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Data-Driven Discovery of a Key Regulator Cyclin A2 as a Promising Therapeutic Target in Hormone-Sensitive Cancers

Suvitha Anbarasu1, Anand Anbarasu2

  • 1Medical and Biological Computing Laboratory, Department of Biotechnology, School of Biosciences and Technology (SBST), Vellore Institute of Technology (VIT), Vellore, 632014, Tamil Nadu, India.

Molecular Biotechnology
|September 11, 2025
PubMed

Insights

This study identifies CCNA2 as a key gene driving resistance in hormone-sensitive cancers (HSCs) like breast, ovarian, and endometrial cancers. CCNA2 shows potential as a therapeutic target to overcome endocrine therapy resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Hormone-sensitive cancers (HSCs) are a leading cause of cancer-related death globally.
  • Therapeutic resistance, particularly to endocrine therapy, remains a significant clinical challenge in managing HSCs.

Purpose of the Study:

  • To identify novel therapeutic targets for hormone-sensitive cancers (HSCs) in women, specifically breast, ovarian, and endometrial cancers.
  • To investigate the role of differentially expressed genes in tamoxifen resistance within these HSCs.

Main Methods:

  • Comparative analysis of differentially expressed genes in breast, ovarian, and endometrial cancers against known tamoxifen resistance genes.
  • Identification and functional screening of hub genes.
  • Evaluation of CCNA2's expression significance, mutational profile, survival impact, and clinical relevance across the studied HSCs.

Main Results:

  • CCNA2 was identified as a significant hub gene across breast, ovarian, and endometrial cancers, strongly associated with cell cycle regulation.
  • CCNA2 positively correlated with multiple resistance-causing genes, validating its role in therapeutic resistance.
  • CCNA2 demonstrated critical hazard ratios and significant expression levels in advanced stages of these cancers, indicating its pivotal role in patient survival.

Conclusions:

  • CCNA2 is a potential therapeutic target for overcoming endocrine therapy resistance in hormone-sensitive cancers.
  • Targeting CCNA2 may offer a novel strategy to improve treatment outcomes for patients with breast, ovarian, and endometrial cancers.
Keywords:
Cell cycleDifferential regulationDrug resistanceHormone dependentTarget screening

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