RIP1 Cancer Research Results

RIP1, Receptor-Interacting Protein 1: Click to Expand ⟱
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RIP1 (Receptor-Interacting Protein 1) is a protein kinase that plays a crucial role in cell signaling pathways, including those involved in inflammation, cell death, and cancer.

RIP1 is often overexpressed, and associated with poor prognosis.

RIP1 and RIP3 are key regulators of necroptosis and are involved in intricate signaling pathways that dictate cell survival, inflammation, and death.
Their dual roles in cancer can have opposing effects on tumor progression: while necroptosis may promote anti-tumor immunity and improve outcomes in some contexts, pro-survival signaling mediated by RIP1 can contribute to tumor aggressiveness and resistance to therapy.
Scientific Papers found: Click to Expand⟱
988- EMD,    Emodin Induced Necroptosis and Inhibited Glycolysis in the Renal Cancer Cells by Enhancing ROS
- in-vitro, RCC, NA
Necroptosis↑, emodin induces necroptosis, but not apoptosis, in renal cancer cells
p‑RIP1↑,
MLKL↑,
ROS↑, levels of ROS increased upon emodin treatment in a dose-dependent manner
Glycolysis↓,
GLUT1↓,
PI3K↓,
Akt↓,

2362- SK,    RIP1 and RIP3 contribute to shikonin-induced glycolysis suppression in glioma cells via increase of intracellular hydrogen peroxide
- in-vitro, GBM, U87MG - in-vivo, GBM, NA - in-vitro, GBM, U251
RIP1↑, we found shikonin activated RIP1 and RIP3 in glioma cells in vitro and in vivo, which was accompanied with glycolysis suppression
RIP3↑,
Glycolysis↓,
G6PD↓, shikonin-induced decreases of glucose-6-phosphate and pyruvate and downregulation of HK II and PKM2
HK2↓,
PKM2↓,
H2O2↑, shikonin also triggered accumulation of intracellular H2O2 and depletion of GSH and cysteine
GSH↓,
ROS↑, It was documented that inhibition of HK II with its inhibitor 3-bromopyruvate or knockdown of its level resulted in accumulation of ROS

2197- SK,    Shikonin derivatives for cancer prevention and therapy
- Review, Var, NA
ROS↑, This compound accumulates in the mitochondria, which leads to the generation of reactive oxygen species (ROS), and deregulates intracellular Ca2+ levels.
Ca+2↑,
BAX↑, shikonin alone by increasing the expression of the pro-apoptotic Bax protein and decreasing the expression of the anti-apoptotic Bcl2 protein
Bcl-2↓,
MMP9↓, This treatment also inhibited metastasis by decreasing the expression of MMP-9 and NF-kB p65 without affecting MMP-2 expression.
NF-kB↓,
PKM2↓, Figure 4
Hif1a↓,
NRF2↓,
P53↑,
DNMT1↓,
MDR1↓,
COX2↓,
VEGF↓,
EMT↓,
MMP7↓,
MMP13↓,
uPA↓,
RIP1↑,
RIP3↑,
Casp3↑,
Casp7↑,
Casp9↑,
P21↓,
DFF45↓,
TRAIL↑,
PTEN↑,
mTOR↓,
AR↓,
FAK↓,
Src↓,
Myc↓,
RadioS↑, shikonin acted as a radiosensitizer because of the high ROS production it induced.

2188- SK,    Molecular mechanism of shikonin inhibiting tumor growth and potential application in cancer treatment
- Review, Var, NA
ROS↑, their induction of reactive oxygen species production, inhibition of EGFR and PI3K/AKT signaling pathway activation, inhibition of angiogenesis and induction of apoptosis and necroptosis
EGFR↓,
PI3K↓,
Akt↓,
angioG↓,
Apoptosis↑,
Necroptosis↑,
GSH↓, leading to the increased consumption of reduced glutathione (GSH) and increased Ca2+ concentration in the cells and destroying the mitochondrial membrane potential.
Ca+2↓,
MMP↓,
ERK↓, 24 h of treatment with shikonin, ERK 1/2 and AKT activities were significantly inhibited, and p38 activity was upregulated, which ultimately led to pro-caspase-3 cleavage and triggered the apoptosis of GC cells.
p38↑,
proCasp3↑,
eff↓, pretreated with the ROS scavengers NAC and GSH before treatment with shikonin, the production of ROS was significantly inhibited, the cytotoxicity of shikonin was attenuated
VEGF↓, shikonin can inhibit the expression of VEGF
FOXO3↑, Activated FOXO3a/EGR1/SIRT1 signaling
EGR1↑,
SIRT1↑,
RIP1↑, Upregulation of RIP1 and RIP3
RIP3↑,
BioAv↓, limitations caused by its poor water solubility, it has a short half-life and nonselective biological distribution
NF-kB↓, Shikonin can also prevent the activation of NF-κB by AKT and then downregulate the expression of Bcl-xl,
Half-Life↓, due to the limitations caused by its poor water solubility, it has a short half-life and nonselective biological distribution.

2222- SK,    The anti-tumor effect of shikonin on osteosarcoma by inducing RIP1 and RIP3 dependent necroptosis
- in-vitro, OS, U2OS - in-vitro, OS, 143B - in-vivo, NA, NA
Necroptosis↑, Shikonin induced necroptosis in osteosarcoma cells
RIP1↑, Shikonin induced necroptosis via upregulating RIP1 and RIP3
RIP3↑,
OS↑, Shikonin prolonged the survival of metastatic disease
P53↑, protein level of p53 was increased after treated with shikonin for 8 hours

5100- SK,    Shikonin-induced necroptosis in nasopharyngeal carcinoma cells via ROS overproduction and upregulation of RIPK1/RIPK3/MLKL expression
- vitro+vivo, NPC, NA
TumCP↓, Shikonin exhibited a strong inhibitory effect on 5-8F cells in vitro and in vivo
RIP1↑, Moreover, RIPK1, RIPK3, and MLKL were upregulated by shikonin in a dose-dependent manner.
ROS↑, Shikonin induced 5-8F cell death via increased ROS production and the upregulation of RIPK1/RIPK3/MLKL expression, resulting in necroptosis.
Necroptosis↑,
Casp3↑, 7.5 μΜ shikonin significantly increased the activity of caspase-8 (Figure 2A) and caspase-3 (Figure 2B) compared with those of the control
Casp8↑,
eff↓, pretreatment with NAC protected the cells from shikonin mediated cell death.
TumCG↓, nude mice. Shikonin significantly inhibited the growth of the NPC tumors

1342- SK,    RIP1 and RIP3 contribute to shikonin-induced DNA double-strand breaks in glioma cells via increase of intracellular reactive oxygen species
- in-vitro, GBM, NA - in-vivo, NA, NA
RIP1↑,
RIP3↑,
DNAdam↑, DNA DSBs in vitro and in vivo
ROS↑,
GSH↓, depletion of GSH


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 3,   H2O2↑, 1,   NRF2↓, 1,   ROS↑, 6,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

G6PD↓, 1,   Glycolysis↓, 2,   HK2↓, 1,   PKM2↓, 2,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 2,   proCasp3↑, 1,   Casp7↑, 1,   Casp8↑, 1,   Casp9↑, 1,   MLKL↑, 1,   Myc↓, 1,   Necroptosis↑, 4,   p38↑, 1,   RIP1↑, 6,   p‑RIP1↑, 1,   TRAIL↑, 1,  

DNA Damage & Repair ⓘ

DFF45↓, 1,   DNAdam↑, 1,   DNMT1↓, 1,   P53↑, 2,  

Cell Cycle & Senescence ⓘ

P21↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 1,   FOXO3↑, 1,   mTOR↓, 1,   PI3K↓, 2,   PTEN↑, 1,   Src↓, 1,   TumCG↓, 1,  

Migration ⓘ

Ca+2↓, 1,   Ca+2↑, 1,   FAK↓, 1,   MMP13↓, 1,   MMP7↓, 1,   MMP9↓, 1,   RIP3↑, 5,   TumCP↓, 1,   uPA↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   EGR1↑, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   eff↓, 2,   Half-Life↓, 1,   MDR1↓, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 1,   Myc↓, 1,  

Functional Outcomes ⓘ

OS↑, 1,  
Total Targets: 66

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: RIP1, Receptor-Interacting Protein 1
6 Shikonin
1 Emodin
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#:942  State#:%  Dir#:2
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