TOP1 Cancer Research Results

TOP1, Topoisomerase I: Click to Expand ⟱
Source:
Type:
Topoisomerase I (TOP1) is an essential nuclear enzyme involved in relieving DNA supercoiling during replication and transcription.
• Elevated TOP1 expression has been observed in several tumor types, such as colorectal, ovarian, breast, and lung cancers.
• Increased TOP1 levels may correlate with higher proliferation rates, as actively dividing tumor cells require efficient relief of DNA.

• In some cancers, high TOP1 expression has been associated with aggressive tumor behavior, higher grade, and potentially poorer clinical outcomes. This may be due in part to increased proliferation and/or a greater propensity for genomic instability.
• In other contexts, TOP1 expression might indicate sensitivity to TOP1-targeted therapies. For example, tumors with high TOP1 activity may respond better to chemotherapeutic agents (e.g., irinotecan) that target the enzyme, potentially improving outcomes when appropriate treatment is administered.

TOP1 is a critical enzyme in maintaining DNA integrity whose expression in cancers can reflect tumor proliferation and genomic instability. While high TOP1 expression is often associated with aggressive tumor behavior and poorer prognosis in several cancer types, it also has therapeutic relevance because tumors with elevated TOP1 may be more sensitive to TOP1 inhibitors.
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
5582- BetA,    Targeting mitochondrial apoptosis by betulinic acid in human cancers
- Review, Var, NA
Apoptosis↑, MMP↓, Cyt‑c↑, ROS↑, NF-kB↑, angioG↓, mtDam↑, TOP1↓, selectivity↑, ChemoSen↑, TumCG↓, chemoPv↑, RadioS↑,
2722- BetA,    Betulinic Acid for Cancer Treatment and Prevention
- Review, Var, NA
MMP↓, Cyt‑c↑, cl‑Casp3↑, cl‑Casp8↑, ROS↑, NF-kB↑, TOP1↓,
2735- BetA,    Betulinic acid as apoptosis activator: Molecular mechanisms, mathematical modeling and chemical modifications
- Review, Var, NA
mt-Apoptosis↑, Casp↑, p38↑, MAPK↓, JNK↓, VEGF↓, AIF↑, Cyt‑c↑, ROS↑, Ca+2↑, ATP↓, NF-kB↓, ATF3↓, TOP1↓, VEGF↓, survivin↓, Sp1/3/4↓, MMP↓, ChemoSen↑, selectivity↑, BioAv↓, BioAv↑, BioAv↑, BioAv↑, BioAv↑,
2737- BetA,    Multiple molecular targets in breast cancer therapy by betulinic acid
- Review, Var, NA
TumCP↓, Cyc↓, TOP1↓, TumCCA↑, angioG↓, NF-kB↓, Sp1/3/4↓, VEGF↓, MMPs↓, ChemoSen↑, eff↑, MMP↓, ROS↑, Bcl-2↓, Bcl-xL↓, Mcl-1↓, lipid-P↑, RadioS↑, eff↑,
2743- BetA,    Betulinic acid and the pharmacological effects of tumor suppression
- Review, Var, NA
ROS↑, MMP↓, Cyt‑c↑, Apoptosis↑, TumCCA↑, Sp1/3/4↓, STAT3↓, NF-kB↓, EMT↓, TOP1↓, MAPK↑, p38↑, JNK↑, Casp↑, Bcl-2↓, BAX↑, VEGF↓, LAMs↓,
2744- BetA,    Betulin and betulinic acid: triterpenoids derivatives with a powerful biological potential
- Review, Var, NA
Apoptosis↓, TumCCA↑, Casp9↑, Casp3↑, Casp7↑, cl‑PARP↑, MMP↓, ROS↑, TOP1↓, NF-kB↓,
2747- BetA,    Betulinic acid, a natural compound with potent anticancer effects
- Review, Var, NA
selectivity↑, Cyt‑c↑, *toxicity↓, TOP1↓, NF-kB↓, ROS↑, RadioS↑, ChemoSen↑,
2752- BetA,    Betulinic acid: a natural product with anticancer activity
- Review, Var, NA
selectivity↑, ChemoSen↑, RadioS↑, MMP↓, cl‑Casp3↑, Cyt‑c↑, ROS↑, NF-kB↑, TOP1↓,
2767- Bos,    The potential role of boswellic acids in cancer prevention and treatment
- Review, Var, NA
*Inflam↓, AntiCan↑, *MAPK↑, *Ca+2↝, p‑ERK↓, TumCI↓, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, p‑RB1↓, *NF-kB↓, *TNF-α↓, NF-kB↓, IKKα↓, MCP1↓, IL1α↓, MIP2↓, VEGF↓, Tf↓, COX2↓, MMP9↓, CXCR4↓, VEGF↓, eff↑, PPARα↓, lipid-P?, STAT3↓, TOP1↓, TOP2↑, 5HT↓, p‑PDGFR-BB↓, PDGF↓, AR↓, DR5↑, angioG↓, DR4↑, Casp3↑, Casp8↑, cl‑PARP↑, eff↑, chemoPv↑, Wnt↓, β-catenin/ZEB1↓, ascitic↓, Let-7↑, miR-200b↑, eff↑, MMP1↓, MMP2↓, eff↑, BioAv↓, BioAv↑, Half-Life↓, toxicity↓, Dose↑, BioAv↑, ChemoSen↑,
6026- CGA,    Chlorogenic Acid: The Conceivable Chemosensitizer Leading to Cancer Growth Suppression
- Review, Var, NA
ChemoSen↑, AMPK↑, EGFR↓, PI3K↓, mTOR↓, Hif1a↓, VEGF↓, MAPK↓, ERK↓, DNAdam↑, TOP1↓, TOP2↓, Apoptosis↑, *BioAv↝, *Half-Life↓,
2781- CHr,  PBG,    Chrysin a promising anticancer agent: recent perspectives
- Review, Var, NA
PI3K↓, Akt↓, mTOR↓, MMP9↑, uPA↓, VEGF↓, AR↓, Casp↑, TumMeta↓, TumCCA↑, angioG↓, BioAv↓, *hepatoP↑, *neuroP↑, *SOD↑, *GPx↑, *ROS↓, *Inflam↓, *Catalase↑, *MDA↓, ROS↓, BBB↑, Half-Life↓, BioAv↑, ROS↑, eff↑, ROS↑, ROS↑, lipid-P↑, ER Stress↑, NOTCH1↑, NRF2↓, p‑FAK↓, Rho↓, PCNA↓, COX2↓, NF-kB↓, PDK1↓, PDK3↑, GLUT1↓, Glycolysis↓, mt-ATP↓, Ki-67↓, cMyc↓, ROCK1↓, TOP1↓, TNF-α↓, IL1β↓, CycB/CCNB1↓, CDK2↓, EMT↓, STAT3↓, PD-L1↓, IL2↑,
2785- CHr,    Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin
- Review, Var, NA
*NF-kB↓, *COX2↓, *iNOS↓, angioG↓, TOP1↓, HDAC↓, TNF-α↓, IL1β↓, cardioP↑, RenoP↑, neuroP↑, LDL↓, BioAv↑, eff↑, cycD1/CCND1↓, hTERT/TERT↓, MMP-10↓, Akt↓, STAT3↓, VEGF↓, EGFR↓, Snail↓, Slug↓, Vim↓, E-cadherin↑, eff↑, TET1↑, ROS↑, mTOR↓, PPARα↓, ER Stress↑, Ca+2↑, ERK↓, MMP↑, Cyt‑c↑, Casp3↑, HK2↓, NRF2↓, HO-1↓, MMP2↓, MMP9↓, Fibronectin↓, GRP78/BiP↑, XBP-1↓, p‑eIF2α↑, *AST↓, ALAT↓, ALP↓, LDH↓, COX2↑, Bcl-xL↓, IL6↓, PGE2↓, iNOS↓, DNAdam↑, UPR↑, Hif1a↓, EMT↓, Twist↓, lipid-P↑, CLDN1↓, PDK1↓, IL10↓, TLR4↓, NOTCH1↑, PARP↑, Mcl-1↓, XIAP↓,
5809- CPT,    Cancer Therapies Utilizing the Camptothecins: A Review of in Vivo Literature
- Review, Var, NA
BioAv↓, TOP1↓, BioAv↑,
5808- CPT,    Repair of Topoisomerase I-Mediated DNA Damage
- Review, Var, NA
TOP1↓, AntiCan↑, Dose?, CHK1↑, Chk2↑,
2814- CUR,    Curcumin in Cancer and Inflammation: An In-Depth Exploration of Molecular Interactions, Therapeutic Potentials, and the Role in Disease Management
- Review, Var, NA
*BioAv↓, *Inflam↓, *antiOx↑, AntiCan↑, CK2↓, GSK‐3β↓, EGFR↓, TOP1↓, TOP2↓, NF-kB↓, COX2↓, CRP↓,
2832- FIS,    Fisetin's Promising Antitumor Effects: Uncovering Mechanisms and Targeting for Future Therapies
- Review, Var, NA
MMP↓, mtDam↑, Cyt‑c↑, Diablo↑, Casp↑, cl‑PARP↑, Bak↑, BIM↑, Bcl-xL↓, Bcl-2↓, P53↑, ROS↑, AMPK↑, Casp9↑, Casp3↑, BID↑, AIF↑, Akt↓, mTOR↓, MAPK↓, Wnt↓, β-catenin/ZEB1↓, TumCCA↑, P21↑, p27↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, TumMeta↓, uPA↓, E-cadherin↑, Vim↓, EMT↓, Twist↓, DNAdam↑, ROS↓, COX2↓, PGE2↓, HSF1↓, cFos↓, cJun↓, AP-1↓, Mcl-1↓, NF-kB↓, IRE1↑, ER Stress↑, ATF4↑, GRP78/BiP↑, MMP2↓, MMP9↓, TCF-4↓, MMP7↓, RadioS↑, TOP1↓, TOP2↓,
2906- LT,    Luteolin, a flavonoid with potentials for cancer prevention and therapy
- Review, Var, NA
*Inflam↓, AntiCan↑, antiOx⇅, Apoptosis↑, TumCP↓, TumMeta↓, angioG↓, PI3K↓, Akt↓, NF-kB↓, XIAP↓, P53↑, *ROS↓, *GSTA1↑, *GSR↑, *SOD↑, *Catalase↑, *other↓, ROS↑, Dose↝, chemoP↑, NF-kB↓, JNK↑, p27↑, P21↑, DR5↑, Casp↑, Fas↑, BAX↑, MAPK↓, CDK2↓, IGF-1↓, PDGF↓, EGFR↓, PKCδ↓, TOP1↓, TOP2↓, Bcl-xL↓, FASN↓, VEGF↓, VEGFR2↓, MMP9↓, Hif1a↓, FAK↓, MMP1↓, Twist↓, ERK↓, P450↓, CYP1A1↓, CYP1A2↓, TumCCA↑,

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 ⓘ

antiOx⇅, 1,   ATF3↓, 1,   CYP1A1↓, 1,   HO-1↓, 1,   lipid-P?, 1,   lipid-P↑, 3,   NRF2↓, 2,   ROS↓, 2,   ROS↑, 14,  

Metal & Cofactor Biology ⓘ

Tf↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 2,   ATP↓, 1,   mt-ATP↓, 1,   MMP↓, 8,   MMP↑, 1,   mtDam↑, 2,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMPK↑, 2,   cMyc↓, 1,   FASN↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   LDH↓, 1,   LDL↓, 1,   PDK1↓, 2,   PDK3↑, 1,   PPARα↓, 2,  

Cell Death ⓘ

Akt↓, 4,   Apoptosis↓, 1,   Apoptosis↑, 4,   mt-Apoptosis↑, 1,   Bak↑, 1,   BAX↑, 2,   Bcl-2↓, 3,   Bcl-xL↓, 4,   BID↑, 1,   BIM↑, 1,   Casp↑, 5,   Casp3↑, 4,   cl‑Casp3↑, 2,   Casp7↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 2,   Chk2↑, 1,   CK2↓, 1,   Cyt‑c↑, 8,   Diablo↑, 1,   DR4↑, 1,   DR5↑, 2,   Fas↑, 1,   hTERT/TERT↓, 1,   iNOS↓, 1,   JNK↓, 1,   JNK↑, 2,   MAPK↓, 4,   MAPK↑, 1,   Mcl-1↓, 3,   p27↑, 2,   p38↑, 2,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 3,  

Transcription & Epigenetics ⓘ

cJun↓, 1,  

Protein Folding & ER Stress ⓘ

p‑eIF2α↑, 1,   ER Stress↑, 3,   GRP78/BiP↑, 2,   HSF1↓, 1,   IRE1↑, 1,   UPR↑, 1,   XBP-1↓, 1,  

DNA Damage & Repair ⓘ

CHK1↑, 1,   DNAdam↑, 3,   P53↑, 2,   PARP↑, 1,   cl‑PARP↑, 3,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 4,   CDK4↓, 2,   Cyc↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   cycE/CCNE↓, 2,   P21↑, 2,   p‑RB1↓, 1,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

cFos↓, 1,   EMT↓, 4,   ERK↓, 3,   p‑ERK↓, 1,   GSK‐3β↓, 1,   HDAC↓, 1,   IGF-1↓, 1,   Let-7↑, 1,   mTOR↓, 4,   NOTCH1↑, 2,   PI3K↓, 3,   STAT3↓, 4,   TCF-4↓, 1,   TOP1↓, 17,   TOP2↓, 4,   TOP2↑, 1,   TumCG↓, 1,   Wnt↓, 2,  

Migration ⓘ

AP-1↓, 1,   Ca+2↑, 2,   CLDN1↓, 1,   E-cadherin↑, 2,   FAK↓, 1,   p‑FAK↓, 1,   Fibronectin↓, 1,   Ki-67↓, 1,   LAMs↓, 1,   miR-200b↑, 1,   MMP-10↓, 1,   MMP1↓, 2,   MMP2↓, 3,   MMP7↓, 1,   MMP9↓, 4,   MMP9↑, 1,   MMPs↓, 1,   PDGF↓, 2,   PKCδ↓, 1,   Rho↓, 1,   ROCK1↓, 1,   Slug↓, 1,   Snail↓, 1,   TET1↑, 1,   TumCI↓, 1,   TumCP↓, 2,   TumMeta↓, 3,   Twist↓, 3,   uPA↓, 2,   Vim↓, 2,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 6,   ATF4↑, 1,   EGFR↓, 4,   Hif1a↓, 3,   p‑PDGFR-BB↓, 1,   VEGF↓, 10,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 4,   COX2↑, 1,   CRP↓, 1,   CXCR4↓, 1,   IKKα↓, 1,   IL10↓, 1,   IL1α↓, 1,   IL1β↓, 2,   IL2↑, 1,   IL6↓, 1,   MCP1↓, 1,   MIP2↓, 1,   NF-kB↓, 11,   NF-kB↑, 3,   PD-L1↓, 1,   PGE2↓, 2,   TLR4↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 2,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 4,   BioAv↑, 9,   ChemoSen↑, 7,   CYP1A2↓, 1,   Dose?, 1,   Dose↑, 1,   Dose↝, 1,   eff↑, 9,   Half-Life↓, 2,   P450↓, 1,   RadioS↑, 5,   selectivity↑, 4,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AR↓, 2,   ascitic↓, 1,   CRP↓, 1,   EGFR↓, 4,   hTERT/TERT↓, 1,   IL6↓, 1,   Ki-67↓, 1,   LDH↓, 1,   PD-L1↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 4,   cardioP↑, 1,   chemoP↑, 1,   chemoPv↑, 2,   neuroP↑, 1,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 195

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 2,   GPx↑, 1,   GSR↑, 1,   GSTA1↑, 1,   MDA↓, 1,   ROS↓, 2,   SOD↑, 2,  

Cell Death ⓘ

iNOS↓, 1,   MAPK↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,  

Migration ⓘ

Ca+2↝, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 4,   NF-kB↓, 2,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↝, 1,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

AST↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,   neuroP↑, 1,   toxicity↓, 1,  
Total Targets: 23

Scientific Paper Hit Count for: TOP1, Topoisomerase I
8 Betulinic acid
2 Chrysin
2 Camptothecin
1 Boswellia (frankincense)
1 Chlorogenic acid
1 Propolis -bee glue
1 Curcumin
1 Fisetin
1 Luteolin
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:26  Cells:%  prod#:%  Target#:1117  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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