ADAM17 Cancer Research Results

ADAM17, A Disintegrin and Metalloprotease 17: Click to Expand ⟱
Source:
Type:
ADAM17 (A Disintegrin and Metalloprotease 17), also known as TACE (Tumor Necrosis Factor-α Converting Enzyme), is a membrane-anchored protease.
– It is best known for cleaving and releasing the extracellular domains (ectodomains) of various cell surface proteins, a process called “ectodomain shedding.”

Numerous studies have documented increased ADAM17 expression in several cancers, such as breast, lung, colon, and pancreatic cancers.
– Upregulation often correlates with enhanced release of growth factors (e.g., EGF family ligands) and cytokines that may drive tumor growth and modify the tumor microenvironment.
– Higher levels of ADAM17 have been linked with more aggressive tumor characteristics, including increased invasiveness, metastasis, and resistance to certain therapies.
– In cancers such as breast and lung, elevated ADAM17 expression is often associated with poor clinical prognosis.


Scientific Papers found: Click to Expand⟱
1091- GA,    Gallic acid reduces cell viability, proliferation, invasion and angiogenesis in human cervical cancer cells
- in-vitro, Cerv, HeLa - in-vitro, Cerv, HTB-35
tumCV↓, decreased cell viability in a dose-dependent manner.
TumCP↓,
ADAM17↓,
EGFR↓,
p‑Akt↓,
p‑ERK↓,

3047- SK,    Shikonin suppresses colon cancer cell growth and exerts synergistic effects by regulating ADAM17 and the IL-6/STAT3 signaling pathway
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW48
TumCG↓, SKN inhibited colon cancer cell growth, suppressed both constitutive and IL-6-induced STAT3 phosphorylation, and downregulated the expression of ADAM17
p‑STAT3↓,
ADAM17↓,
Apoptosis↑, SKN promoted cell apoptosis, as evidenced by increased expression levels of cleaved caspase-3 and cleaved PARP in both cell lines
Casp3↑,
cl‑PARP↑,
cycD1/CCND1↓, SKN decreased the expression of cyclin D1 and cyclin E1, thus suggesting the disruption of the cell cycle and the suppression of cell growth
cycE/CCNE↓,
TumCCA↑,
JAK1?, The inhibitory effects of SKN on the phosphorylation of both JAK1 and JAK2 in the two cell lines were also observed
p‑JAK1↓,
p‑JAK2↓,
p‑eIF2α↑, phosphorylation levels of eIF2α were enhanced by SKN (20 µM) in the HCT116 and SW480 colon cancer cells
eff↓, NAC decreased SKN-induced p-eIF2α expression and reversed the SKN-mediated downregulation of ADAM17 protein expression
ROS↑, suppressed the expression of ADAM17 mediated by ROS-associated p-eIF2α expression in the HCT116 and SW480 colon cancer cells
IL6↓, demonstrated that the antitumor effects of SKN on colon cancer cells were associated with its inhibition of the IL-6/STAT3 signaling pathway.


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

ROS↑, 1,  

Cell Death

p‑Akt↓, 1,   Apoptosis↑, 1,   Casp3↑, 1,  

Transcription & Epigenetics

tumCV↓, 1,  

Protein Folding & ER Stress

p‑eIF2α↑, 1,  

DNA Damage & Repair

cl‑PARP↑, 1,  

Cell Cycle & Senescence

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

Proliferation, Differentiation & Cell State

p‑ERK↓, 1,   p‑STAT3↓, 1,   TumCG↓, 1,  

Migration

TumCP↓, 1,  

Angiogenesis & Vasculature

EGFR↓, 1,  

Immune & Inflammatory Signaling

IL6↓, 1,   JAK1?, 1,   p‑JAK1↓, 1,   p‑JAK2↓, 1,  

Cellular Microenvironment

ADAM17↓, 2,  

Drug Metabolism & Resistance

eff↓, 1,  

Clinical Biomarkers

EGFR↓, 1,   IL6↓, 1,  
Total Targets: 23

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ADAM17, A Disintegrin and Metalloprotease 17
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#:994  State#:%  Dir#:1
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