p65 Cancer Research Results

p65, RelA: Click to Expand ⟱
Source:
Type:
P65, also known as RelA, is a subunit of the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) transcription factor complex. NF-κB plays a crucial role in regulating immune response, inflammation, and cell survival.
Due to its role in cancer progression, p65 and the NF-κB pathway are considered potential therapeutic targets. Inhibitors of NF-κB signaling are being explored in preclinical and clinical studies as potential cancer treatments.
Many studies have reported that p65 is overexpressed in various types of cancers, including breast, prostate, lung, and colorectal cancers.
In some cancers, elevated p65 levels correlate with higher grades of tumors and advanced stages of disease.

"RELA proto-oncogene, NF-κB subunit." It encodes the p65 protein, which is a central component of the NF‑κB transcription factor complex.
-Chronic activation of RELA and the NF‑κB pathway is frequently associated with cancer progression, promoting inflammation-driven tumorigenesis, chemoresistance, and metastasis.
-RELA interacts with other oncogenic signaling networks (for example, STAT3 and MAPK pathways), further integrating environmental signals that favor cancer progression.

RELA (p65) is a critical subunit of the NF‑κB transcription factor complex, involved in the regulation of genes that control inflammation, cell survival, and proliferation. In the context of cancer, aberrant activation and overexpression of RELA are frequently associated with aggressive tumor behavior, therapy resistance, and poorer patient outcomes in cancers such as breast, lung, colorectal, and pancreatic cancers, among others.

RELA emerges as a potential key contributor to the suppression of glycolysis, mitochondrial respiration, and ATP production in cancer cells. (RELA knockdown signifcantly reduced the tumorigenic.
potential of various pancreatic cancer cell lines).
Park, Parkinson's Disease (PD): Click to Expand ⟱
Parkinson's disease (PD) is a neurodegenerative disorder characterized by motor and non-motor symptoms, and is due to the degeneration of dopaminergic neurons. It is multifactorial, caused by genetic and environmental factors and currently has no definitive cure.
-CoQ10 deficiency was observed at a higher frequency in Parkinson's disease
Scientific Papers found: Click to Expand⟱
3597- PI,    Chronic diseases, inflammation, and spices: how are they linked?
- Review, AD, NA - Review, Park, NA - Review, Var, NA
*NF-kB↓, *MAPK↓, *AP-1↓, *COX2↓, *NOS2↓, *IL1β↓, *TNF-α↓, *PGE2↓, *STAT3↓, *IL10↑, *IL4↓, *IL5↓, P53↑, MMP9↓, MMP2↓, cMyc↓, VEGF↓, STAT3↓, survivin↓, p65↓,
3003- RosA,    Comprehensive Insights into Biological Roles of Rosmarinic Acid: Implications in Diabetes, Cancer and Neurodegenerative Diseases
- Review, Var, NA - Review, AD, NA - Review, Park, NA
*Inflam↓, *antiOx↑, *neuroP↑, *IL6↓, *IL1β↓, *NF-kB↓, *PGE2↓, *COX2↓, *MMP↑, *memory↑, *ROS↓, *Aβ↓, *HMGB1↓, TumCG↓, MARK4↓, Zeb1↓, MDM2↓, BNIP3↑, ASC↑, NLRP3↓, PI3K↓, Akt↓, Casp1↓, E-cadherin↑, STAT3↓, TLR4↓, MMP↓, ICAM-1↓, AMPK↓, IL6↑, MMP2↓, Warburg↓, Bcl-xL↓, Bcl-2↓, TumCCA↑, EMT↓, TumMeta↓, mTOR↓, HSP27↓, Casp3↑, GlucoseCon↓, lactateProd↓, VEGF↓, p‑p65↓, GIT1↓, FOXM1↓, cycD1/CCND1↓, CDK4↓, MMP9↓, HDAC2↓,

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:


Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,   cMyc↓, 1,   GlucoseCon↓, 1,   lactateProd↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp1↓, 1,   Casp3↑, 1,   MDM2↓, 1,   survivin↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↓, 1,  

Autophagy & Lysosomes ⓘ

BNIP3↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   FOXM1↓, 1,   HDAC2↓, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↓, 2,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   GIT1↓, 1,   MARK4↓, 1,   MMP2↓, 2,   MMP9↓, 2,   TumMeta↓, 1,   Zeb1↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

ASC↑, 1,   ICAM-1↓, 1,   IL6↑, 1,   p65↓, 1,   p‑p65↓, 1,   TLR4↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Clinical Biomarkers ⓘ

FOXM1↓, 1,   IL6↑, 1,  
Total Targets: 43

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Cell Death ⓘ

MAPK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

STAT3↓, 1,  

Migration ⓘ

AP-1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   HMGB1↓, 1,   IL10↑, 1,   IL1β↓, 2,   IL4↓, 1,   IL5↓, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 2,   PGE2↓, 2,   TNF-α↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,   NOS2↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,   neuroP↑, 1,  
Total Targets: 22

Scientific Paper Hit Count for: p65, RelA
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:75  Cells:%  prod#:%  Target#:238  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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