An integrative analysis of the tumor suppressors and oncogenes from sexual dimorphism and gene expression alteration features in thyroid cancer

Cancer Biomark. 2023;38(1):1-16. doi: 10.3233/CBM-230029.

Abstract

Background: The incidence of thyroid cancer has risen rapidly over the last decades. Although mortality rates are relatively low compared to other cancers, the rate of new cases started to increase in the early 2000s. While tumor suppressors and oncogenes were recently identified in thyroid cancer, the potential roles of these genes in thyroid cancer remain unclear.

Objective: Analyze the roles and functions of tumor suppressors and oncogenes in thyroid cancer.

Methods: Thyroid cancer data were collected from public databases, such as the UCSC Xena database of TCGA thyroid cancer, TISIDB, and UALCAN. The genes frequently associated with unfavorable thyroid cancer were examined and validated. The association of these target genes with thyroid tumorigenesis, stages, subtypes, and survival rates were analyzed. Additionally, the genes aberrantly expressed in thyroid cancer and significantly involved in thyroid tumorigenesis, stages, subtypes, and survival rates were identified.

Results: Female sex was identified as a risk factor for thyroid cancer. The expression of PAPSS2, PDLIM3, COPZ2, ALDH1B1, ANTXR1, GUF1, and SENP6 negatively correlated with thyroid cancer prognosis.

Conclusion: Female sex was a risk factor for thyroid cancer. In addition, our analysis suggested that PAPSS2, PDLIM3, COPZ2, ALDH1B1, ANTXR1, GUF1, and SENP6 are negatively correlated with the prognosis of thyroid cancer. The expression of ANTXR1, GUF1, and PDLIM3 was weakly associated with thyroid cancer's immune and molecular subtypes.

Keywords: Database; anticancer drugs; prognosis gene; sex differences; thyroid cancer.

MeSH terms

  • Carcinogenesis / genetics
  • Cysteine Endopeptidases / genetics
  • Female
  • Gene Expression
  • Humans
  • Male
  • Microfilament Proteins / genetics
  • Oncogenes
  • Prostatic Hyperplasia* / genetics
  • Prostatic Hyperplasia* / metabolism
  • Receptors, Cell Surface / genetics
  • Sex Characteristics
  • Thyroid Neoplasms* / genetics

Substances

  • SENP6 protein, human
  • Cysteine Endopeptidases
  • ANTXR1 protein, human
  • Microfilament Proteins
  • Receptors, Cell Surface