Genes & Cancer

Gene signatures of cyclin-dependent kinases: a comparative study in naïve early and advanced stages of lung metastasis breast cancer among pre- and post-menopausal women

Muhammad Fazal Hussain Qureshi1, Muzna Shah1, Mahira Lakhani1, Zain Jawed Abubaker1, Danish Mohammad1, Hira Farhan1, Iman Zia1, Rida Tafveez1, Samahir Tariq Khan1, Rubina Ghani2, Shamim Mushtaq3, Ghulam Haider4

1 Medical students, Ziauddin University, Clifton, Karachi, Pakistan

1 Department of Biochemistry, Sohail University, Karachi, Pakistan

1 Department of Biochemistry, Ziauddin University, Clifton, Karachi, Pakistan

1 Oncology Department, Jinnah Postgraduate Medical Center, Karachi, Pakistan

Correspondence:

Shamim Mushtaq, email:[email protected]

Keywords: cyclin-dependent kinases, breast cancer, menopause, human epidermal growth factor receptor 2

Received: July 17, 2020 Accepted: December 03, 2020 Published: February 10, 2021

Abstract

The Human epidermal growth factor receptor 2 positive (HER2+) breast cancer (BC) is a more aggressive tumor with 5 years median survival rates after metastasis. Despite successful treatment, unfortunately, the majority of affected patients die. Defects in cell cycle and transcription regulation phases which are governed by cyclin-dependent kinases (CDKs) are the hallmark of many cancers that underpinning the progression of the disease. Therefore, the current study looked at the alteration of six CDKs mRNA expression levels in pre- and postmenopausal lung metastasis BC groups; the majority were HER2+. Two hundred pre-and postmenopausal lung metastasis breast cancer and healthy control blood samples were taken for RNA isolation. Quantitative PCR was done for CDKs mRNA expressions. We observed overexpression of CDK11, CDK12, CDK17, CDK18, and CDK19 in both pre- and postmenopausal groups. However, CDK20 showed progressive downregulation from early to advanced stages in both groups of patients. Collectively, this data revealed that CDKs overexpression levels may predict BC disease progression and provide further rationale for novel anticancer strategies for HER2+ BC cancers.


PII: 209