CAFs with elevated VCAN levels promoted the proliferation, migration, and invasion of high-stemness adenocarcinoma cells via the MDK-NCL and MIF-CD74-CD44 signaling pathways, while also enhancing immune evasion and self-renewal. These results position VCAN as a potential new therapeutic target for STAD.
We established a non-invasive 8-SPCG signature that may serve as a potential predictor for GC prognosis and TME features. SERPINE1 was identified as a promising mediator linking GC progression to CAFs interactions, supporting its further investigation as a therapeutic target.
TMB (Tumor Mutational Burden) • EGF (Epidermal growth factor) • SERPINE1 (Serpin Family E Member 1) • IGFBP1 (Insulin Like Growth Factor Binding Protein 1) • IL1F10 (Interleukin 1 Family Member 10) • GCG (Glucagon)
Randomized controlled clinical trials are required to further demonstrate its efficacy and optimal application scenario. https://clinicaltrials.gov/study/NCT04675866?term=Hou%20Xinfang&rank=1, identifier NCT04675866.
Additionally, it functions as a novel "metabolic immune checkpoint" across multiple cancer types. SPHK1 may bridge sphingolipid metabolism with tumor immune suppression and represents a potential promising integrated target for metabolically informed immunotherapy strategies.
High INHBA expression predicts poor survival of GC patients. INHBA, upregulated by C/EBPβ, induces M2 macrophage polarization to promote tumor metastasis and growth via activating PI3K/AKT pathway in GC. INHBA may be a potential therapeutic target for GC.
Anti-mouse CLDN18.2 CAR-T cells suppressed tumor growth of mice bearing the syngeneic graft of S6M but not the CLDN18.2-low S1M cell line. Dual inhibition of immunosuppressive molecules TGF-β and PD-L1 enhanced the in vivo efficacy of anti-mouse CLDN18.2 CAR-T against S6M cells by recruiting NK cells to tumor microenvironment, suggesting the potential utility of our novel syngeneic gastric cancer cell line model in designing innovative clinical therapeutic approaches.
8 days ago
Preclinical • Journal
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PD-L1 (Programmed death ligand 1) • TP53 (Tumor protein P53) • CLDN18 (Claudin 18) • SMAD4 (SMAD family member 4) • CDH1 (Cadherin 1) • TGFB1 (Transforming Growth Factor Beta 1) • PDX1 (Pancreatic And Duodenal Homeobox 1)
CLDN18.2 overexpression is associated with poor prognosis in GC patients. Transcriptomic and proteomic analyses demonstrate that CLDN18.2 promotes tumor progression and metastasis, underscoring its potential as an independent prognostic factor in regions with a high incidence of GC.