LGALS4 (Galectin 4)

Shortening the peptide linker between the CRDs altered protein binding to the membrane, suggesting the linker likely facilitates stabilizing contacts between the CRDs. Overall, this work helps to illustrate the conformational dynamics of tandem-repeat galectins, emphasizing the roles of ligand affinity, linker peptide dynamics, and contacts between CRDs.

Collectively, these findings demonstrate a novel role for TP53-mediated LGALS4 in regulating tumor progression. This work identifies LGALS4 as a promising therapeutic target and provides a foundation for the development of combined immunotherapy based on galectin for CRC.

Our prognosis-related risk model based on DEGs between RCC and LCC may provide better prediction of clinical outcomes for patients with colon cancer.

Key findings revealed that SM dysregulation correlated with poor clinical outcomes and eight pivotal prognostic genes (ATP13A2, PCSK2, NR2F1, GSDMB, NFASC, NTF3, LGALS4, and SREBF1) were identified...These results suggest that SM dysregulation may drive immunomodulatory changes in BLCA microenvironments, offering mechanistic insights into tumor immune evasion. This study provides a novel biomarker tool for risk stratification and highlights SM pathways as potential therapeutic targets for BLCA patients with immune microenvironment dysregulation.

Additionally, enrichment analysis revealed tumor progression-related pathways unique to each histotype, offering insights into the molecular mechanisms underlying disease progression and potential therapeutic targets. These findings provide valuable insights into the molecular landscape of advanced-stage EOC, paving the way for more effective diagnostic and prognostic tools across diverse histotypes.

Activation of the galectin-4/LDHA/HIF-1α and CXCL6 axis plays a pivotal role in ATZ/BVZ therapy resistance. Galectin-4 serves as a promising therapeutic target to improve immunotherapy efficacy and an effective predictive biomarker for immunotherapy response in HCC.

Molecular docking revealed that the binding energy between LGALS4 and lactose, dendronobiloside A, and dendronobiloside B was-7.22,-9.05, and-8.05 kcal/mol, respectively, forming 5, 11, and 8 hydrogen bonds. Overall, DO effectively suppresses the viability and migration of COAD HCT116 or Caco-2 cells, with LGALS4 potentially serving as a key target.

We identified several glyco-associated biomarkers in NSCLC, including Galectin-4, Galectin-7, MUC21, ST6GALNAC1, and ST6GALNAC2. Galectin-7 is a promising clinical biomarker for detection in plasma.

In a FIT-positive population, CELTiC did not reach 90% sensitivity at the pre-defined threshold. At post hoc thresholds corresponding to 90% sensitivity, specificity was low. CELTiC cannot currently be recommended as an add-on test to detect AN in FIT-positive screenees in a CRC screening programme.

Our study identified MTHFD1 and LGALS4 as potential preventive targets for PRAD. However, future experiments are warranted to assess the utility and effectiveness of these candidate proteins.

LGALS4 overexpression inhibited CRC cell growth, induced cell cycle arrest and enhanced 5-fluorouracil (5-FU)-induced apoptosis...The downregulatory effect of LGALS4 on glycolysis-related genes was further enhanced by the addition of the β-catenin inhibitor XAV-939...Overexpression of LGALS4 reduced the proliferation and glycolytic capacity of CRC cells and also enhanced their sensitivity to 5-FU. These results may potentially provide new perspectives for CRC treatment and targets for future clinical intervention strategies.

In the pilot study, we found promising copy number variation biomarkers of bevacizumab response in FFPE samples of mCRC patients. The validation phase should be focused especially on the genes associated with angiogenesis (AGRN, MAPK8, ARHGAP22, LGALS13, LGALS4, ZFP36, and MYC), tumorigenesis (DVL1), and tumor proliferation (IFNL1, IFNL2, IFNL3, MAP3K10, and MAP4K1).