Affiliations 

  • 1 Research Follower, INTI International University, 71800 Negeri Sembilan, Malaysia; Electronic Marketing and Social Media, Economic and Administrative Sciences, Zarqa University, Jordan. Electronic address: dr_sliman@yahoo.com
  • 2 Faculty of Business and Communications, INTI International University, 71800, Negeri Sembilan, Malaysia. Electronic address: vasudevan@newinti.edu
  • 3 Department of Medical Analysis, Medical Laboratory Technique College, The Islamic University, Najaf, Iraq; Department of Medical Analysis, Medical Laboratory Technique College, The Islamic University of Al Diwaniyah, Al Diwaniyah, Iraq; Department of Medical Analysis, Medical Laboratory Technique College, The Islamic University of Babylon, Babylon, Iraq
  • 4 Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia
  • 5 Department of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India
  • 6 Centre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, 140401, Punjab, India
  • 7 Department of Biomedical, Sathyabama Institute of Science and Technology, Chennai, Tamil Nadu, India
  • 8 Department of Biochemistry, IMS and SUM Hospital, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, Odisha, 751003, India
  • 9 Department of Allied Science, Graphic Era Hill University, Dehradun, India; Graphic Era Deemed to be University, Dehradun, Uttarakhand, India
  • 10 Department of Medical Laboratories Technology, Al-Nisour University College, Nisour Seq. Karkh, Baghdad, Iraq
Exp Cell Res, 2025 Mar 22;447(2):114508.
PMID: 40122505 DOI: 10.1016/j.yexcr.2025.114508

Abstract

The tumor microenvironment (TME) 's primary constituents that promote cancer development are cancer-associated fibroblasts (CAFs). Metabolic remodeling has been shown to control CAF activity, particularly aberrant lipid metabolism. SCD1 can be thought of as the primary enzyme controlling the fluidity of lipid bilayers by gradually converting saturated fatty acids into monounsaturated fatty acids. Furthermore, its crucial function in the onset and spread of cancer is well acknowledged. Even with the increasing amount of research on changes in lipid metabolism, this problem remains a relatively understudied aspect of cancer research. Blocking several fatty acid synthesis-related enzymes highly expressed in cancerous cells inhibits cell division and encourages apoptosis. This is the situation with SCD1, whose overexpression has been linked to several changed tumors and cells. Both genetic and pharmacological silencing of SCD1 in cancer cells prevents glucose-mediated lipogenesis and tumor cell growth. However, its role in CAFs, hence, cancer biology, has been less studied. This study aimed to review the role of SCD1 in CAF biology, shedding light on their function in cancer cell biology.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.