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Journal Article Review Epublish 10 citations

PubMed: 37869088 DOI: 10.3389/fonc.2023.1235418

Unraveling the relationship between the renin-angiotensin system and endometrial cancer: a comprehensive review.

Front Oncol 13:1235418

Authors: Nihad Ashraf Khan, Deena Elsori, Gowhar Rashid, Sonia Tamanna, Ananya Chakraborty, Adeeba Farooqi, Ayman Kar, Niti Sambyal, Mohammad Azhar Kamal

Affiliations

  • Department of Biosciences, Faculty of Natural Sciences, Jamia Millia Islamia, Delhi, India.
  • Faculty of Resillience, Deans Office Rabdan Academy, Abu Dhabi, United Arab Emirates.
  • Amity Medical School, Amity University, Gurgaon, Haryana, India.
  • Department of Biochemistry and Molecular Biology, University of Dhaka, Dhaka, Bangladesh.
  • Department of Biotechnology, Adamas University, Kolkata, West Bengal, India.
  • Department of Biotechnology, Central University of Kashmir, Ganderbal, India.
  • Department of Biotechnology, Shri Mata Vashino Devi University, Katra, Jammu, India.
  • Department of Pharmaceutics, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Alkharj, Saudi Arabia.

Abstract

Endometrial cancer (EC), the most common adenocarcinoma, represents 90% of uterine cancer in women with an increased incidence of occurrence attributed to age, obesity, hypertension, and hypoestrogenism. Being the most common gynecological malignancy in women, it shows a relation with the activation of different components of the renin-angiotensin system (RAS), which is predominantly involved in maintaining blood pressure, salt, water, and aldosterone secretion, thereby playing a significant role in the etiology of hypertension. The components of the RAS, i.e., ACE-I, ACE-II, AT1R, AT2R, and Pro(renin) receptor, are widely expressed in both glandular and stromal cells of the endometrium, with varying levels throughout the different phases of the menstrual cycle. This causes the endometrial RAS to implicate angiogenesis, neovascularization, and cell proliferation. Thus, dysfunctioning of the endometrial RAS could predispose the growth and spread of EC. Interestingly, the increased expression of AngII, AGTR1, and AGTR2 showed advancement in the stages and progression of EC via the prorenin/ATP6AP2 and AngII/AGTR1 pathway. Therefore, this review corresponds to unraveling the relationship between the progression and development of endometrial cancer with the dysfunction in the expression of various components associated with RAS in maintaining blood pressure.

MeSH

Cells, Hypertension, Blood, Neoplasms, Blood Pressure, Renin, Angiotensins, Renin-Angiotensin System, Endometrial Neoplasms

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