LATS2 and FAT4 as key candidate genes of hippo pathway associated with the risk and progression of breast cancer: an in-silico approach

Sci Rep. 2024 Nov 21;14(1):28857. doi: 10.1038/s41598-024-79688-2.

Abstract

Background: The 2020 cancer report states that breast cancer remains a significant cause of death for females, despite the use of various strategies for early detection and treatment. However, there are still gaps in the fight against this disease. Researchers are exploring the hippo pathway, one of eight significant pathways involved in cancer progression, for potential biomarkers to use in personalized therapeutics.

Methods: The current study used bioinformatic tools such as DEGs analysis, Methsurv, Km Plotter to generate data that can predict molecular biomarkers associated with hippo pathway in breast cancer development and treatment. The protein-protein interaction pathway was generated using the STRING database to find associations of hippo pathway genes with other dysregulated genes in breast cancer datasets. A disease enrichment study was also done to explore the potential of the hippo pathway in various aspects.

Results: LATS2 and FAT4 genes of the hippo pathway have shown an interesting association with overall survival, hypermethylation, genetic alterations, and decreased expression levels in the breast cancer cohort. Our findings suggest that both of these genes are associated with breast cancer progression and diagnosis and can be utilized as predictive biomarkers by oncologists for personalized therapy in patients.

MeSH terms

  • Biomarkers, Tumor / genetics
  • Biomarkers, Tumor / metabolism
  • Breast Neoplasms* / genetics
  • Breast Neoplasms* / metabolism
  • Breast Neoplasms* / mortality
  • Breast Neoplasms* / pathology
  • Cadherins
  • Computational Biology / methods
  • Computer Simulation
  • Disease Progression*
  • Female
  • Gene Expression Regulation, Neoplastic
  • Hippo Signaling Pathway*
  • Humans
  • Protein Interaction Maps / genetics
  • Protein Serine-Threonine Kinases* / genetics
  • Protein Serine-Threonine Kinases* / metabolism
  • Signal Transduction / genetics
  • Tumor Suppressor Proteins* / genetics
  • Tumor Suppressor Proteins* / metabolism

Substances

  • Protein Serine-Threonine Kinases
  • LATS2 protein, human
  • Tumor Suppressor Proteins
  • FAT4 protein, human
  • Biomarkers, Tumor
  • Cadherins