the patient's beneficial prognosis. These findings suggest that advanced liquid biopsy techniques may provide complementary insights into prognostic biomarkers and therapeutic targets in HGSOC.

SGML-4 exerts anti-insomnia effects through multi-target and multi-pathway mechanisms. Apigenin, luteolin, and piplartine are the core active components, and EGFR is identified as the central target, potentially acting through serotonergic synapses and calcium signaling pathways.

Altogether, Q-Tw-Cs@Se NPs show potential as neuroprotective adjuvants to reduce cisplatin-induced neurotoxicity. However, further in vitro and in vivo studies are required to confirm their therapeutic value.

Serum analysis revealed that superoxide dismutase (SOD) activity in group C was significantly elevated versus CON, Network pharmacology identified 150 potential antioxidant targets of EHE, primarily enriched in pathways associated with cancer, hepatic injury, apoptosis, and viral infection, suggesting immune-modulatory effects. Based on these findings, it can be inferred that supplementing milk replacer with EHE enhances calf growth performance, regulating oxidative stress, and it regulates signaling pathways related to immune response and apoptosis through interactions with key targets such as IL6, TP53, MAPK1, AKT1, TNF, BCL2, and ESR1.

And AMT overexpression reduces the expression of PI3K and AKT1 by increasing the level of H3K27me3. This work reveals that the negative role of AMT in regulating NSCLC progression, which emerges potential therapeutic implications.