ALDH1A3 Cancer Research Results

ALDH1A3, Aldehyde Dehydrogenase 1 Family Member A3: Click to Expand ⟱
Source:
Type:

ALDH1A3 - Aldehyde Dehydrogenase 1 Family Member A3

Type: Aldehyde dehydrogenase / retinaldehyde dehydrogenase / metabolic enzyme / cancer stem-cell-associated marker

Function: ALDH1A3 is an NAD+-dependent aldehyde dehydrogenase that oxidizes retinaldehyde to retinoic acid and also contributes to detoxification of reactive aldehydes, redox homeostasis, differentiation, cellular metabolism, and stem-cell biology.

Cancer: ↑ Frequently overexpressed or enriched in aggressive and stem-like tumor-cell populations. Increased ALDH1A3 is associated with cancer stemness, proliferation, migration, invasion, metastasis, metabolic adaptation, treatment resistance, and poor prognosis in several malignancies. ALDH1A3 inhibition or knockdown can reduce tumor growth and stem-like properties in experimental models.

Favorable Direction in Cancer:ALDH1A3 expression or activity is generally favorable in cancers where ALDH1A3 is tumor-promoting.



Scientific Papers found: Click to Expand⟱
8193- LGE,    Targets and pathways involved in the antitumor activity of citral and its stereo-isomers
- Review, Var, NA
TumCP↓, CIT inhibits cancer cell proliferation and induces cancer cell apoptosis
Apoptosis↑,
ROS↑, (i) a drug-induced accumulation of reactive oxygen species in cancer cells leading to an oxidative burst and DNA damages,
DNAdam↑,
MARK4↓, (ii) a colchicine-like inhibition of tubulin polymerization and promotion of microtubule depolymerization, associated with an inhibition of the microtubule affinity-regulating kinase MARK4
ALDH1A3↓, (iii) a potent inhibition of the aldehyde dehydrogenase isoform ALDH1A3 which is associated with cancer stem cell proliferation and chemoresistance.
CSCs↓,
chemoR↓,
BioAv↓, intrinsic potency of CIT is limited, mainly because the drug is not very stable and has a low bioavailability and it does not present a high selectivity for cancer cells versus non-tumor cells.
selectivity↝,

8186- LGE,    Citral reduces breast tumor growth by inhibiting the cancer stem cell marker ALDH1A3
- vitro+vivo, BC, NA
ALDH1A3↓, Citral was identified as the best inhibitor of ALDH1A3, reducing the Aldefluor fluorescence in breast cancer cell lines and in a patient‐derived tumor xenograft.
TumCG↓, Nanoparticle encapsulated citral specifically reduced the enhanced tumor growth of MDA‐MB‐231 cells overexpressing ALDH1A3.


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0)

ALDH1A3↓, 2,  

Redox & Oxidative Stress(tgid=1)

ROS↑, 1,  

Cell Death(tgid=5)

Apoptosis↑, 1,  

DNA Damage & Repair(tgid=10)

DNAdam↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

CSCs↓, 1,   TumCG↓, 1,  

Migration(tgid=13)

MARK4↓, 1,   TumCP↓, 1,  

Drug Metabolism & Resistance(tgid=21)

BioAv↓, 1,   chemoR↓, 1,   selectivity↝, 1,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ALDH1A3, Aldehyde Dehydrogenase 1 Family Member A3
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#:1774  State#:%  Dir#:1
wNotes=on sortOrder:rid,rpid

 

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