CIP2A Cancer Research Results

CIP2A, Cancerous Inhibitor of Protein Phosphatase 2A: Click to Expand ⟱
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Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) is an oncoprotein that plays a critical role in promoting tumorigenesis by inhibiting the activity of protein phosphatase 2A (PP2A), a tumor suppressor.

-CIP2A inhibits PP2A, leading to sustained activation of oncogenic signaling pathways such as AKT, MYC, and others that drive cell proliferation, survival, and growth.
-By stabilizing these oncoproteins, CIP2A contributes to tumor initiation, progression, and resistance to apoptosis.


-CIP2A is frequently overexpressed in various cancers, including breast, lung, colorectal, and head and neck cancers, among others.
-Elevated CIP2A expression promotes the malignant phenotype by deregulating key pathways that control cell cycle progression and survival.


-High CIP2A levels are generally associated with a poor prognosis. Increased expression often correlates with more aggressive tumor behavior, higher rates of metastasis, and reduced overall survival.
-In many cancer types, CIP2A overexpression is considered an independent prognostic marker, indicating a greater likelihood of treatment resistance and disease recurrence.
Scientific Papers found: Click to Expand⟱
6185- Cuc,    Cucurbitacin B: A review of its pharmacology, toxicity, and pharmacokinetics
- Review, Var, NA - Review, Arthritis, NA - Review, AD, NA
*Inflam↓, results showed that CuB exhibits potent anti-inflammatory, antioxidant, antiviral, hypoglycemic, hepatoprotective, neuroprotective, and anti-cancer activities
*antiOx↑,
*hepatoP↑,
*neuroP↑,
*AntiCan↑,
*toxicity↝, Studies of its toxicity and pharmacokinetic properties showed that CuB has non-specific toxicity and low bioavailability.
*BioAv↓,
*HO-1↑, CuB can exert its anti-inflammatory effect via the induction of heme oxygenase-1 (HO-1) by the activation Nrf2 [25].
*NRF2↑,
*NLRP3↑, CuB could act as an anti-inflammatory agent to inhibit gouty arthritis in mice [28]. The mechanism of action was mainly attributed to inhibition of the formation and activation of the NOD-like receptor thermal protein domain associated protein 3 (NLR
*SOD↑, Its antioxidant activity may be indirectly realized by increasing the activities of the antioxidant enzymes total SOD and SOD-1, and thereby eliminating excessive ROS and other free radicals in cells
*SOD1↑,
*ROS↓,
*AntiAge↑, this study also confirmed that CuB could exert anti-aging effects by regulating autophagy, ROS, and aging-related genes, which suggested that CuB might be a promising anti-aging drug
*ARE↑, activating the Nrf2/ARE signaling pathway and inhibiting the STAT/NF-κB signaling pathway, and thereby exerting a protective effect on cortical neurons
*STAT↓,
*NF-kB↓,
*neuroG↑, CuB (0.1 mg/kg) could also promote neurogenesis in APP/PS1 mice and alleviate memory deficits associated with enhanced neurogenesis in mice.
*memory↑,
ROS↑, Figure 2
NLRP3↑,
CIP2A↓,
Akt↓,
STAT3↑,
VEGFR2↓,
DNMTs↓, tudies have shown that in H1299 human lung cancer cells CuB (6, 60, 600, and 860 nM) can inhibit DNA methyltransferases (DNMTs)
MAPK↓,
YAP/TEAD↓,
PI3K↓,
Wnt↓,
NOTCH↓,
TumCCA↑,
TumCG↓, Inhibit cell growth and proliferation
TumCP↓,
FAK↑, CuB inhibited the migration, invasion, and adhesion of KKU-452 CCA cells in a dose-dependent manner by suppressing the activation of FAK and down-regulating MMP-9,
MMP9↓,
TumAuto↑, CuB ccould induce autophagy in BEL-7402 hepatocellular carcinoma cells by affecting autophagy-related proteins, such as up-regulating the expression of light chain 3 (LC3)-II
toxicity↝, Most experiments have demonstrated that CuB is moderately cytotoxic, both to human cancer cells and to normal cells
BioAv↓, When Wistar rats were given CuB orally at a dose of 8 mg/kg, the absorption degree was low and the absorption speed was slowest, which was specifically reflected in the fact that the time to peak concentration was longest (180 min, Tmax = 3 h). T
Half-Life↝, When CuB was administered intravenously at 0.1 mg/kg and orally at 1 mg/kg, the clearance rates of CuB in Wistar rats were similar, with a half-life (t1/2) of 5.08 ± 2.87 h and 5.09 ± 2.20 h, respectively [139].
BioAv↑, CuB-loaded mixed micelles with collagen peptides as a carrier, which improved the solubility of CuB and enhanced the absorption of orally administered CuB, and its relative bioavailability increased by a factor of 3.43
selectivity∅, Although CuB displays potent activity against tumor cells, its non-selective toxicity has limited its clinical applications.

1621- EA,    The multifaceted mechanisms of ellagic acid in the treatment of tumors: State-of-the-art
- Review, Var, NA
AntiCan↑, Studies have shown its anti-tumor effect in gastric cancer, liver cancer, pancreatic cancer, breast cancer, colorectal cancer, lung cancer and other malignant tumors
Apoptosis↑,
TumCP↓,
TumMeta↓,
TumCI↓,
TumAuto↑,
VEGFR2↓, inhibition of VEGFR-2 signaling
MAPK↓, MAPK and PI3K/Akt pathways
PI3K↓,
Akt↓,
PD-1↓, Downregulation of VEGFR-2 and PD-1 expression
NOTCH↓, Inhibition of Akt and Notch
PCNA↓, regulation of the expression of proliferation-related proteins PCNA, Ki67, CyclinD1, CDK-2, and CDK-6
Ki-67↓,
cycD1/CCND1↓,
CDK2↑,
CDK6↓,
Bcl-2↓,
cl‑PARP↑, up-regulated the expression of cleaved PARP, Bax, Active Caspase3, DR4, and DR5
BAX↑,
Casp3↑,
DR4↑,
DR5↑,
Snail↓, down-regulated the expression of Snail, MMP-2, and MMP-9
MMP2↓,
MMP9↓,
TGF-β↑, up-regulation of TGF-β1
PKCδ↓, Inhibition of PKC signaling
β-catenin/ZEB1↓, decreases the expression level of β-catenin
SIRT1↓, down-regulates the expression of anti-apoptotic protein, SIRT1, HuR, and HO-1 protein
HO-1↓,
ROS↑, up-regulates ROS
CHOP↑, activating the CHOP signaling pathway to induce apoptosis
Cyt‑c↑, releases cytochrome c
MMP↓, decreases mitochondrial membrane potential and oxygen consumption,
OCR↓,
AMPK↑, activates AMPK, and downregulates HIF-1α expression
Hif1a↓,
NF-kB↓, inhibition of NF-κB pathway
E-cadherin↑, Upregulates E-cadherin, downregulates vimentin and then blocks EMT progression
Vim↓,
EMT↓,
LC3II↑, Up-regulation of LC3 – II expression and down-regulation of CIP2A
CIP2A↓,
GLUT1↓, regulation of glycolysis-related gene GLUT1 and downstream protein PDH expression
PDH↝,
MAD↓, Downregulation of MAD, LDH, GR, GST, and GSH-Px related protein expressio
LDH↓,
GSTs↑,
NOTCH↓, inhibited the expression of Akt and Notch protein
survivin↓, survivin and XIAP was also significantly down-regulated
XIAP↓,
ER Stress↑, through ER stress
ChemoSideEff↓, could improve cisplatin-induced hepatotoxicity in colorectal cancer cells
ChemoSen↑, Enhancing chemosensitivity

4779- Lyco,    Lycopene Inhibits Reactive Oxygen Species-Mediated NF-κB Signaling and Induces Apoptosis in Pancreatic Cancer Cells
- in-vitro, PC, PANC1
ROS↓, The results show that the lycopene decreased intracellular and mitochondrial ROS levels, mitochondrial function (determined by the mitochondrial membrane potential and oxygen consumption rate),
NF-kB↓, NF-κB activity, and expression of NF-κB-dependent survival genes in PANC-1 cells.
tumCV↓, Lycopene reduced cell viability with increases in active caspase-3 and the Bax to Bcl-2 ratio in PANC-1 cells
Casp3↑,
Apoptosis↑, Lycopene Induces Apoptosis in PANC-1 Cells
OCR↓, Lycopene Decreases Intracellular and Mitochondrial ROS Levels and OCR in PANC-1 Cells
MMP↓, Lycopene Decreases MMP in PANC-1 Cells
CIP2A↓, Lycopene Decreases Expression of cIAP1, cIAP2, and Survivin in PANC-1 Cells
survivin↓,
Casp3↑, Thus, lycopene induces caspase-3-dependent apoptosis and increased the Bax to Bcl-2 ratio in PANC-1 cells.
Bax:Bcl2↑,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSTs↑, 1,   HO-1↓, 1,   MAD↓, 1,   ROS↓, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,   OCR↓, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   LDH↓, 1,   PDH↝, 1,   SIRT1↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp3↑, 3,   Cyt‑c↑, 1,   DR4↑, 1,   DR5↑, 1,   MAPK↓, 2,   survivin↓, 2,   YAP/TEAD↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↑, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CIP2A↓, 3,   EMT↓, 1,   NOTCH↓, 3,   PI3K↓, 2,   STAT3↑, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   FAK↑, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP9↓, 2,   PKCδ↓, 1,   Snail↓, 1,   TGF-β↑, 1,   TumCI↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,   VEGFR2↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 2,   PD-1↓, 1,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 1,   Half-Life↝, 1,   selectivity∅, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   ChemoSideEff↓, 1,   toxicity↝, 1,  
Total Targets: 72

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ARE↑, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,   SOD1↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

neuroG↑, 1,   STAT↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 1,   toxicity↝, 1,  
Total Targets: 19

Scientific Paper Hit Count for: CIP2A, Cancerous Inhibitor of Protein Phosphatase 2A
1 Cucurbitacin
1 Ellagic acid
1 Lycopene
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

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