LTBP1 (Latent-transforming growth factor beta-binding protein 1)

Higher LTBP1 expression is associated with a worse prognosis and advanced stage in bladder cancer patients. In conclusion, this study revealed that LTBP1 may be a potential target for alleviating chemoresistance in bladder cancer.

These mechanisms lay a solid foundation for its clinical translation: LTBP1 is established as a multidimensional biomarker and constitutes a novel target for a range of intervention strategies, from targeted therapies and cell therapies to functionalized biomaterials. In summary, establishing LTBP1 as a key pathological integrator in systematic studies, provides a new framework and direction for understanding common mechanisms of complex diseases and developing precision medicine strategies.

This study provides new perspectives on the development of IPF and may help identify novel therapeutic targets. Further research may reveal how core genes influence cellular function and disease progression, providing novel insights into the intricate mechanisms underlying IPF.

One loci mapping to MCTP2 was associated with lower overall mortality risk: rs7171579 (per allele HR: 0.59, CI: 0.50-0.71, p = 2.13 × 10-8). In conclusion, evidence from the present study supports LTBP1 and MCTP2 as important to CRC mortality.

The BRGs signature is a reliable biomarker for predicting the prognosis of MM and helps optimize clinical decision-making for treatment, and identifies key gene ARID5B downregulation as an adverse prognostic factor in multiple myeloma.

This signature highlights the clinical relevance of OXPHOS in LUSC prognosis and may guide personalized therapeutic strategies targeting metabolic vulnerabilities. Study limitations include its retrospective design and lack of experimental validation.

Consistently, BRD4S drove cancer cell dissemination in vitro and metastasis in vivo, which could be blocked by BET or TGF-β signaling pathway inhibitors. Overall, this study identifies IPA usage at the BRD4 gene locus induced by CDK12 deficiency as a mechanism responsible for BRD4S genesis, which represents an important mechanism driving cancer metastasis and a potential target for therapeutic intervention in CDK12-deficient cancers.

LTBP1 efficiently reduces severe pneumonia by activating the TGF-β1/Smad signaling pathway, highlighting its potential as a therapeutic target for treating this condition.

Using a GC liver metastasis model in combination with PET-CT imaging, inhibition of the CCL11/CCR3 axis was shown to suppress CEH-driven tumor growth and metastatic potential. These findings identify LTBP1-enriched EVs from PDPN⁺LTBP1⁺ CAFs as a viable therapeutic target to impede GC liver metastasis.

A 10 anoikis-related-gene prognostic model (MGP, TPM2, CRIP2, TUBB6, C1orf54, NOTCH3, LTBP1, CSRP2, FSTL3, and VIM) was developed and the area under the curve (AUC) values of the model in predicting 1-, 3- and 5-year survival probabilities reached 0.744, 0.797, and 0.755, respectively. In conclusion, anoikis related genes could be promising prognostic factors for risk stratification of CRC patients.

Elevated FBXW7 increased the radiosensitivity of TNBC cells in vitro and in vivo, and radioresistance was partially rescued after CREM upregulation. These results indicate that inhibition of protein degradation of CREM due to FBXW7 loss promotes radioresistance and immune escape in TNBC by increasing LTBP1 transcription, providing a new potential target for improving radiotherapy sensitivity in TNBC.

Combination therapy targeting TGF-β and PD-1 significantly improves the immunotherapy resistance of LTA4H-knockout Hepa1-6 tumors. Our findings reveal the previously unreported role of LTA4H in regulating the tumor microenvironment and provide insights into potential diagnostic and therapeutic strategies for patients with LTA4H-deficient HCC.