AMP Cancer Research Results

AMP, Adenosine Monophosphate: Click to Expand ⟱
Source:
Type: nucleotide
AMP (Adenosine Monophosphate) is a nucleotide that plays a crucial role in various cellular processes, including energy metabolism, cell growth, and differentiation,
AMP is a key energy currency in cells, serving as a intermediate in the production of ATP (Adenosine Triphosphate) from ADP (Adenosine Diphosphate).
AMP expression associated with Tumor growth, angiogensis, metastasis
Scientific Papers found: Click to Expand⟱
2879- HNK,    Honokiol Inhibits Lung Tumorigenesis through Inhibition of Mitochondrial Function
- in-vitro, Lung, H226 - in-vivo, NA, NA
tumCV↓, honokiol significantly reduced the percentage of bronchial that exhibit abnormal lung SCC histology from 24.4% bronchial in control to 11.0% bronchial in honokiol treated group (p= 0.01) while protecting normal bronchial histology (present in 20.5%
selectivity↑,
TumCP↓, In vitro studies revealed that honokiol inhibited lung SCC cells proliferation, arrested cells at the G1/S cell cycle checkpoint, while also leading to increased apoptosis.
TumCCA↑,
Apoptosis↑,
mt-ROS↑, interfering with mitochondrial respiration is a novel mechanism by which honokiol increased generation of reactive oxygen species (ROS) in the mitochondria, : mitochondrial ROS generation
Casp3↑, cells treated with honokiol showed a significant increase in caspase 3/7 activity, which occurred in dose- and time-dependent manners
Casp7↑,
OCR↓, Honokiol caused a fast and concentration-dependent decrease in basal oxygen consumption rate (OCR) in both cell lines
Cyt‑c↑, cytochrome c release was increased in honokil treated mouse lung SCC tissue
ATP↓, found a dramatic decrease in cellular ATP content
mitResp↓, Honokiol inhibits mitochondrial respiration and decreases ATP levels in H226 and H520 cells, which may elevate AMP and the intracellular AMP/ATP ratio, leading to activation of the AMPK
AMP↑,
AMPK↑,

5800- MET,    Metformin as anticancer agent and adjuvant in cancer combination therapy: Current progress and future prospect
- Review, Var, NA
ChemoSen↑, Some combination therapy strategies including metformin combined with chemotherapy, radiotherapy, targeted therapy and immunotherapy have been proven to have more significant antitumor effects
RadioS↑,
Imm↑,
*AntiDiabetic↑, Metformin, the preferred glucose-lowering drug for patients with T2DM, is typically an adenosine monophosphate-activated protein kinase (AMPK) activator
*AMPK↑,
TumCP↓, AMPK restores the normal function of the liver and other tissues in diabetic patients as well as stops the metabolism of rapidly proliferating tumors
hepatoP↑,
ATP↓, . This leads to a decrease in intracellular ATP and an increase in AMP levels, which inhibits gluconeogenesis and further activates AMPK.
AMP↑,
glucoNG↓,
ROS↑, metformin can also promote reactive oxygen species (ROS) production by inhibiting mitochondrial respiratory-chain complex I, which can lead to DNA damage and gene mutation [23]
compI↓,
DNAdam↑,
CSCs↓, The advantage of metformin combined with chemotherapy is related to killing cancer stem cells [30].
NP/CIPN↓, metformin could improve the adverse effects of neuropathy (PN) in paclitaxel-treated breast cancer patients
chemoP↑, Thus, metformin may be able to be used as a chemoprotective agent, reducing the toxicity of chemotherapy and ameliorating adverse effects.
toxicity↓, The safety and tolerability of metformin were confirmed, but a large number of phase III clinical trials are still needed to follow up the study
Trx↓, Metformin radiosensitizes ductal breast cancer MCF7 cells by increasing intracellular reactive oxygen species (ROS) production through decreased thioredoxin (Trx) expression
eff↑, In addition, metformin may act in combination with the aspirin metabolite salicylic acid to enhance the proliferation inhibition of radiotherapy on prostate cancer
cycD1/CCND1↓, addition of metformin reduced the expression levels of cyclin D1, CDK4, CDK6, cyclin E, and CDK2 in gastric cancer cells
CDK4↓,
CDK6↓,
cycE/CCNE↓,
CDK2↓,

5609- NaHCO3,    Alkalization of cellular pH leads to cancer cell death by disrupting autophagy and mitochondrial function
- in-vitro, Var, NA
eff↑, We then reported that alternate infusion of bicarbonate and anticancer agent into tumors via tumor feeding artery markedly enhanced the efficacy of transarterial chemoembolization (TACE) in the local control of hepatocellular carcinoma (HCC).
e-pH↑, Alkalizing cellular pH by bicarbonate decreased pH gradient (ΔpH), membrane potential (ΔΨm), and proton motive force (Δp) across the inner membrane of mitochondria;
MMP↓,
OXPHOS↝, disruption of oxidative phosphorylation (OXPHOS) due to collapsed Δp
AMP↑, led to a significant increase in adenosine monophosphate (AMP), which activated the classical AMPK-mediated autophagy.
TumAuto↑,
MPT↑, Bicarbonate also induced persistent mitochondrial permeability (MPT) and damaged mitochondria.
mtDam↑,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

compI↓, 1,   OXPHOS↝, 1,   ROS↑, 1,   mt-ROS↑, 1,   Trx↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   mitResp↓, 1,   MMP↓, 1,   MPT↑, 1,   mtDam↑, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMP↑, 3,   AMPK↑, 1,   glucoNG↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Casp3↑, 1,   Casp7↑, 1,   Cyt‑c↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,  

Migration ⓘ

TumCP↓, 2,  

Immune & Inflammatory Signaling ⓘ

Imm↑, 1,  

Cellular Microenvironment ⓘ

e-pH↑, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 2,   RadioS↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   hepatoP↑, 1,   NP/CIPN↓, 1,   toxicity↓, 1,  
Total Targets: 39

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,  
Total Targets: 2

Scientific Paper Hit Count for: AMP, Adenosine Monophosphate
1 Honokiol
1 Metformin
1 Bicarbonate(Sodium)
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#:794  State#:%  Dir#:2
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