Smo Cancer Research Results

Smo, G-protein-coupled receptor-like 7-pass transmembrane protein Smoothened: Click to Expand ⟱
Source: CGL-Driver Genes
Type: HH Oncogene
Smoothened homolog (Drosophila)
SMO, or Smoothened, is a protein that plays a crucial role in the Hedgehog signaling pathway, which is important for cell growth, differentiation, and tissue patterning during embryonic development. Inhibitors of SMO, such as vismodegib and sonidegib, have been developed as targeted therapies for cancers associated with aberrant Hedgehog signaling.
SMO (Smoothened):
- A G protein-coupled receptor (GPCR)-like protein that is a critical component of the Hedgehog (Hh) signaling pathway.
- Functions in transmitting the Hedgehog signal from the cell surface to intracellular effectors, culminating in changes in gene expression.
Aberrant Activation of the Hedgehog Pathway:
- In many cancers, mutations or dysregulations in pathway components lead to ligand-independent or ligand-dependent activation of SMO.
- This inappropriate activation can result in enhanced cell proliferation, survival, and stem cell-like
Several cancers exhibit overexpression of SMO or activating mutations leading to Hedgehog pathway activation.
Smoothened (SMO) is a critical mediator of the Hedgehog signaling pathway, with aberrant activation contributing to tumor growth, progression, and resistance to therapy. High expression or activating mutations in SMO are linked with a poor prognosis in certain cancer types, particularly in cancers that are dependent on Hedgehog pathway signaling such as basal cell carcinoma and medulloblastoma. By targeting SMO with specific inhibitors, researchers and clinicians are addressing one of the key drivers of tumorigenesis in these settings.
Scientific Papers found: Click to Expand⟱
8010- itraC,    Itraconazole induces apoptosis and cell cycle arrest via inhibiting Hedgehog signaling in gastric cancer cells
- vitro+vivo, GC, MKN45
TumCP↓, Itraconazole could remarkably inhibit the proliferation of gastric cancer cells
ChemoSen↑, When in combination with 5-FU, itraconazole significantly reduced the proliferation rate of cancer cells.
TumCCA↑, itraconazole could regulate the G1-S transition and induce apoptosis of gastric cancer cells.
Apoptosis↑,
Gli1↓, expression of glioma-associated zinc finger transcription factor 1 (Gli1) was decreased at both transcriptional and translational levels after treatment with itraconazole.
TumCG↓, In vivo studies demonstrated that monotherapy with itraconazole by oral administration could inhibit the growth of xenografts, and that itraconazole could significantly enhance the antitumor efficacy of the chemotherapeutic agent 5-FU.
HH↓, Itraconazole regulates Hh signaling by inhibition of Gli1 transcription
Smo∅, Smo was unchanged in itraconazole-treated gastric cancer cells


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Gli1↓, 1,   HH↓, 1,   Smo∅, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,  
Total Targets: 8

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Smo, G-protein-coupled receptor-like 7-pass transmembrane protein Smoothened
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#:287  State#:%  Dir#:6
  wNotes=on  sortOrder:rid,rpid

 

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