Rictor Cancer Research Results

Rictor, Rapamycin-insensitive companion of mTOR: Click to Expand ⟱
Source:
Type:

Rapamycin-insensitive companion of mTOR (RICTOR) is an essential scaffold component of mTOR complex 2 (mTORC2). RICTOR enables mTORC2-dependent signalling through substrates including AKT, particularly AKT phosphorylation at Ser473, as well as SGK and protein kinase C family members. In many cancers, RICTOR expression, amplification, or activity ↑ promotes cell survival, proliferation, metabolism, migration, invasion, metastasis, and treatment resistance. Conversely, RICTOR knockdown, degradation, or mTORC2 inhibition ↓ commonly reduces AKT Ser473 phosphorylation and suppresses tumour-cell growth and motility. Record RICTOR gene amplification, mRNA expression, protein abundance, and mTORC2 activity as separate endpoints when available. RICTOR is separate from RPTOR/Raptor, which is a component of mTORC1. Cancer review; RICTOR and RTK signalling review.
-Typical cancer direction: RICTOR/mTORC2 ↑ = usually adverse; RICTOR/mTORC2 ↓ = usually anticancer.



Scientific Papers found: Click to Expand⟱
6984- Form,    Formononetin suppresses colitis-associated colon cancer by targeting lipid synthesis and mTORC2/Akt signaling
- in-vitro, Colon, HCT116 - Review, IBD, RAW264.7
*Inflam↓, Modern research highlights Formononetin (FN) for its significant anti-inflammatory and extensively studied anti-cancer properties;
AntiCan↑,
*NF-kB↓, FN can inhibit the activation of the NF-κB/MAPK signaling pathways in LPS-induced RAW264.7 cells, thereby exerting its anti-inflammatory effects.
*MAPK↓,
*colonLen↑, FN significantly enhanced the colon length and DAI score in mice, notably suppressed the production of inflammatory cytokines, and inhibited the NF-κB/MAPK signaling pathway, leading to an improvement in DSS-induced colitis.
TumCG↓, FN significantly inhibited CT-26 and HCT116 cell growth, reduced tumor growth rate, improved pathological damage in CAC mice, and inhibited inflammatory factor production, enhancing intestinal mucosa protection.
Apoptosis↑, FN promoted apoptosis of colon cancer cells by increasing autophagy proteins (LC3, Beclin-1) and apoptosis proteins (CL-Caspase3, Bax), while reducing Bcl-2 expression.
LC3II↑,
Beclin-1↑,
cl‑Casp3↑,
BAX↑,
Bcl-2↓,
IGF-1↓, FN reduced IGF-1, ACLY, A-CoA, FAS, HSL, ATGL, and FFA levels, and increased GSK-3 levels
ACLY↓,
Acetyl-CoA↓,
Fas↓,
HSL/LIPE↓,
ATGL/PNPLA2↓,
FFA/NEFA↓,
GSK‐3β↑,
p‑mTOR↓, FN also inhibited the expression of P-mTOR, Rictor, P-Akt, ACLY, PDE3B, P-PKA, and P-HSL
Rictor↓,
p‑Akt↓,
PDE3B↓,
p‑PKA↓,
p‑HSL/LIPE↑,
TumAuto↑, FN significantly inhibits colon cancer cell growth and exerts anti-CAC effects by activating autophagy and apoptosis pathways and regulating lipid metabolism.


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)

ATGL/PNPLA2↓, 1,   FFA/NEFA↓, 1,   HSL/LIPE↓, 1,   p‑HSL/LIPE↑, 1,   PDE3B↓, 1,   Rictor↓, 1,  

Core Metabolism/Glycolysis(tgid=4)

Acetyl-CoA↓, 1,   ACLY↓, 1,  

Cell Death(tgid=5)

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

Autophagy & Lysosomes(tgid=9)

Beclin-1↑, 1,   LC3II↑, 1,   TumAuto↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

GSK‐3β↑, 1,   IGF-1↓, 1,   p‑mTOR↓, 1,   TumCG↓, 1,  

Migration(tgid=13)

p‑PKA↓, 1,  

Functional Outcomes(tgid=23)

AntiCan↑, 1,  
Total Targets: 23

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0)

colonLen↑, 1,  

Cell Death(tgid=5)

MAPK↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

Inflam↓, 1,   NF-kB↓, 1,  
Total Targets: 4

Scientific Paper Hit Count for: Rictor, Rapamycin-insensitive companion of mTOR
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#:1552  State#:%  Dir#:1
wNotes=on sortOrder:rid,rpid

 

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