GSTA1 Cancer Research Results

GSTA1, Glutathione S-Transferase A1: Click to Expand ⟱
Source:
Type:
GSTA1 belongs to the glutathione S-transferase (GST) superfamily of enzymes. These enzymes catalyze the conjugation of glutathione (GSH) to a variety of electrophilic substrates, thereby aiding in their detoxification.
By facilitating the detoxification of reactive metabolites, carcinogens, and drugs, GSTA1 helps protect cells against oxidative stress and chemical-induced damage.
In tumor cells, upregulation of GSTA1 may be a defensive response to increased oxidative stress. While this can protect normal cells, in a tumor setting, enhanced detoxification may allow cancer cells to survive in a hostile microenvironment.
Elevated levels of GSTA1 have been linked to resistance to chemotherapy. As GSTA1 helps metabolize and clear chemotherapeutic agents, its overexpression in tumors can contribute to treatment resistance
-GSTA1 expression levels are being evaluated as a prognostic marker. In some studies, its overexpression has correlated with aggressive tumor behavior, higher rates of recurrence, and reduced overall survival.
Scientific Papers found: Click to Expand⟱
2717- BetA,    Betulinic Acid Induces ROS-Dependent Apoptosis and S-Phase Arrest by Inhibiting the NF-κB Pathway in Human Multiple Myeloma
- in-vitro, Melanoma, U266 - in-vivo, Melanoma, NA - in-vitro, Melanoma, RPMI-8226
Apoptosis↑, BA mediated cytotoxicity in MM cells through apoptosis, S-phase arrest, mitochondrial membrane potential (MMP) collapse, and overwhelming reactive oxygen species (ROS) accumulation.
TumCCA↑, S-Phase Arrest in U266 Cells
MMP↓,
ROS↑, exhibited concentration-dependent increases in intracellular ROS
eff↓, ROS scavenger N-acetyl cysteine (NAC) effectively abated elevated ROS, the BA-induced apoptosis was partially reversed
NF-kB↓, BA resulted in marked inhibition of the aberrantly activated NF-κB pathway in MM
Cyt‑c↑, BA mediated the release of cyt c and activated cleaved caspase-3, caspase-8, and caspase-9 and cleaved PARP1
Casp3↑,
Casp8↑,
Casp9↑,
cl‑PARP1↑,
MDA↑, here is a concentration-dependent increase in MDA contents and reduction in SOD activities, especially for the high concentration group.
SOD↓,
SOD2↓, expression of genes SOD2, FHC, GCLM, and GSTM was all decreased following treatment with BA (40 μM)
GCLM↓,
GSTA1↓,
FTH1↓, FHC
GSTs↓, GSTM
TumVol↓, BA Inhibits the Growth of MM Xenograft Tumors In Vivo. BA-treated group were significantly reduced (inhibition ratio of approximately 72.1%).

4964- PEITC,    Irreversible Inhibition of Glutathione S-Transferase by Phenethyl Isothiocyanate (PEITC), a Dietary Cancer Chemopreventive Phytochemical
- in-vitro, Var, NA
GSH↓, . The primary route of isothiocyanate metabolism is its conjugation with glutathione (GSH), a reaction catalyzed by glutathione S-transferase (GST).
GSTA1↓,
chemoPv↑, a Dietary Cancer Chemopreventive Phytochemical

2953- PL,    Piperlongumine Acts as an Immunosuppressant by Exerting Prooxidative Effects in Human T Cells Resulting in Diminished TH17 but Enhanced Treg Differentiation
- in-vitro, Nor, NA
*ROS↑, PL increased the levels of intracellular reactive oxygen species and decreased glutathione in PBTs.
*GSTA1↓,
eff↝, promising agent for therapeutic immunosuppression by exerting prooxidative effects in human T cells resulting in a diminished TH17 but enhanced Treg cell differentiation.
*toxicity↓, In the present study, we found that PL was not toxic to primary human T cells, as opposed to the malignant T leukemia line Jurkat
ROS↑, Similar to primary human T cells, the ROS levels in Jurkat leukemia cells also increased significantly after PL treatment
*Hif1a↓, PL strongly inhibits the expression of HIF-1α in a dose-dependent manner starting already at a concentration of 1 μM PL

5163- PLB,    Plumbagin suppresses epithelial to mesenchymal transition and stemness via inhibiting Nrf2-mediated signaling pathway in human tongue squamous cell carcinoma cells
- in-vitro, SCC, SCC25
TumCP↓, PLB inhibited cell proliferation, activated death receptor-mediated apoptotic pathway,
NRF2↓, PLB induces intracellular ROS generation and regulates redox homeostasis via suppressing Nrf2-mediated oxidative signaling pathway in SCC25 cells
TumCCA↑, PLB markedly induced cell cycle arrest at G2/M phase and extrinsic apoptosis
EMT↓, and inhibited epithelial to mesenchymal transition (EMT) and stemness in SCC25 cells.
CSCs↓,
eff↓, Of note, N-acetyl-l-cysteine (NAC) and l-glutathione (GSH) abolished the effects of PLB on cell cycle arrest, apoptosis induction, EMT inhibition, and stemness a
ROS↑, PLB on ROS generation-related molecules
CycB/CCNB1↓, PLB induces G2/M arrest in SCC25 cells via downregulation of cyclin B1, CDK1/cdc2, and cdc25
CDK1↓,
CDK2↓,
CDC25↓,
Vim↓, PLB inhibited the expression of vimentin in a concentration- and time-dependent manner
OCT4↓, PLB significantly decreased the expression level of Oct-4, Sox-2, Nanog, and Bmi-1.
SOX2↓,
Nanog↓,
BMI1↓,
NQO1↓, The expression levels of NQO1, GST, and HSP90 were all markedly decreased
GSTA1↓,
HSP90↓,
toxicity↓, PLB exhibits anticancer activities with minimal side effect in vitro and in vivo,

2106- TQ,    Cancer: Thymoquinone antioxidant/pro-oxidant effect as potential anticancer remedy
- Review, Var, NA
Apoptosis↑, The anticancer power of TQ is accomplished by several aspects; including promotion of apoptosis, arrest of cell cycle and ROS generation.
TumCCA↑,
ROS↑,
*Catalase↑, activation of antioxidant cytoprotective enzymes including, CAT, SOD, glutathione reductase (GR) [80], glutathione-S-transferase (GST) [81] and glutathione peroxidase (GPx) - scavenging H2O2 and superoxide radicals and preventing lipid peroxidation
*SOD↑,
*GR↑,
*GSTA1↓,
*GPx↑,
*H2O2↓,
*ROS↓,
*lipid-P↓,
*HO-1↑, application of TQ to HaCaT (normal) cells promoted the expression of HO-1 in a concentration and time-dependent pattern
p‑Akt↓, TQ could induce ROS which provoked phosphorylation and activation of Akt and AMPK-α
AMPKα↑,
NK cell↑, TQ was outlined to enhance natural killer (NK) cells activity
selectivity↑, Many researchers have noticed that the growth inhibitory potential of TQ is particular to cancer cells
Dose↝, Moreover, TQ has a dual effect in which it can acts as both pro-oxidant and antioxidant in a dose-dependent manner; it acts as an antioxidant at low concentration whereas, at higher concentrations it possess pro-oxidant property
eff↑, Pro-oxidant property of TQ occurs in the presence of metal ions including copper and iron which induce conversion of TQ into semiquinone. This leads to generation of reactive oxygen species (ROS) causing DNA damage and induction of cellular apoptosis
GSH↓, TQ for one hour resulted in three-fold increase of ROS while reduced GSH level by 60%
eff↓, pre-treatment of cells with N-acetylcysteine, counteracted TQ-induced ROS production and alleviated growth inhibition
P53↑, TQ provokes apoptosis in MCF-7 cancer cells by up regulating the expression of P53 by time-dependent manner.
p‑STAT3↓, TQ inhibited the phosphorylation of STAT3
PI3K↑, via up regulation of PI3K and MPAK signalling pathway
MAPK↑,
GSK‐3β↑, TQ produced apoptosis in cancer cells and modulated Wnt signaling by activating GSK-3β, translocating β-catenin
ChemoSen↑, Co-administration of TQ and chemotherapeutic agents possess greater cytotoxic influence on cancer cells.
RadioS↑, Treatment of cells with both TQ and IR enhanced the antiproliferative power of TQ as observed by shifting the IC50 values for MCF7 and T47D cells from ∼104 and 37 μM to 72 and 18 μM, respectively.
BioAv↓, TQ cannot be used as the primary therapeutic agent because of its poor bioavailability [177,178] and lower efficacy
NRF2↑, TQ to HaCaT cells promoted the expression of HO-1 in a concentration and time-dependent pattern. This was achieved via increasing stabilization of Nrf2


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GCLM↓, 1,   GSH↓, 2,   GSTA1↓, 3,   GSTs↓, 1,   MDA↑, 1,   NQO1↓, 1,   NRF2↓, 1,   NRF2↑, 1,   ROS↑, 4,   SOD↓, 1,   SOD2↓, 1,  

Metal & Cofactor Biology ⓘ

FTH1↓, 1,  

Mitochondria & Bioenergetics ⓘ

CDC25↓, 1,   MMP↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 2,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   MAPK↑, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,  

Protein Folding & ER Stress ⓘ

HSP90↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   cl‑PARP1↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   CycB/CCNB1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

BMI1↓, 1,   CSCs↓, 1,   EMT↓, 1,   GSK‐3β↑, 1,   Nanog↓, 1,   OCT4↓, 1,   PI3K↑, 1,   SOX2↓, 1,   p‑STAT3↓, 1,  

Migration ⓘ

TumCP↓, 1,   Vim↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,   NK cell↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 1,   Dose↝, 1,   eff↓, 3,   eff↑, 1,   eff↝, 1,   RadioS↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,   toxicity↓, 1,   TumVol↓, 1,  
Total Targets: 53

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GPx↑, 1,   GSTA1↓, 2,   H2O2↓, 1,   HO-1↑, 1,   lipid-P↓, 1,   ROS↓, 1,   ROS↑, 1,   SOD↑, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Hormonal & Nuclear Receptors ⓘ

GR↑, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 12

Scientific Paper Hit Count for: GSTA1, Glutathione S-Transferase A1
1 Betulinic acid
1 Phenethyl isothiocyanate
1 Piperlongumine
1 Plumbagin
1 Thymoquinone
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

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