PTN Cancer Research Results

PTN, Pleiotrophin, HARP, HBNF, HB-GAM, HBGF8, NEGF1: Click to Expand ⟱
Source:
Type:

PTN - Pleiotrophin

Abbreviation: PTN

Alternative Names: Pleiotrophin, HARP, HBNF, HB-GAM, HBGF8, NEGF1

Type: Secreted heparin-binding growth factor / cytokine-like signaling protein / angiogenic factor

Function: Pleiotrophin is a secreted heparin-binding growth factor that regulates cell growth, survival, migration, differentiation, neurite outgrowth, angiogenesis, and tissue remodeling. PTN can signal through receptors including PTPRZ1/RPTPβζ and can influence downstream pathways involving ALK, Fyn, β-catenin, PKC, and other signaling proteins.

Cancer: ↑ PTN is overexpressed in multiple cancers and can promote tumor-cell proliferation, survival, migration, invasion, angiogenesis, metastasis, and remodeling of the tumor microenvironment. High PTN expression has been associated with advanced tumor stage and poorer overall survival in several cancer types.

Favorable Direction in Cancer: ↓ PTN expression or signaling is generally favorable where PTN drives tumor growth, angiogenesis, invasion, or metastasis.
Scientific Papers found: Click to Expand⟱
8384- LT,    Current situation and research progress of luteolin in the treatment of gastrointestinal malignant tumors
- Review, GC, NA
Apoptosis↑, TumAuto↑, TumCCA↑, EMT↓, *ROS↓, *antiOx↑, ROS↑, P53↑, LC3II↑, Beclin-1/ATG6↑, p‑MAP2K1/MEK1↓, p‑ERK↓, BAX↑, cl‑Casp3↑, Bcl-2↓, p‑MAPK↓, DNArepair↓, HMGB1↓, XRCC1↓, ERCC3↑, CycB/CCNB1↓, CDC2↓, p‑CHK1↑, TumCCA↑, TumCP?, Wnt↓, β-catenin/ZEB1↓, miR-384↑, PTN↓, MMP2↓, MMP3↓, MMP9↓, MMP16↓, Ferroptosis↑, GPx4↓, eff↑, Ki-67↓, GSH↓, ChemoSen↑, TumCP↓, TumCMig↓, TumCI↓, PI3K↓, Akt↓, mTOR↓, NF-kB↓, NOTCH↓, miR-139-5p↑, miR-34a↑, miR-422a↑, miR-107↑, miR-21↓, miR-155↓, miR-224↓, miR-340↓, E-cadherin↑, N-cadherin↓, Vim↓, HK1↓, FOXO1↓, compI↓, compIII↓, compV↓, ETC↓, BioAv↝,

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:


NA, unassigned(tgid=0) ⓘ

compV↓, 1,   ERCC3↑, 1,   miR-107↑, 1,   miR-224↓, 1,   miR-422a↑, 1,   MMP16↓, 1,   PTN↓, 1,   XRCC1↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

compI↓, 1,   Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   HK1↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC2↓, 1,   compIII↓, 1,   ETC↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   cl‑Casp3↑, 1,   Ferroptosis↑, 1,   p‑MAPK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

miR-21↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1/ATG6↑, 1,   LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

p‑CHK1↑, 1,   DNArepair↓, 1,   P53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CycB/CCNB1↓, 1,   TumCCA↑, 2,  

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

EMT↓, 1,   p‑ERK↓, 1,   FOXO1↓, 1,   p‑MAP2K1/MEK1↓, 1,   miR-34a↑, 1,   mTOR↓, 1,   NOTCH↓, 1,   PI3K↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

E-cadherin↑, 1,   Ki-67↓, 1,   miR-139-5p↑, 1,   miR-155↓, 1,   miR-340↓, 1,   miR-384↑, 1,   MMP2↓, 1,   MMP3↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP?, 1,   TumCP↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

HMGB1↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   ChemoSen↑, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Ki-67↓, 1,  
Total Targets: 64

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↓, 1,  
Total Targets: 2

Scientific Paper Hit Count for: PTN, Pleiotrophin, HARP, HBNF, HB-GAM, HBGF8, NEGF1
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#:1819  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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