NOTCH1 expression

P=N/A, N=420, Recruiting, Fuwai Hospital,Chinese Academy of Medical Sciences and Peking Union Medical College; Fuwai Hospital,Chinese Academy of Medical Sciences and Peking Uni

Targeting NOTCH1 and ATM is a promising strategy to overcome sorafenib resistance in HCC, particularly through the combined use of VPA and sorafenib.

Overall, this study provides crucial evidence that EGFL8 inhibits the proliferation and cancer aggressiveness of human OC cells by suppressing ERK/MAPK signaling. Therefore, EGFL8 may serve as a valuable prognostic biomarker and a potential target for developing novel human OC therapies.

RT-qPCR detection of NOLC1 and FOXA1 expression, colony formation assay of cell proliferation, Transwell assay of cell invasion, sphere formation assay of cell stemness, western blot detection of CD133, OCT4, GLI1, NOTCH1 and Hes1 expression, CCK-8 assay of IC50 value of cisplatin, and ChIP and dual-luciferase reporter validation of binding relationship between NOLC1 and FOXA1 were done...Activation of NOLC1 transcription by FOXA1 through NOTCH pathway promoted stemness of LUAD. FOXA1/NOLC1 axis is expected to become a new target for inhibiting stemness of LUAD cells.

AKT1 induces the Notch1 phosphorylation and promotes the activation and nuclear translocation of Notch1-IC by targeting the regulation of IRS-1, thereby advancing the progression of GC.

The NCSTN knockout mouse might be employed as HS animal model; Reducing nicastrin may affect the expression of notch1-hes1 pathway molecules in skin, brain, and liver tissues; low dose (10 mg/kg/d) tamoxifen could be used to induce the deletion of the target gene in mice.

Numb expression is decreased and Notch-1 expression is increased in colon cancer tissue and metastatic lymph node tissue, suggesting that the interaction between the two proteins may play a promote role in the development, invasion, and metastasis of colon cancer. There was no relationship between the expression of Numb and Notch-1 protein in colon cancer and metastatic lymph node tissue, suggesting that there is no obvious enhancement of the cancer cells; in the process of lymph node metastasis, the degree of malignant biological behavior remains relatively stable.

Mechanistically, the co-treatment with drugs-loaded Cs NPs was found to downregulate the expression of NOTCH-1 and HIF-1α, two key transcription factors involved in tumor cell survival and adaptation, suggesting that their inhibition is a crucial component of the therapeutic efficacy of this treatment strategy. Collectively, the findings of this study suggest that the co-delivery of Met and Dig via chitosan Cs NPs represents a promising therapeutic strategy for breast cancer, as it effectively targets key pathways involved in tumor growth and progression, and underscores the potential of Cs NPs as a versatile platform for cancer therapy.

The expression of GINS1 enhances the expression of Notch1 and Notch3 receptors, and then phosphorylates and activates the downstream PI3K/AKT/mTORC1 signaling pathway to enhance the glycolysis, proliferation and metastasis of LUAD cells.

ZGP protects ovarian function in CTX-induced ovarian aging rats by regulating the Notch1/Nrf2 pathway. It restores serum sex hormone levels, maintains normal follicle development, promotes the proliferation of aged OSCs, optimizes the cell cycle, reduces apoptosis, and preserves stemness, thereby alleviating ovarian aging.

Mechanistically, DUSP6 dephosphorylates phospho-Y2116, which in turn reduces NTM ubiquitination, leading to increased NTM stability and transcriptional activity. As a result, the expression of Notch1-targeted proliferation genes is increased to promote tumour cell growth.

NOTCH1 was conducive to cancer-associated fibroblasts (CAFs) immune infiltration, while the metastatic process was more dependent on the differentiation and angiogenesis function of NOTCH1. Accordingly, the heterogeneity of NOTCH1 in immune infiltration was extensively analyzed in this study based on the pan-cancer study, which can contribute to the formulation of specific immunotherapy strategies.