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

Pathway enrichment implicated SFXN1 is involved in the PI3K-AKT-mTOR and p53 signaling pathways. These findings highlight the involvement of SFXN1 in cancer-related pathways and its potential role in OSCC, suggesting potential therapeutic targeting opportunities that need further investigation.

GO and KEGG analyses indicated that the main pathways included the hypoxia-inducible factor 1 (HIF-1) signaling pathway, phosphatidylinositol 3-kinase-protein kinase B (PI3K-AKT) signaling pathway, and advanced glycation end products-receptor for advanced glycation end products (AGE-RAGE) signaling pathway, involving processes such as signal transduction, receptor complex formation, and cytokine activity. The core acupoint prescription for PCOS might exert therapeutic effects through multiple targets and pathways, providing a theoretical basis for mechanistic research on acupoint prescriptions.

Additionally, suppressing AKT1 expression diminished the impact of INSR on promoting AML cells proliferation, invasion, and migration. This study indicates that INSR expression is elevated in AML cells after treating with chidamide and that INSR promotes AML cells proliferation and migration by upregulating AKT1 expression.

Overall, C. pentandra exhibits potent, multi-target anticancer activity against colorectal cancer by modulating key oncogenic pathways. These findings integrate in silico predictions with in vitro validation, highlighting C. pentandra as a promising natural therapeutic candidate warranting further mechanistic and preclinical investigations.

β-PGG exhibits potent anti-HCC activity by modulating PCID2 expression, PI3K/Akt signaling, and cell cycle regulation, and it represents a promising lead compound with PCID2-targeting potential. This study not only support a rationale for further exploration of PCID2 as a therapeutic target in HCC but also provide valuable insights into the discovery of novel lead compounds from TCM for liver cancer treatment.

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.