Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Lipolysis gone rogue: the HSL connection in feeding cancer

Hemadri K., Subramanian P., Aravindan S., Periyasamy L., Aravindan N.

Narrative Review on Immune Modulation, published in Cell Biol Toxicol (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Cell Biol Toxicol (2025)
Reported sample size
—
Source database
Europe PMC
PMID
41186614
PMCID
PMC12586420
DOI
10.1007/s10565-025-10098-4

Abstract (original English)

Lipolysis, a tightly regulated metabolic process, is hijacked by cancer cells to meet their energy and biosynthetic demands under stress. Central to this process is hormone-sensitive lipase (HSL), a key enzyme that orchestrates lipid mobilization by hydrolyzing diacylglycerols into free fatty acids (FFAs). This review explores the pivotal and multifaceted role of HSL in cancer metabolism, focusing on its dual function acting as both a tumor promoter and suppressor depending on the cancer type and microenvironment. Lipolysis, the breakdown of triglycerides into free fatty acids (FFAs), is essential for maintaining energy homeostasis, and is co-opted by tumor cells to fuel growth. Enzymes such as ATGL, HSL, and MGL synergistically regulate lipolysis, with HSL being the driver in this process. Dysregulation of HSL can either promote or inhibit cancer growth, depending on the tumor type. We examine how deregulated HSL activity contributes to tumor progression, metastasis, and therapy resistance through metabolic reprogramming, particularly in the context of cancer-associated adipocytes (CAAs) and fibroblasts (CAFs). CAAs and CAFs within the tumor microenvironment modulate lipid metabolism, influencing tumor progression. The review also discusses the interplay between HSL and oncogenic signaling pathways, its regulation by hormonal and transcriptional networks, and its impact on imm

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AdipocytesAnimalsHumansNeoplasmsSignal TransductionEnergy MetabolismLipolysisLipid MetabolismSterol EsteraseTumor Microenvironment

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