THBS1 (Thrombospondin 1)

Within the perivascular microenvironment, EV-mediated interactions between glioblastoma cells and astrocytes support the induction of stemness and the differentiation of GBM cells toward a pericyte-like phenotype, promoting perivascular niche formation and microvascular proliferation. The hydrogel-based co-culture model thus provides a simple and effective platform for dissecting tumor-stroma communication in the glioblastoma microenvironment.

ENL has potent inhibitory effects on ovarian cancer and suppresses malignant angiogenesis by binding to THBS1-3TSR. ENL ameliorates gut dysbacteriosis.

SRSF2 mutations promoted DNR resistance through multiple mechanisms, and targeted combination therapy with PDGFB pathway inhibitors may represent a novel strategy to improve therapeutic outcomes in patients with mutations.

Chemotherapy intensified senescence in hepatocytes by 5-fold relative to aging and led to unique CDKN2A+ populations. Across conditions, senescent cells shared AP-1 activation, pro-inflammatory cytokines, and apoptosis resistance, suggesting therapeutic opportunities.

Therefore, it has antileukemic actions. One of the main targets for anti-AML treatment is THBS1.

SPP1 may be a potential marker for the differentiation between benign and malignant ovarian masses, while IGFBP2 can differentiate between healthy females and females with ovarian masses. Combining SPP1 with CA125 or TSP1 provides high sensitivity and specificity for the detection of EOC patients.

These results indicate that radiotherapy promotes the release of Thbs1+ EVs, which drive cardiac muscle wasting via PERK-eIF2α-Atf4 signaling, revealing a novel mechanism underlying cancer-associated cardiac damage.

Our findings reveal a novel RNA-binding function of FSCN1 in posttranscriptional regulation of THBS1, establishing the FSCN1/THBS1/TGF-β axis as a critical driver of ESCC progression. The acetylation-dependent modulation of this pathway highlights the potential therapeutic vulnerability of metastatic ESCC cells.

We knocked down THBS1 in rat (BRL, BRL-3A) and human (THLE-2) hepatocytes using siRNA and applied Ruxolitinib to inhibit the JAK2/STAT3 pathway, further clarifying the role of THBS1 in this signaling process...In addition, plasma ELISA revealed that the concentration of THBS1 in plasma increased with increasing radiation dose and degree of RILI, which was consistent with the expression level in the liver tissue. This study provides new insights into the pathogenesis of RILI, and identifies THBS1 as a potential biomarker for RILI diagnosis and monitoring.

THBS1 promotes platinum resistance in OCCC through EMT activation and may serve as a prognostic biomarker and therapeutic target.

THBS1, carried by ovarian cancer-derived exosomes, promotes M2 polarization of TAMs by modulating TGFBI expression. The subsequent M2 polarization of TAMs contributes to the establishment of an immunosuppressive tumor microenvironment, thereby facilitating disease progression. Consequently, targeting the exosome-mediated signaling axis between cancer cells and macrophages represents a promising avenue for developing novel therapeutic interventions.

Importantly, disrupting the TSP-1-CD47 axis prevents T cell exhaustion and enhances tumor control. Our findings identify a novel pathway promoting T cell dysfunction and suggest that targeting the TSP-1-CD47 axis is a promising strategy to enhance T cell immunity and immunotherapy efficacy.