HES1 (Hes Family BHLH Transcription Factor 1)

In conclusion, ATOX1 is crucial for cisplatin resistance in liver cancer and linked to poor prognosis. Targeting ATOX1 with compound 8 may be a novel therapeutic strategy for overcoming cisplatin resistance.

In addition to these mechanisms, Notch2 acts as a transcription factor that directly controls the expression of key targets, such as CD23 and Hes1, that are fundamental for B cell proliferation, differentiation, and survival in CLL. All of these circuits represent important therapeutic targets and help explain the cells' dependence on their niche, the formation of proliferation centers, and resistance to modern targeted agents.

MFAP-5 expression in human HCC samples and conserved signaling pathways between mice and humans underscore the translational relevance of this target. Our findings highlight the therapeutic potential of CAF-targeted siRNA delivery using polycarbonate-based nanogels to inhibit stromal-driven angiogenesis and tumor progression in HCC.

Activation of Jag1/Notch1/Hes1 signaling pathway protects the intestinal mucosal barrier from inflammatory injury by abrogating MLCK-dependent TJ dysregulation.

Our work delineates the epigenetic and transcriptional circuitry that establishes TAM heterogeneity as potential therapeutic levers to enhance cancer immunotherapy.

These cells were then exposed to norepinephrine (NE), epinephrine (EPI), or corticosterone (CC)...Moreover, tumors from mice subjected to restraint stress had elevated expression of Notch1, Jagged 2, NICD, HES1, GR, ADRB2, and pS9-GSK3β. These data indicate that chronic stress leads to MDSCs infiltration and suppressive activity, which contributes to an immunosuppressive TME and OC progression.

After IL-17A addition to PDAC cell lines, the inhibitory effect of FGF21 on the Notch signaling pathway was significantly reduced. FGF21 suppresses invasion and metastasis in PDAC by inhibiting the IL-17A-Notch signaling axis, which reveals a novel therapeutic strategy for this malignancy.

The capsule was kept in place to preserve critical anatomical structures; however, it should be removed when possible depending on tumor configuration. The patient, who consented to the procedure and to the publication of her images, recovered within a few days.

Our findings suggest that HIF-1α promotes radiotherapy resistance in HNSCC by activating the Notch1 signaling axis. Targeting this pathway may enhance radiosensitivity and provide a new strategy for overcoming hypoxia-driven resistance.

Molecular docking supported the binding of Ardisiaoside A to NANOG, OCT4, CD44, and Notch proteins (NOTCH1, HES1, DLL1, DLL4), consistent with target inhibition. In conclusion, Ardisiaoside A, a newly identified triterpenoid glycoside from Ardisia gigantifolia, represents a promising candidate that inhibits cell proliferation by reducing cancer stem-cell populations and inducing cellular senescence in gastric cancer.

Our research identifies SPTAN1-kla as a novel oncogenic driver in HBV-related HCC, functioning via metabolic reprogramming and immune modulation. These findings position SPTAN1-kla as a promising therapeutic target for developing precision interventions against HBV-related HCC.

Background: Myelosuppression is one of the most common chemotherapy side effects, seriously threatening the quality of life of cancer patients. The application of the PI3K inhibitor LY294002 and the Notch1 inhibitor DAPT demonstrated that the ameliorative effect of VAPs on myelosuppression was dependent on the activation of both the Notch1 and PI3K/AKT pathways. Our study indicates that VAPs may achieve treatment of myelosuppression by improving the hematopoietic microenvironment, inhibiting apoptosis of mouse bone marrow cells, and regulating the Notch1 and PI3K/AKT signaling pathways.