TfR1/CD71 Cancer Research Results

TfR1/CD71, Transferrin receptor protein 1,: Click to Expand ⟱
Source:
Type: gene/protein
Also called CD71
A protein that in humans is encoded by the TFRC gene. A protein that mediates iron uptake from transferrin into cells.
Transferrin receptor, which can control iron metabolism, is frequently expressed in tumor cells.
As is well known, TfR1 binds to iron-loaded transferrin and plays a pivotal role in cellular uptake of iron as well as ferritin sequesters and stores the cellular iron.


Scientific Papers found: Click to Expand⟱
1069- AL,    Allicin promotes autophagy and ferroptosis in esophageal squamous cell carcinoma by activating AMPK/mTOR signaling
- vitro+vivo, ESCC, TE1 - vitro+vivo, ESCC, KYSE-510 - in-vitro, Nor, Het-1A
TumCP↓,
LC3‑Ⅱ/LC3‑Ⅰ↑,
p62↓,
p‑AMPK↑,
mTOR↓,
TumAuto↑,
NCOA4↑,
MDA↑,
Iron↑, elevated malondialdehyde and Fe2+ production levels
TumW↓,
TumVol↓,
ATG5↑,
ATG7↑,
TfR1/CD71↓,
FTH1↓, suppressed the expression of ferritin heavy chain 1 (the major intracellular iron-storage protein)
ROS↑,
Iron↑,
Ferroptosis↑,
*toxicity↓, 80 μg/mL allicin for 24 h did not change the viability of Het-1A cells. A slight reduction in cell viability was observed when Het-1A cells were treated with 160 μg/mL allicin for 24 h

5132- ART/DHA,    Dihydroartemisinin Exerts Its Anticancer Activity through Depleting Cellular Iron via Transferrin Receptor-1
- in-vitro, Liver, HepG2 - in-vitro, BC, MCF-7
Iron↓, In the current study, we found that dihydroartemisinin caused cellular iron depletion in time- and concentration-dependent manners.
TfR1/CD71↓, Moreover, dihydroartemisinin reduced the level of transferrin receptor-1 associated with cell membrane.
ROS↑, which may be a new action mechanism of DHA independently of oxidative damage.

576- ART/DHA,    Profiling of Multiple Targets of Artemisinin Activated by Hemin in Cancer Cell Proteome
- Analysis, NA, NA
GSTP1/GSTπ↓, IC50 value of 2 μM
TfR1/CD71↓,

3679- BBR,    Berberine alleviates Alzheimer's disease by activating autophagy and inhibiting ferroptosis through the JNK-p38MAPK signaling pathway
- in-vivo, AD, NA
*Beclin-1↑, autophagy-related markers Beclin1 and LC3B were upregulated and P62 was downregulated after BBR treatment.
*LC3B↑,
*p62↓,
*ROS↓, ROS and lipid peroxide MDA decreased significantly after BBR treatment.
*lipid-P↓,
*MDA↓,
*Ferroptosis↓, expression levels of ferroptosis-related genes TFR1, ASCL4, DMT1, and IREB2 were decreased, while the expression levels of FTH1 and SLC7A11 increased after BBR treatment.
*TfR1/CD71↓,
*FTH1↑,
*memory↑, BBR treatment enhanced spatial memory impairment in 5xFAD mice.
*JNK↓, inhibited ferroptosis by inhibiting the JNK-P38MAPK signaling pathway.
*p38↓,
*Aβ↓, further reducing Aβ plaque deposition, inhibiting inflammatory response,
*Inflam↓,

2426- GamB,    Anti-cancer natural products isolated from chinese medicinal herbs
- Review, Var, NA
TfR1/CD71↓, Transferrin receptor (TfR) significantly over-expressed in a variety of cancers cells may be the primary target of GA
MMP2↓, (MMP-2) and matrix metallopeptidase-9 (MMP-9) inhibition
MMP9↓,
ChemoSen↑, GA in combined use with 5-fluorouracil (5-FU) induced considerably higher apoptosis rates in BGC-823 human gastric cells and inhibited tumor growth in human xenografts

3803- Hup,    Huperzine A and Its Neuroprotective Molecular Signaling in Alzheimer’s Disease
- Review, AD, NA
*AChE↓, effects of this alkaloid have been attributed to its ability to inhibit the cholinergic enzyme acetylcholinesterase (AChE), acting as an acetylcholinesterase inhibitor (AChEI).
*neuroP↑, summarize the neuroprotective effects of HupA on AD,
*BBB↑, HupA is an unsaturated sesquiterpene alkaloid compound that effectively crosses the blood-brain barrier (BBB), acting as a mixed-competitive, reversible, and selective AChE inhibitor
*Half-Life↑, with a half-life of 5 h in the bloodstream, reaching a peak concentration at approximately 60 min in humans
*cognitive↑, hows evidence of improved cognition
*Dose↝, significant cognitive enhancement in patients receiving 0.4 mg of HupA twice a day.
*BACE↓, while downregulating the membrane translocation of BACE1
*IronCh↑, HupA might act directly as an Fe2+ chelator, reducing the capacity of IRP-1 to induce APP translation
*TfR1/CD71↓, HupA also downregulates TFR1 expression in mice in vivo, which reduces the uptake of transferrin-bound iron (TBI) in neurons
*ROS↓, HupA indirectly reduces ROS

4213- Hup,    Huperzine A-Liposomes Efficiently Improve Neural Injury in the Hippocampus of Mice with Chronic Intermittent Hypoxia
- in-vivo, NA, NA
*cognitive↑, HuA-LIP significantly ameliorated cognitive dysfunction and neuronal damage in CIH mice.
*SOD↑, HuA-LIP elevated T-SOD and GSH-Px abilities and decreased MDA content to resist oxidative stress damage induced by CIH.
*GPx↑,
*MDA↓,
*ROS↓,
*Iron↓, HuA-LIP reduced brain iron levels by downregulating TfR1, hepcidin, and FTL expression.
*TfR1/CD71↓,
*FTL↓,
*ERK↑, HuA-LIP activated the PKAα/Erk/CREB/BDNF signaling pathway and elevated MAP2, PSD95, and synaptophysin to improve synaptic plasticity.
*PKA↑,
*CREB↑,
*BDNF↑,
*PSD95↑,
*neuroP↑, HuA-LIP showed a superior performance against neuronal damage induced by CIH.

4209- Hup,    Huperzine A, reduces brain iron overload and alleviates cognitive deficit in mice exposed to chronic intermittent hypoxia
- in-vivo, NA, NA
*ROS↓, HuA improves synaptic plasticity and decreases ROS level in CIH mice
*cognitive↑, HuA significantly improved cognitive impairment and neuronal damage in the hippocampus of CIH mice via increasing the ratio of Bcl-2/Bax and inhibiting caspase-3 cleavage.
*neuroP↑,
*Bax:Bcl2↓,
*Casp3↑,
*NADPH↓, HuA considerably decreased ROS levels by downregulating the high levels of NADPH oxidase (NOX 2, NOX 4) mediated by CIH.
*NOX↓,
*TfR1/CD71↓, Decreased levels of TfR1 and FTL proteins observed in HuA treated CIH group, could reduce iron overload in hippocampus. HuA increased PSD 95 protein expression, CREB activation and BDNF protein expression
*Iron↓,
*PSD95↑,
*BDNF↑,

222- MFrot,  MF,    LF-MF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathway
- in-vitro, Lung, A549
TumCG↓,
OS↑,
miR-34a↑, enhanced miR-34a transcription
E2Fs↓, E2F1/E2F3
P53↑,
TfR1/CD71↓, TfR1 protein levels
Ferritin↓, inhibits iron metabolism

3039- RosA,    Rosmarinic acid liposomes suppress ferroptosis in ischemic brain via inhibition of TfR1 in BMECs
- in-vivo, Nor, NA - in-vivo, Stroke, NA
*Ferroptosis↓, RosA-LIP inhibited ferroptosis by ameliorating mitochondrial abnormalities, increasing GPX4 levels, and decreasing ACSL4/LPCAT3/Lox-dependent lipid peroxidation.
*GPx4↑,
*ACSL4↓,
*BBB↑, RosA-LIP effectively improved blood‒brain barrier (BBB) permeability, increased tight junctions (TJs) protein expression
*IronCh↑, reduced iron levels in ischemic tissue and brain microvascular endothelial cells (BMECs) by modulating FPN1 and TfR1 levels.
*TfR1/CD71↓, Furthermore, RosA-LIP suppressed TfR1 to attenuate ACSL4/LPCAT3/Lox-mediated ferroptosis in TfR1EC cKO mice subjected to dMCAO.
*neuroP↑, proposed neuroprotection of RosA-LIP during ischemic stroke.


Showing Research Papers: 1 to 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GSTP1/GSTπ↓, 1,   Iron↓, 1,   Iron↑, 2,   MDA↑, 1,   ROS↑, 2,  

Metal & Cofactor Biology ⓘ

Ferritin↓, 1,   FTH1↓, 1,   NCOA4↑, 1,   TfR1/CD71↓, 5,  

Core Metabolism/Glycolysis ⓘ

p‑AMPK↑, 1,   ATG7↑, 1,  

Cell Death ⓘ

Ferroptosis↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

E2Fs↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

miR-34a↑, 1,   mTOR↓, 1,   TumCG↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 1,   TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  

Clinical Biomarkers ⓘ

Ferritin↓, 1,  

Functional Outcomes ⓘ

OS↑, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 30

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↓, 2,   GPx↑, 1,   GPx4↑, 1,   Iron↓, 2,   lipid-P↓, 1,   MDA↓, 2,   ROS↓, 4,   SOD↑, 1,  

Metal & Cofactor Biology ⓘ

FTH1↑, 1,   FTL↓, 1,   IronCh↑, 2,   TfR1/CD71↓, 5,  

Core Metabolism/Glycolysis ⓘ

ACSL4↓, 1,   CREB↑, 1,   NADPH↓, 1,  

Cell Death ⓘ

Bax:Bcl2↓, 1,   Casp3↑, 1,   Ferroptosis↓, 2,   JNK↓, 1,   p38↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3B↑, 1,   p62↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,  

Migration ⓘ

PKA↑, 1,  

Barriers & Transport ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   BDNF↑, 2,   PSD95↑, 2,  

Protein Aggregation ⓘ

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,   Half-Life↑, 1,  

Functional Outcomes ⓘ

cognitive↑, 3,   memory↑, 1,   neuroP↑, 4,   toxicity↓, 1,  
Total Targets: 39

Scientific Paper Hit Count for: TfR1/CD71, Transferrin receptor protein 1,
3 Huperzine A/Huperzia serrata
2 Artemisinin
1 Allicin (mainly Garlic)
1 Berberine
1 Gambogic Acid
1 Magnetic Field Rotating
1 Magnetic Fields
1 Rosmarinic acid
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#:465  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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