HMGCS2 Cancer Research Results

HMGCS2, 3-Hydroxy-3-Methylglutaryl-CoA Synthase 2: Click to Expand ⟱
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HMGCS2 - 3-Hydroxy-3-Methylglutaryl-CoA Synthase 2

Abbreviation: HMGCS2, mitochondrial HMG-CoA synthase

Type: Mitochondrial metabolic enzyme / ketogenesis enzyme

Function: Catalyzes the condensation of acetyl-CoA with acetoacetyl-CoA to form HMG-CoA and is the rate-limiting enzyme of mitochondrial ketogenesis. HMGCS2 regulates production of ketone bodies including β-hydroxybutyrate and acetoacetate and links fatty-acid oxidation, mitochondrial metabolism, cellular energy status, and metabolic signaling.

Cancer: ↕ Context-dependent. HMGCS2 functions as a tumor suppressor in several cancers, where reduced expression can promote proliferation, migration, invasion, and tumor progression and restoration of HMGCS2 can suppress malignant behavior. However, HMGCS2-dependent ketogenesis can support metabolic adaptation and survival in selected tumor contexts, making its role dependent on cancer type and metabolic state.
Scientific Papers found: Click to Expand⟱
7483- H2,  Cisplatin,    Molecular hydrogen attenuates cisplatin-induced nephrotoxicity by modulating β-hydroxybutyrate metabolism
- in-vivo, Nor, HK-2
RenoP↑, H2 inhalation significantly attenuated cisplatin-induced kidney injury by reducing inflammation and apoptosis in renal tissue.
BHB↑, H2 upregulated the ketone body metabolic pathway, particularly enhancing β-hydroxybutyrate (β-HOB) synthesis via increased expression of the ketogenic enzyme 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2).
HMGCS2↑,
chemoP↑, Molecular hydrogen confers protection against cisplatin-induced nephrotoxicity by modulating β-HOB metabolism through upregulation of HMGCS2, thereby suppressing renal inflammation and apoptosis.
*IL2↓, IL-1β, IL-6, MCP-1, and TNF-α in kidney tissue. Levels of these proinflammatory mediators were significantly elevated following cisplatin treatment. H2 inhalation significantly suppressed these cytokines,
*IL6↓,
*MCP1/CCL2↓,
*TNF-α↓,
*KeyT↝, H2 upregulated HMGCS2 to enhance ketone body metabolism
*Inflam↓, H2 has been demonstrated protective effects in various inflammatory and oxidative stress-related conditions
*ROS↓,
*MMP↑, Several studies have shown that H2 can preserve mitochondrial membrane potential, boost ATP generation, and improve mitochondrial dynamics and biogenesis by activating pathways such as mitofusin-2 (Mfn2) and PGC-1α
*ATP↑,
*MFN2↑,
*PGC-1α↑,
*BUN↓, Our work confirmed that H2 inhalation significantly ameliorated cisplatin-induced histological damage, elevated BUN and creatinine levels, renal inflammation, and tubular apoptosis.
*creat↓,


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

BHB↑, 1,   HMGCS2↑, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1,   RenoP↑, 1,  
Total Targets: 4

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

MFN2↑, 1,   ROS↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   MMP↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

BUN↓, 1,   KeyT↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL2↓, 1,   IL6↓, 1,   Inflam↓, 1,   MCP1/CCL2↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

creat↓, 1,   IL6↓, 1,  
Total Targets: 14

Scientific Paper Hit Count for: HMGCS2, 3-Hydroxy-3-Methylglutaryl-CoA Synthase 2
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1646  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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