PTCH1 Cancer Research Results

PTCH1, 12-transmembrane cell surface receptor Patched1: Click to Expand ⟱
Source: CGL-Driver
Type: TSG Gene
When not bound by Hh ligands, PTCH1 restrains the activity of Smo. The protein functions as a receptor protein for sonic hedgehog, desert hedgehog, and indian hedgehog proteins.
PTCH1 (Patched 1) is a gene that plays a crucial role in the Hedgehog signaling pathway, which is important for cell growth, differentiation, and tissue patterning during embryonic development. Mutations in the PTCH1 gene are associated with several types of cancer.

PTCH1 and PTCH2 act as tumor suppressors by maintaining control over Hedgehog signaling. Their loss—whether by mutation or reduced expression—leads to unchecked pathway activation, supporting cell proliferation and survival. Such abnormalities are associated with a more aggressive tumor phenotype and poorer clinical outcomes in cancers where the Hedgehog pathway is a driver of tumorigenesis.
Scientific Papers found: Click to Expand⟱
1- Aco,    Acoschimperoside P, 2'-acetate: a Hedgehog signaling inhibitory constituent from Vallaris glabra
- in-vitro, PC, PANC1 - in-vitro, Pca, DU145
HH↓, Compound 1 was active in the assay for Hedgehog signaling inhibition.
PTCH1↓, The expression of GLI-related proteins (PTCH and BCL-2) in a dose-dependent manner was also inhibited by 1.
Bcl-2↓,
Gli1↓,

7- BBR,    Berberine, a natural compound, suppresses Hedgehog signaling pathway activity and cancer growth
- vitro+vivo, MB, LS174T
HH↓, BBR significantly inhibited the Hh pathway activity.
Gli1∅, observations ruled out the possibility that BBR inhibited the Hh signaling pathway activity by targeting Gli.
PTCH1↓,
Smo↓, BBR inhibited the Hh pathway activity by targeting Smo,
TumCG↓, BBR inhibits the Hh-dependent medulloblastoma cell growth in vitro

8- BetA,    Hedgehog/GLI-mediated transcriptional inhibitors from Zizyphus cambodiana
- in-vitro, PC, HaCaT - in-vitro, Pca, PANC1
HH↓,
Gli1↓, The expressions of GLI-related proteins PTCH and BCL2 were clearly inhibited by 1 or 2.
PTCH1↓,
Bcl-2↓,

2736- BetA,  Chemo,    Multifunctional Roles of Betulinic Acid in Cancer Chemoprevention: Spotlight on JAK/STAT, VEGF, EGF/EGFR, TRAIL/TRAIL-R, AKT/mTOR and Non-Coding RNAs in the Inhibition of Carcinogenesis and Metastasis
- Review, Var, NA
chemoPv↑, reviews about cancer chemopreventive role of betulinic acid against wide variety of cancers [18,19,20,21].
p‑STAT3↓, betulinic acid reduced the levels of p-STAT3 in tumor tissues derived from KB cells
JAK1↓, Betulinic acid exerted inhibitory effects on the constitutive phosphorylation of JAK1 and JAK2
JAK2↓,
VEGF↓, betulinic acid mediated inhibition of VEGF
EGFR↓, evaluation of betulinic acid as a next-generation EGFR inhibitor
Cyt‑c↑, release of SMAC/DIABLO and cytochrome c from mitochondria in SHEP neuroblastoma cells
Diablo↑,
AMPK↑, Betulinic acid induced activation of AMPK and consequently reduced the activation of mTOR.
mTOR↓,
Sp1/3/4↓, Betulinic acid significantly reduced the quantities of Sp1, Sp3 and Sp4 in the tissues of the tumors derived from RKO cells
DNAdam↑, Betulinic acid efficiently triggered DNA damage (γH2AX) and apoptosis (caspase-3 and p53 phosphorylation) in temozolomide-sensitive and temozolomide-resistant glioblastoma cells.
Gli1↓, Betulinic acid effectively reduced GLI1, GLI2 and PTCH1 in RMS-13 cells.
GLI2↓,
PTCH1↓,
MMP2↓, betulinic acid exerted inhibitory effects on MMP-2 and MMP-9 in HepG2 cells.
MMP9↓,
miR-21↓, Collectively, p53 increased miR-21 levels and inhibited SOD2 levels, leading to significant increase in the accumulation of ROS levels and apoptotic cell death.
SOD2↓,
ROS↑,
Apoptosis↑,

12- CUR,    Curcumin inhibits the Sonic Hedgehog signaling pathway and triggers apoptosis in medulloblastoma cells
- in-vitro, MB, DAOY
HH↓, Curcumin inhibits the Sonic Hedgehog signaling pathway
Shh↓, curcumin inhibited the Shh-Gli1 signaling pathway by downregulating the Shh protein
Gli1↓,
PTCH1↓,
cMyc↓,
n-MYC↓,
cycD1/CCND1↓,
Bcl-2↓,
NF-kB↓,
Akt↓,
β-catenin/ZEB1↓, curcumin reduced the levels of beta-catenin
survivin↓,
Apoptosis↑, Consequently, apoptosis was triggered by curcumin through the mitochondrial pathway via downregulation of Bcl-2, a downstream anti-apoptotic effector of the Shh signaling.
ChemoSen↑, curcumin enhances the killing efficiency of nontoxic doses of cisplatin and gamma-rays.
RadioS↑,
eff↑, we present clear evidence that piperine, an enhancer of curcumin bioavailability in humans

19- Deg,    Deguelin inhibits proliferation and migration of human pancreatic cancer cells in vitro targeting hedgehog pathway
- in-vitro, PC, Bxpc-3 - in-vitro, PC, PANC1
HH↓, The activation of the hedgehog (Hh) signaling pathway, as well as matrix metalloproteinases (MMP)-2 and MMP-9, was suppressed by deguelin.
Gli1↓,
PTCH1↓,
Sufu↓,
MMP2↓, Deguelin downregulates MMP-2 and MMP-9 in Bxpc-3 and Panc-1 cells
MMP9↓,
PI3K/Akt↓,
HIF-1↓,
VEGF↓,
IKKα↓,
NF-kB↓,
EMT↓,
AMPK↑,
mTOR↓,
survivin↓,
TumCG↓, Deguelin treatment was observed to inhibit growth and induce apoptosis in two PC cell lines (Bxpc-3 and Panc-1)
Apoptosis↑,
TumCMig↓, Deguelin inhibits migration and invasion of PC cells
TumCI↓,

21- EGCG,    Tea polyphenols EGCG and TF restrict tongue and liver carcinogenesis simultaneously induced by N-nitrosodiethylamine in mice
- in-vivo, Liver, NA
HH↓, The up-regulation of self renewal Wnt/β-catenin, Hh/Gli1 pathways and their associated genes Cyclin D1, cMyc and EGFR along with down regulation of E-cadherin seen during the carcinogenesis processes were found to be modulated during the restriction
PTCH1↓,
Smo↓,
Gli1↓,
CD44↓, Both EGCG and TF significantly reduced (P b 0.05) CD44 positive cells in all the treated groups
β-catenin/ZEB1↓, GCG and TF could reduce β-catenin expression and its nu- clear activation in different cancers (

22- EGCG,    Inhibition of sonic hedgehog pathway and pluripotency maintaining factors regulate human pancreatic cancer stem cell characteristics
- in-vitro, PC, CD133+ - in-vitro, PC, CD44+ - in-vitro, PC, CD24+ - in-vitro, PC, ESA+
HH↓, EGCG also inhibited the components of Shh pathway (smoothened, patched, Gli1 and Gli2)
Smo↓,
PTCH1↓,
PTCH2↓,
Gli1↓,
GLI2↓,
Gli↓,
Bcl-2↓, inhibiting the expression of Bcl-2 and XIAP, and activating caspase-3
XIAP↓,
Shh↓,
survivin↓,
Casp3↑,
Casp7↑,
CSCs↓, EGCG inhibited the expression of pluripotency maintaining transcription factors (Nanog, c-Myc and Oct-4), and self-renewal capacity of pancreatic CSCs.
Nanog↓,
cMyc↓,
OCT4↓,
EMT↓, EGCG inhibited EMT by inhibiting the expression of Snail, Slug and ZEB1, and TCF/LEF transcriptional activity,
Snail↓,
Slug↓,
Zeb1↓,
TumCMig↓, significantly reduced CSC’s migration and invasion, suggesting the blockade of signaling involved in early metastasis.
TumCI↓,
eff↑, combination of quercetin with EGCG had synergistic inhibitory effects on self-renewal capacity of CSCs through attenuation of TCF/LEF and Gli activities

23- EGCG,    (-)-Epigallocatechin-3-gallate induces apoptosis and suppresses proliferation by inhibiting the human Indian Hedgehog pathway in human chondrosarcoma cells
- in-vitro, Chon, SW1353 - in-vitro, Chon, CRL-7891
HH↓, EGCG inhibited the human Indian Hedgehog pathway, down-regulated PTCH and Gli-1 levels,
Gli1↓,
PTCH1↓,
Bcl-2↓, Bcl-2 were significantly decreased and the levels of Bax were significantly increased.
BAX↑,
TumCG↓, EGCG is effective for growth inhibition of a chondrosarcoma cell lines in vitro, and suggest that EGCG may be a new therapeutic option for patients with chondrosarcoma.

31- GlaB,    Gli1/DNA interaction is a druggable target for Hedgehog-dependent tumors
- in-vitro, BCC, NA
HH↓, robust inhibitory effect on Gli1 activity, Glabrescione B inhibited the growth of Hedgehog-dependent tumor cells in vitro and in vivo
Gli1↓, GlaB inhibits Hh signaling by impairing Gli1 function
PTCH1↓,
CSCs↓, as well as the self-renewal ability and clonogenicity of tumor-derived stem cells.

32- GlaB,    Gli1/DNA interaction is a druggable target for Hedgehog-dependent tumors
- in-vivo, MB, NA
HH↓, GlaB inhibits Hh signaling by imparing Gli1/DNA binding and transcriptional activity
Gli1↓, impairing Gli1 activity by interfering with its interaction with DNA
PTCH1↓,
TumCG↓, Glabrescione B inhibited the growth of Hedgehog-dependent tumor cells in vitro and in vivo
CSCs↓, s well as the self-renewal ability and clonogenicity of tumor-derived stem cells.

34- PFB,    Naturally occurring small-molecule inhibitors of hedgehog/GLI-mediated transcription
- in-vitro, PC, PANC1
HH↓, 1, 9, 17, and 18 decreased Hh-related component expressions.
Gli1↓,
GLI2↓, We identified zerumbone (1), zerumbone epoxide (2), staurosporinone (9), 6-hydroxystaurosporinone (10), arcyriaflavin C (11) and 5,6-dihydroxyarcyriaflavin A (12) as inhibitors of GLI-mediated transcription.
PTCH1↓,
Bcl-2↓,

3098- RES,    Regulation of Cell Signaling Pathways and miRNAs by Resveratrol in Different Cancers
- Review, Var, NA
NOTCH2↓, resveratrol has been reported to target multiple proteins in ovarian cancer, markedly reducing NOTCH2 and HES1 in OVCAR-3 and CAOV-3 cells
Wnt↓, In CAOV-3 cells, resveratrol downregulated WNT2 and reduced the nuclear accumulation of β-catenin
β-catenin/ZEB1↓,
p‑SMAD2↓, Resveratrol effectively inhibits SMAD proteins
p‑SMAD3↓, Resveratrol has been reported to reduce phosphorylated-SMAD2/3 in colorectal cancer LoVo cells
PTCH1↓, PTCH, SMO, and GLI-1 were also inhibited in resveratrol-treated colorectal cancer HCT116 cells
Smo↓,
Gli1↓,
E-cadherin↑, resveratrol upregulated E-cadherin
NOTCH⇅, Although some reports document efficient inhibition of different proteins of the NOTCH pathway by resveratrol to inhibit cancer, there are conflicting reports that resveratrol can activate the NOTCH pathway, leading to its anticancer activity.
TAC?,
NKG2D↑, Resveratrol has been found to increase the cell-surface expression of NKG2D ligands and DR4 along
DR4↑,
survivin↓, Resveratrol dose-dependently downregulated survivin in HepG2 cells.
DR5↑, resveratrol upregulated DR4, DR5, Bax, and p27(/KIP1) and inhibited the expression of cyclin D1 and Bcl-2
BAX↑,
p27↑,
cycD1/CCND1↓,
Bcl-2↓,
STAT3↓, Resveratrol exerts inhibitory effects on the constitutive activation of STAT3 and STAT5.
STAT5↓,
JAK↓, Resveratrol has also been shown to prevent the activation of JAK,
DNAdam↑, Resveratrol induced DNA damage, as evidenced by the presence of multiple γ-H2AX foci after treatment with 25 μM resveratrol.
γH2AX↑,

102- RES,    Effect of resveratrol on proliferation and apoptosis of human pancreatic cancer MIA PaCa-2 cells may involve inhibition of the Hedgehog signaling pathway
- in-vitro, PC, MIA PaCa-2
HH↓, the levels of Ihh, Ptch and Smo were decreased by Res treatment
PTCH1↓,
Smo↓,
HH↓, Ihh
EMT↓,
PI3K/Akt↓, thru PI-3K/Akt/NF-κB↓
NF-kB↓,
TumCP↓, Res can inhibit the cell proliferative ability in a time- and dose-dependent manner.
Apoptosis↑, Res further induced apoptosis of MIA PaCa-2 cells in a dose-dependent manner.
ChemoSen↑, The apoptotic rate was significantly increased in cells treated with 5-Fu and Res, and the number of apoptotic cells increased with the increasing concentrations of Res

4900- Sal,    Anticancer Mechanisms of Salinomycin in Breast Cancer and Its Clinical Applications
- Review, BC, NA
CSCs↓, Salinomycin, a monocarboxylic polyether antibiotic isolated from Streptomyces albus, can precisely kill cancer stem cells (CSCs), particularly BCSCs, by various mechanisms, including apoptosis, autophagy, and necrosis.
Apoptosis↑,
TumAuto↑,
necrosis↑,
TumCP↓, salinomycin can inhibit cell proliferation, invasion, and migration in BC and reverse the immune-inhibitory microenvironment to prevent tumor growth and metastasis.
TumCI↓,
TumCMig↓,
TumCG↓,
TumMeta↓,
eff↑, Salinomycin is over 100 times more effective against BCSCs than paclitaxel, the traditional chemotherapy drug for the treatment of BC
Bcl-2↓, downregulation of Bcl-2 expression, and decreases their migration capacity, which is accompanied by downregulation of c-Myc and Snail expression
cMyc↓,
Snail↓,
ALDH↓, salinomycin reduces aldehyde dehydrogenase activity and the expression of MYC, AR, and ERG; it induces oxidative stress and inhibits nuclear factor (NF)-κB activity
Myc↓,
AR↓,
ROS↑, Salinomycin also induces autophagy by increasing intracellular ROS level, which is accompanied by MAPK signaling pathway activation
NF-kB↓,
PTCH1↓, significantly reduces tumor growth, which is accompanied by decreased PTCH, SMO, Gli1, and Gli2 expression
Smo↓,
Gli1↓,
GLI2↓,
Wnt↓, Figure 2
mTOR↓,
GSK‐3β↓,
cycD1/CCND1↓,
survivin↓,
P21↑,
p27↑,
CHOP↑,
Ca+2↑, cytosolic
DNAdam↑,
Hif1a↓,
VEGF↓,
angioG↓,
MMP↓, salinomycin can affect the cell membrane potential and reduce the level of ATP to induce mitophagy and mitoptosis.
ATP↓,
p‑P53↑, Salinomycin increases DNA breaks in BC cells as well as the expression of phosphorylated p53 and γH2AX in Hs578T cells.
γH2AX↑,
ChemoSen↑, Table 3 Synergistic anticancer co-action of salinomycin with other agents in BC.

107- SS,    Saikosaponin B1 and Saikosaponin D inhibit tumor growth in medulloblastoma allograft mice via inhibiting the Hedgehog signaling pathway
- vitro+vivo, MB, LS174T
HH↓, SSB1 and SSD inhibit Hedgehog signaling pathway activity in vitro
Smo↓, SSB1 and SSD potentially inhibit the Hedgehog pathway by targeting SMO
Gli↓, luciferase
Gli1↓,
PTCH1↓,
TumCG↓, Inhibition of cell proliferation and tumor growth tumor growth inhibition ratios were approximately 50% and 70%,

112- SuD,    Inhibition of Gli/hedgehog signaling in prostate cancer cells by “cancer bush” Sutherlandia frutescens extract
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
HH↓, S. frutescens extract (SLE) suppressed the Gli/Hh signaling in Shh Light II cell line
Gli1↓, S. frutescens extract also inhibited Gli/Hh signaling activity by reducing Gli1 and PTCH1 gene expression in TRAMP-C2 and PC3 cells
PTCH1↓,
TumCG↓, S. frutescens extract (SLE) inhibited the growth of human and mouse prostate cancer cell lines
chemoPv↑, Furthermore, major triterpenoids of S. frutescens are structurally related to cycloartane-type tritepenoids which have cancer chemopreventive activity (
eff↑, S. frutescens extract is potentially safe and effective for the prevention and treatment of advanced prostate cancers with upregulated Gli/Hh signaling activity.


Showing Research Papers: 1 to 17 of 17

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 17

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 2,   SOD2↓, 1,   TAC?, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   cMyc↓, 3,   PI3K/Akt↓, 2,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 5,   BAX↑, 2,   Bcl-2↓, 8,   Casp3↑, 1,   Casp7↑, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   DR4↑, 1,   DR5↑, 1,   Myc↓, 1,   necrosis↑, 1,   p27↑, 2,   survivin↓, 5,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

miR-21↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 3,   p‑P53↑, 1,   γH2AX↑, 2,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 3,   P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   CD44↓, 1,   CSCs↓, 4,   EMT↓, 3,   Gli↓, 2,   Gli1↓, 15,   Gli1∅, 1,   GSK‐3β↓, 1,   HH↓, 15,   mTOR↓, 3,   n-MYC↓, 1,   Nanog↓, 1,   NOTCH⇅, 1,   NOTCH2↓, 1,   OCT4↓, 1,   PTCH1↓, 17,   PTCH2↓, 1,   Shh↓, 2,   Smo↓, 7,   STAT3↓, 1,   p‑STAT3↓, 1,   STAT5↓, 1,   Sufu↓, 1,   TumCG↓, 7,   Wnt↓, 2,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↑, 1,   GLI2↓, 4,   MMP2↓, 2,   MMP9↓, 2,   Slug↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   Snail↓, 2,   TumCI↓, 3,   TumCMig↓, 3,   TumCP↓, 2,   TumMeta↓, 1,   Zeb1↓, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   HIF-1↓, 1,   Hif1a↓, 1,   VEGF↓, 3,  

Immune & Inflammatory Signaling ⓘ

IKKα↓, 1,   JAK↓, 1,   JAK1↓, 1,   JAK2↓, 1,   NF-kB↓, 4,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   eff↑, 4,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 1,   Myc↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 2,   NKG2D↑, 1,  
Total Targets: 91

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PTCH1, 12-transmembrane cell surface receptor Patched1
3 EGCG (Epigallocatechin Gallate)
2 Betulinic acid
2 Glabrescione B
2 Resveratrol
1 Acoschimperoside P, 2’-acetate
1 Berberine
1 Chemotherapy
1 Curcumin
1 Deguelin
1 Physalin F & B
1 salinomycin
1 Saikosaponin B1 and D
1 Sutherlandioside D
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

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