RAS Cancer Research Results

RAS, RAS: Click to Expand ⟱
Source: CGL-CS
Type: oncogene
Family of RAS proteins (KRAS, NRAS, and HRAS) have been well described to cause oncogenic transformation.

- The expression and mutational status of RAS isoforms are critical in several cancers and are generally linked with a poorer prognosis when mutated.
RAS is one of the most frequently activated oncogenic drivers in human cancer. Mutations lock RAS in its GTP-bound active state, making signaling:
-Constitutive
-Growth-factor independent
-Resistant to normal feedback control

Key framing: RAS is a true driver oncogene, not just an amplifier.

Core Oncogenic Pathways Downstream of RAS
RAS sits at the apex of multiple essential signaling cascades:
a. MAPK Pathway (RAF–MEK–ERK)
-Drives proliferation
-Induces cell-cycle genes (Cyclin D, MYC, FOS/AP-1)
-Supports invasion and differentiation blockade

b. PI3K–AKT–mTOR
-Promotes survival and metabolic reprogramming
-Enhances resistance to apoptosis
-Supports protein synthesis and growth

c. RAL-GDS and Others
-Cytoskeletal remodeling
-Vesicle trafficking
-Metastatic behavior

Together, these create a multi-axis growth and survival program.


NA, Not Available: Click to Expand ⟱
none (reserved)
Scientific Papers found: Click to Expand⟱
1807- NarG,    A Systematic Review of the Preventive and Therapeutic Effects of Naringin Against Human Malignancies
- Review, NA, NA
AntiTum↑, TumCP↓, tumCV↓, TumCCA↑, Mcl-1↓, RAS↓, e-Raf↓, VEGF↓, AntiAg↑, MMP2↓, MMP9↓, TIMP2↑, TIMP1↑, p38↓, Wnt↓, β-catenin/ZEB1↑, Casp↑, P53↑, BAX↑, COX2↓, GLO-I↓, CYP1A1↑, lipid-P↓, p‑Akt↓, p‑mTOR↓, VCAM-1↓, P-gp↓, survivin↓, Bcl-2↓, ROS↑, ROS↑, MAPK↑, STAT3↓, chemoP↑,
3350- QC,    Quercetin and the mitochondria: A mechanistic view
- Review, NA, NA
*antiOx↑, *Inflam↓, *NRF2↑, ROS⇅, *NRF2↑, *HO-1↑, *PPARα↑, *PGC-1α↑, *SIRT1↑, *ATP↑, ATP↓, ERK↓, cl‑PARP↑, Casp9↑, Casp8↑, BAX↑, MMP↓, Cyt‑c↑, Casp3↑, HSP27↓, HSP72↓, RAS↓, Raf↓,

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:


Redox & Oxidative Stress ⓘ

CYP1A1↑, 1,   lipid-P↓, 1,   ROS↑, 2,   ROS⇅, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,   Raf↓, 1,   e-Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

GLO-I↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   BAX↑, 2,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   MAPK↑, 1,   Mcl-1↓, 1,   p38↓, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↓, 1,   HSP72↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   p‑mTOR↓, 1,   RAS↓, 2,   STAT3↓, 1,   Wnt↓, 1,  

Migration ⓘ

AntiAg↑, 1,   MMP2↓, 1,   MMP9↓, 1,   TIMP1↑, 1,   TIMP2↑, 1,   TumCP↓, 1,   VCAM-1↓, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   chemoP↑, 1,  
Total Targets: 45

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   HO-1↑, 1,   NRF2↑, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

PPARα↑, 1,   SIRT1↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  
Total Targets: 8

Scientific Paper Hit Count for: RAS, RAS
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:0  Cells:%  prod#:%  Target#:269  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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