GAS1 (Growth Arrest Specific 1)

The Gli-targeting agent GANT61 may inhibit ALK + ALCL cell growth, trigger cell cycle arrest and induce apoptosis through Gli1 inhibition, potentially leading to PIK3IP1 upregulation and subsequent attenuation of PI3K/Akt pathway activity. These findings indicate that the Hh-PIK3IP1-Akt signaling axis may participate in ALK + ALCL tumorigenesis, showing that conventional target drugs can be employed for ALK + ALCL treatment.

Mechanistically, A3C enhances the expression of the STING1 and its downstream related molecules Caspase-1, IL-18, and IL-1β; upregulates DNA damage-protective genes (GSTP1 and GPX3); and enhances the expression of cell cycle regulator GAS1. This study establishes A3C as a suppressor in PCa, which impedes tumor progression by regulating key molecules involved in cellular inflammation, cell cycle arrest, and DNA damage response.

BPA perturbates adipose differentiation, creating a dysfunctional adipocyte that fosters cancer growth and invasiveness in TNBC. This study underscores the impact of environmental pollutants on tumour progression by revealing the importance of BPA perturbation on tissue homeostasis and how this could promote cancer.

These 8 candidate genes (MSMB, PLG, CHMP2B, ATF6B, EGF, TAPBP, GAS1 and MMP7) were validated. After combining single-cell sequencing, Mendelian randomization, and Bayesian co-localization analyses, we identified 1 gene (TAPBP) that is strongly associated with prostate cancer.

Importantly, we effectively translated this tissue-based biomarker into a liquid biopsy predictor for anti-EGFR response (AUC: 76.9%), highlighting its non-invasive potential. In conclusion, circ-EGFR is a significant predictor of cetuximab efficacy in mCRC, potentially aiding in patient selection and treatment management, especially for patients with low circ-EGFR expression.

This study highlights the critical role of macrophage-associated transcriptomic remodeling in liver disease progression. The machine learning-based predictive models offer a promising approach for early diagnosis and clinical decision-making in patients with cirrhosis.

We show that the IGSF10-RET-GAS1-cdc42 pathway regulates migration of GnRH neurons and that IGSF10 mutants linked to delayed puberty are defective in RET-cdc42 regulation. These results reveal a critical role of IGSF10 as a RET antagonist in Ewing sarcoma and GnRH neurons.

The results showed that GAS1 (Growth arrest specific 1) exhibited a higher expression pattern in fibroblasts from ovarian cancer patients The assessment of resistance and immune checkpoint differences across various risk score groups indicates that the CAFs regulatory factor survival model is practical for guiding systemic treatment. In summary, this study establishes a prognostic model composed of 22 CAFs regulatory factors to predict the prognosis of ovarian cancer (OC), providing new perspectives for the clinical treatment of OC.

The observed high CTLA4 suggests that this inhibitory signal may be preventing a robust antitumor immune response. Taken together, this study identified multiple targets to be explored for biomarkers of malignancy, prediction of tumor behavior, and potential targets for development of novel therapies.

Additionally, hsa-let-7a-5p and hsa-miR-34a-5p were identified as potential therapeutic regulators for PCa treatment. In conclusion, this research offers novel perspectives into the progression of PCa, providing robust scientific support for the development of personalized treatment strategies for PCa patients.

Remarkably, they are multipotent and more gliogenic than Gas1low/- qNSCs, continuously generating oligodendrocytes in the adult and aged brain, and can be mobilized for myelin repair upon demyelination. Together, our study uncovers a subpopulation of dorsally derived, multipotent long-term qNSCs in the adult and aged SVZ with enhanced gliogenic potential, shedding light on the heterogeneity and plasticity of NSCs in normal, aging, and disease conditions.

We also provide evidence that MHC-II transcripts in the FT are differentially regulated throughout the menstrual cycle, with lower expression in follicular phase. These results suggest spatially regulated expression of FT transcripts with implications for fertilization and early neoplastic changes contributing to HGSOC.