Fap1 Cancer Research Results
Fap1, PTPN13: Click to Expand ⟱
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Fas-associated phosphatase-1 (Fap-1), also known as PTPN13 (protein tyrosine phosphatase non-receptor type 13).
Fap-1 negatively regulates Fas-mediated apoptosis by dephosphorylating or modulating components of the Fas signaling pathway. Overexpression of Fap-1 in tumor cells can result in resistance to apoptosis, potentially contributing to tumor cell survival and resistance to therapy.
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Scientific Papers found: Click to Expand⟱
TumCG↓, Exposure to capsaicin inhibited cancer cell growth and increased G1 phase cell cycle arrest.
TumCCA↑,
TumAuto↑, induced autophagy via involvement of the class III PI3K/Beclin-1/Bcl-2 signaling pathway.
Casp3↑, increasing caspase-3 activity to induce apoptosis
Ca+2↑, involves increased intracellular Ca2+ levels [19,24], the generation of reactive oxygen species
ROS↑,
MMP↓, disruption of mitochondrial membrane potential
LC3‑Ⅱ/LC3‑Ⅰ↑, Capsaicin Upregulates LC3-II and Atg5 Expression and Downregulates p62 and Fap-1 Expression in NPC-TW01 Cells
ATG5↑,
p62↓,
Fap1↓,
PI3K↓, Capsaicin Inhibits PI3K Expression and the Phosphorylation of Downstream Effectors of the PI3K/Akt/mTOR Pathway in NPC-TW01 Cells
DNAdam↑, have found that capsaicin may induce DNA and chromosomal damage in human lung (A549) and prostate (DU145) cancer cells
chemoPv↑, Capsaicin has shown significant prospects as an effective chemopreventive agent
Ca+2↑, Capsaicin was shown to cause upstream activation of Ca2+
antiOx↑, Another plausible mechanism implicated in the chemopreventive action of capsaicin is its anti-oxidative effects.
*ROS↓, capsaicin inhibits ROS release and the subsequent mitochondrial membrane potential collapse, cytochrome c expression, chromosome condensation, and caspase-3 activation induced by oxidized low-density lipoprotein in normal human HUVEC cells
*MMP∅,
*Cyt‑c∅,
*Casp3∅,
*eff↑, dietary curcumin and capsaicin concurrent administration in high-fat diet-fed rats were shown to mitigate the testicular and hepatic antioxidant status by increasing GSH levels, glutathione transferase activity, and Cu-ZnSOD expression
*Inflam↓, Anti-inflammation is another mechanism implicated in the chemopreventive action of capsaicin.
*NF-kB↓, inhibition of NF-kB by capsaicin
*COX2↓, compound elicits COX-2 enzyme activity inhibition and downregulation of iNOS
iNOS↓,
TRPV1↑, major pro-apoptotic mechanisms of capsaicin is via the vanilloid receptors, primarily TRPV1
i-Ca+2?, causing a concomitant influx of Ca2+: severe condition of mitochondria calcium overload. at high concentration (> 10 µM), capsaicin induces a slow but persistent increase in intracellular Ca2+
MMP↓, depolarization of mitochondria membrane potential
Cyt‑c↑, release of cytochrome C
Bax:Bcl2↑, activation of Bax and p53 through C-jun N-terminal kinase (JNK) activation
P53↑,
JNK↑,
PI3K↓, blocking the Pi3/Akt/mTOR signalling pathway, capsaicin increases levels of autophagic markers (LC3-II and Atg5)
Akt↓,
mTOR↓,
LC3II↑,
ATG5↑,
p62↑, enhances p62 and Fap-1 degradation and increases caspase-3 activity to induce apoptosis in human nasopharyngeal carcinoma cells
Fap1↓,
Casp3↑,
Apoptosis↑,
ROS↑, generation of ROS in human hepatoma (HepG2 cells)
MMP9↓, inhibition of MMP9 by capsaicin occurs via the suppression of AMPK-NF-κB, EGFR-mediated FAK/Akt, PKC/Raf/ERK, p38 MAPK, and AP-1 signaling pathway
eff↑, capsaicin 8% patch could promote the regeneration and restoration of skin nerve fibres in chemotherapy-induced peripheral neuropathy in addition to pain relief
eff↓, capsaicin has shown several unpleasant side effects, including stomach cramps, skin and gastric irritation, and burning sensation
eff↑, liposomes and micro-emulsion-based drugs have been known to significantly improve oral bioavailability and reduce the irritation of drugs
selectivity↑, In addition, these delivery systems can be surfaced-modified to perform site-directed/cell-specific drug delivery, thereby ensuring increased cell death of cancer cells while sparing non-selective normal cells
eff↑, Furthermore, owing to its antioxidant potential, capsaicin has been applied as a bioreduction and capping agent to synthesize biocompatible silver nanoparticles
ChemoSen↑, capsaicin has been combined with other anticancer therapies for more pronounced anticancer effects
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:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, ROS↑, 2,
Mitochondria & Bioenergetics ⓘ
MMP↓, 2,
Cell Death ⓘ
Akt↓, 1, Apoptosis↑, 1, Bax:Bcl2↑, 1, Casp3↑, 2, Cyt‑c↑, 1, Fap1↓, 2, iNOS↓, 1, JNK↑, 1, TRPV1↑, 1,
Autophagy & Lysosomes ⓘ
ATG5↑, 2, LC3‑Ⅱ/LC3‑Ⅰ↑, 1, LC3II↑, 1, p62↓, 1, p62↑, 1, TumAuto↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1, P53↑, 1,
Cell Cycle & Senescence ⓘ
TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
mTOR↓, 1, PI3K↓, 2, TumCG↓, 1,
Migration ⓘ
Ca+2↑, 2, i-Ca+2?, 1, MMP9↓, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 1, eff↓, 1, eff↑, 3, selectivity↑, 1,
Functional Outcomes ⓘ
chemoPv↑, 1,
Total Targets: 32
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
ROS↓, 1,
Mitochondria & Bioenergetics ⓘ
MMP∅, 1,
Cell Death ⓘ
Casp3∅, 1, Cyt‑c∅, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, Inflam↓, 1, NF-kB↓, 1,
Drug Metabolism & Resistance ⓘ
eff↑, 1,
Total Targets: 8
Scientific Paper Hit Count for: Fap1, PTPN13
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#:1229 State#:% Dir#:1
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