AKR1C3/17β-HSD5/PGF Synthase Cancer Research Results

AKR1C3/17β-HSD5/PGF Synthase, Aldo-Keto Reductase Family 1 Member C3: Click to Expand ⟱
Source:
Type:

AKR1C3 - Aldo-Keto Reductase Family 1 Member C3

Abbreviation: AKR1C3, 17β-HSD5, PGF Synthase

Type: Aldo-keto reductase / hydroxysteroid dehydrogenase / prostaglandin-metabolizing enzyme

Function: AKR1C3 is an NADPH-dependent oxidoreductase involved in steroid hormone and prostaglandin metabolism. It converts weak androgen precursors into more active androgens, can convert estrone to estradiol, and reduces prostaglandin D2 to 11β-PGF2α. Through these activities, AKR1C3 regulates hormone-receptor signaling, prostaglandin signaling, cellular proliferation, and metabolic adaptation.

Cancer: ↑ Frequently overexpressed in multiple cancers and associated with enhanced proliferation, invasion, metastasis, tumor recurrence, and resistance to anticancer therapy. In hormone-dependent cancers, increased AKR1C3 can enhance local androgen and estrogen production and thereby activate androgen- or estrogen-receptor signaling. AKR1C3 inhibition can suppress tumor progression and restore treatment sensitivity in experimental models.
Scientific Papers found: Click to Expand⟱
8054- KAE,    Kaempferol Improves Alzheimer's Disease by Inhibiting Neuronal Ferroptosis via Activating GPX4/AKR1C3 Signaling Pathway
- vitro+vivo, AD, NA
*AKR1B10↝, Kaempferol treatment facilitated the expression of AKR1B1 in PC12 cells exposed to Aβ1–42
*MDA↓, Kaempferol treatment mitigated the Aβ1–42‐induced increases in Fe2+, MDA, and lipid ROS and Aβ1–42‐induced decreases in GSH synthesis and SOD activity.
*ROS↓,
*GSH↑,
*SOD↑,
*GPx4↑, The reduction in ferroptosis‐related proteins (GPX4, NQO1, SLC7A11, AKR1C1, and AKR1C3) and the inhibition of Nrf2 nuclear translocation and Nrf2/HO‐1 signaling caused by Aβ1–42 were also reversed by kaempferol.
*NQO1↑,
*xCT/SLC7A11↑,
*NRF2↑,
*HO-1↑,
*cognitive↑, In vivo studies revealed that kaempferol improved cognitive impairments, reduced deposition of Aβ and p‐Tau, and alleviated neuronal ferroptosis in the hippocampal tissues of an AD mouse model
*Aβ↓,
*p‑tau↓,
*Ferroptosis↓,
*AKR1C3/17β-HSD5/PGF Synthase↑, inhibiting neuronal ferroptosis through the activation of the Nrf2/HO‐1/GPX4/AKR1C3 signaling via upregulation of AKR1B1
*AKR1B1/ALR2↑,


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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AKR1B1/ALR2↑, 1,   AKR1B10↝, 1,   AKR1C3/17β-HSD5/PGF Synthase↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↓, 1,   GPx4↑, 1,   GSH↑, 1,   HO-1↑, 1,   MDA↓, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,   xCT/SLC7A11↑, 1,  

Cell Death(tgid=5) ⓘ

Ferroptosis↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,  
Total Targets: 17

Scientific Paper Hit Count for: AKR1C3/17β-HSD5/PGF Synthase, Aldo-Keto Reductase Family 1 Member C3
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#:1751  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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