PINK1 Cancer Research Results

PINK1, PTEN-induced kinase 1: Click to Expand ⟱
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PINK1 (PTEN-induced kinase 1) is a mitochondrial kinase that plays a critical role in maintaining mitochondrial quality control through mitophagy.
- Many studies indicate that lower PINK1 expression tends to correlate with more aggressive disease and poorer prognosis—likely due to compromised mitochondrial quality control.
Scientific Papers found: Click to Expand⟱
6510- BCP,  CBD,    Cannabidiol and Beta-Caryophyllene Combination Attenuates Diabetic Neuropathy by Inhibiting NLRP3 Inflammasome/NFκB through the AMPK/sirT3/Nrf2 Axis
- in-vivo, Nor, NA
*MMP↓, BC and CBD diminished HG-induced hyperglycemia in Schwann cells, in part by reducing mitochondrial membrane potential, reactive oxygen species, and mitochondrial superoxides.
*ROS↑,
*BloodF↑, while improving blood flow
*Pain↓, CBD and BC treatments also reduced pain hypersensitivity to hyperalgesia and allodynia, with increased antioxidant and anti-inflammatory action in diabetic rats.
*antiOx↑,
*Inflam↓,
*AMPK↑, in vivo effects were attributed to significant upregulation of AMPK, sirT3, Nrf2, PINK1, PARKIN, LC3B, Beclin1, and TFAM functions
*SIRT3↑,
*NRF2↑,
*PINK1↑,
*PARK2↑,
*LC3B↑,
*Beclin-1↑,
*TFAM↑,
*NLRP3↓, while downregulation of NLRP3 inflammasome, NFκB, COX2, and p62 activity was noted
*NF-kB↓,
*COX2/PTGS2↓,
*p62↓,
*NP/CIPN↓, CBD and BC combination ameliorates DN by modulating the mitochondrial quality control system.

2047- Buty,    Sodium butyrate inhibits migration and induces AMPK-mTOR pathway-dependent autophagy and ROS-mediated apoptosis via the miR-139-5p/Bmi-1 axis in human bladder cancer cells
- in-vitro, CRC, T24/HTB-9 - in-vitro, Nor, SV-HUC-1 - in-vitro, Bladder, 5637 - in-vivo, NA, NA
HDAC↓, Sodium butyrate (NaB) is a histone deacetylase inhibitor and exerts remarkable antitumor effects in various cancer cells
AntiTum↑,
TumCMig↓, NaB inhibited migration
AMPK↑, induced AMPK/mTOR pathway-activated autophagy and reactive oxygen species (ROS) overproduction via the miR-139-5p/Bmi-1 axis
mTOR↑,
TumAuto↑,
ROS↑, NaB initiates ROS overproduction
miR-139-5p↑, NaB upregulates miR-139-5p and depletes Bmi-1 in bladder cancer cells
BMI1↓,
TumCI?, NaB significantly inhibited cell migration dose-dependently
E-cadherin↑, E-cadherin was markedly increased, while the expression of N-cadherin, Vimentin, and Snail was decreased
N-cadherin↓,
Vim↓,
Snail↓,
cl‑PARP↑, increased expression levels of cleaved PARP, cleaved caspase-3, and Bax and the concurrent decrease in Bcl-2 and Bcl-xl
cl‑Casp3↑,
BAX↑,
Bcl-2↓,
Bcl-xL↓,
MMP↓, impairs mitochondrial membrane potential
PINK1↑, activates the PINK1/ PARKIN pathway
PARK2↑,
TumMeta↓, NaB inhibits tumor metastasis and growth in vivo
TumCG↓,
LC3II↑, a significant increase in the levels of cleaved caspase3, p-AMPK, and LC3B-II along with decreased Bmi-1 and Vimentin
p62↓, elevated LC3B-II levels and degradation of p62
eff↓, NAC abolished the impairment of MMP and ROS overproduction. Interestingly, NAC also significantly inhibited apoptosis induced by NaB

7438- CYN,    Cynaropicrin Suppresses Cell Proliferation by Inducing Mitophagy through p38 MAPK-Mediated Mitochondrial ROS Generation in Human Hepatocellular Carcinoma Cells
- in-vitro, HCC, NA
tumCV↓, cynaropicrin significantly induced cytotoxicity and autophagy in HCC cells, but not in immortalized non-cancerous hepatocytes,
TumAuto↑,
selectivity↑,
mt-ROS↑, which was related to the generation of mitochondrial reactive oxygen species (mtROS) and induction of mitochondrial membrane potential loss.
MMP↓,
LC3B↑, Under cynaropicrin treatment, the expression of microtubule-associated protein light chain 3, which is involved in the elongation of the phagophore membrane, was upregulated
Beclin-1↓, whereas the expression of Beclin-1 and p62, which are essential for the formation of autophagosomes, was downregulated.
p62↓,
PINK1↑, expression of mitophagy regulators PTEN-induced kinase 1 (PINK1) and Parkin in the mitochondria increased, suggesting the induction of autophagic flux in the mitochondria.
PARK2↑,
eff↓, However, N-acetyl-l-cysteine(NAC), a ROS scavenger, counteracted cynaropicrin-induced effects.
p‑MAPK↑, cynaropicrin increased the phosphorylation of p38 mitogen-activated protein kinase (MAPK), and the p38 MAPK inhibitor, SB203580, specifically attenuated cynaropicrin-induced cytotoxicity and mtROS production.

6881- FA,    Potential Therapeutic Efficacy of Ferulic Acid and Its Derivatives in the Management of Cancers: A Comprehensive Analysis With Mechanistic Insight
- Review, Var, NA
ROS↑, FA showed promising anticancer activity through underlying mechanisms, including induction of oxidative stress, cytotoxic effect, cell cycle arrest, apoptotic effect, suppression of invasion and migration, antiproliferative effect, autophagy, and gen
TumCCA↑,
TumCI↓,
TumCMig↓,
TumCP↓,
BioAv↑, FA, indicating lower oral bioavailability is affected by the liver's fast conjugation process; this limitation is overcome by applying a nanoformulation of FA.
BioAv↑, medication's bioavailability is 100% when administered intravenously (IV)
TP53↑, FA could impede cell growth by upregulating the gene expression of TP53 and downregulating the gene expression of CDK2, CDK4, and CDK6 in prostate cancer PC-3 cells, resulting in cell cycle arrest in PC-3 cells
CDK2↓,
CDK4↓,
CDK6↓,
JAK2↓, blocking the JAK2/STAT6 immune signaling pathway
STAT6↓,
tyrosinase↓, FA could also decrease tyrosinase activity by directly binding to enzymes
p‑Akt↓, FA lowered phosphorylation of AKT and PI3K in CaSki cells in a dose-dependent way,
p‑PI3K↓,
mTOR↓, FA reduced the amount of mTOR mRNA and Ki-67 protein in A549 lung
Ki-67↓,
Casp3↑, increased the levels of caspase-3 protein
proCasp8↑, FA elevated pro-caspase-3, pro-caspase-8, and pro-caspase-9 and PARP cleavage, Bax, and ROS and decreased Bcl-2, Mcl-1, AKT, and PI3K pathway levels in a dose-dependent way
cl‑PARP↑,
BAX↑,
Bcl-2↓,
Mcl-1↓,
MMP9↓, reducing cell invasion, MMP9 mRNA expression, and cyclin D1 and cyclin E levels
cycD1/CCND1↓,
cycE/CCNE↓,
PINK1↑, FA (100 μg/mL) enhanced apoptosis via increasing PINK-1, Parkin and reducing the MMP expression
PARK2↑,
MMP↓,
CycD3↓, reducing the gene expressions of CCND1, CCND2, CCND3, CDK2, CDK4, and CDK6 level in PC-3 cells
TumAuto⇅, FA has shown anticancer activity via the increase and decrease of autophagy in different types of cancer.
eff↑, by combining with other compounds like 2-deoxy-D-glucose (2DG) [164], epirubicin, gamma radiation [165], aspirin, thyoquinine [166], phenolic and flavonoids, P-coumaric acid [167], 4-vinylguaiacol, caffeic [168], coumaric, and gemcitabine [169].
eff↑, FA and aspirin could trigger apoptotic cell death, p-RB, p21, and p-ERK1/2, cytotoxicity and reduce PCNA and MKI67, growth of tumor in pancreatic cancer.
ALAT↓, figure 5
AST↓,
ALP↓,
VEGF↓,
MMPs↓,
angioG↓,

7383- MF,    Magneto mitochondrial dysfunction mediated cancer cell death using intracellular magnetic nano-transducers
- vitro+vivo, Var, NA
mtDam↑, magnetic nano-transducers, which convert external magnetic fields into physical stress, are designed to induce mitochondrial dysfunction to remotely kill cancer cells.
Apoptosis↑, magneto-mechanical transduction of nano-transducers in mitochondria enhances cancer cell apoptosis by promoting a mitochondrial quality control mechanism, referred to as mitophagy.
MitoP↑,
Dose↝, The synthesized magnetic nano-transducers were approximately 40 nm in length and 15 nm in width with an aspect ratio of approximately 2.5
Dose↝, The nanotransducers were effectively responsive to an external magnetic field of 2 Hz.
eff↑, highest anti-proliferative effect after 24 h exposed with a well-resonated frequency of 2.0 Hz magnetic field for 15 minutes
PINK1↑, Additionally, an increase in PINK1 and Parkin expression levels was observed in the McA-RH7777 cells under the same conditions, suggesting that Parkin promotes the degradation of OMM proteins, causing mitophagy
PARK2↑,

4874- Uro,  EGCG,    A Combination Therapy of Urolithin A+EGCG Has Stronger Protective Effects than Single Drug Urolithin A in a Humanized Amyloid Beta Knockin Mice for Late-Onset Alzheimer's Disease
- in-vivo, AD, NA
*motorD↑, increased positive effects of urolithin A and a combination treatment of urolithin A+EGCG in hAbKI mice for phenotypic behavioral changes including motor coordination, locomotion/exploratory activity, spatial learning and working memory
*memory↑,
*MitoP↑, mitophagy and autophagy genes were upregulated
*Aβ↓, The levels of amyloid beta (Aβ) 40 and Aβ42 are reduced in both treatments, however, the reduction is higher for combined treatment
*mitResp↑, Mitochondrial respiration is stronger for urolithin A compared to EGCG, indicating that mitophagy enhancer, urolithin A is a better and more promising molecule to enhance mitophagy activity.
*Nrf1↑, table4
*PINK1↑,
*PARK2↑,
*ATG5↑,
*Bcl-2↑,
*H2O2↓, we found hydrogen peroxide levels were reduced in urolithin A (p = 0.0008) and urolithin A+EGCG (p = 0.0004) treated hAbKI mice relative to untreated mice.
*ROS↓, urolithin A and EGCG act as free radical scavengers in hAbKI mice
*lipid-P↓, (lipid peroxidation) were also significantly reduced in urolithin A (p = 0.0003) and urolithin A+EGCG (p = 0.0002) treated hAbKI mice relative to untreated hAbKI mice
*mt-ATP↑, mitochondrial ATP levels were increased in urolithin A (p = 0.007) and urolithin A+EGCG (p = 0.0002) treated hAbKI mice relative to hAbKI untreated mice.

4875- Uro,    Impact of the Natural Compound Urolithin A on Health, Disease, and Aging
- Review, AD, NA - Review, Stroke, NA - Review, ostP, NA - Review, IBD, NA
*MitoP↓, Experimental models consistently show that UA increases mitophagy and mitochondrial function and blunts excessive inflammatory responses.
*Strength↑, UA is a promising strategy to target health and disease conditions of aging, especially those linked to mitochondrial and muscle dysfunction.
*PINK1↑, UA can activate. PTEN-induced kinase 1 (PINK1)/Parkin-dependent mitophagy starts with the stabilization of the kinase PINK1,
*PARK2↑, which recruits and phosphorylates the ubiquitin-conjugating protein Parkin.
*Inflam↓, anti-inflammatory effect of UA was reported for the first time as a decrease in mRNA and protein levels of the inflammatory marker cyclooxygenase 2 (COX2)
*COX2/PTGS2↓,
*IL1β↓, In neuronal tissues, UA treatment reduced levels of IL-1β, IL-6, and TNFα in the brains of the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of AD
*IL6↓,
*TNF-α↓,
*OS↑, impact on worm longevity showed that UA extends lifespan by 45%,
*cardioP↑, reduction in IRI markers, such as circulating creatine kinase and lactate dehydrogenase levels, and by fewer apoptotic cells in the heart
*memory↑, Increased learning, memory retention, neuronal survival, and neurogenesis in the hippocampus was achieved with UA administration in the APP/PS1 mouse model of AD
*neuroG↑,
*neuroP↑, UA was shown to have neuroprotective effects in the EAE mouse model of multiple sclerosis (MS)
*Cartilage↑, In a model of osteoarthritis, an age-related and disabling joint disease caused by a slow degeneration of cartilage,
*Inflam↓, UA has protective effects against a chronic DSS-induced model of IBD, leading to reduced levels of colon inflammation markers and to better mucosal integrity.
*RenoP↑, UA consistently reduced tubular damage induced by cisplatin, as shown by histopathology and by a reduction in circulating markers of kidney damage
*eff↑, When administered as nanoparticles to increase its bioavailability, UA even improved the survival of mice that received a lethal dose of cisplatin
*Dose↝, UA showed a favorable safety profile, with no observed side effects following either single oral administration of UA up to 2000 mg or multiple oral dosing (28 days) of UA up to 1000 mg daily.
*Half-Life↑, It showed a relatively long-half life (t1/2 = 17–22 hours),
*NRF2↑, Other mechanisms of action have been proposed for UA, such as the activation of the Ahr/Nrf2 pathway and its downstream antioxidative stress response
*GutMicro↑, A recent report also showed an impact of direct UA supplementation on gut microflora in obese rats

2274- VitK2,    Vitamin K2 Modulates Mitochondrial Dysfunction Induced by 6-Hydroxydopamine in SH-SY5Y Cells via Mitochondrial Quality-Control Loop
- in-vitro, Nor, SH-SY5Y
*Bcl-2↓, Vitamin K2 played a significant part in apoptosis by upregulating and downregulating Bcl-2 and Bax protein expressions, respectively, which inhibited mitochondrial depolarization, and ROS accumulation to maintain mitochondrial structure and function
*BAX↑,
*MMP↑, vitamin K2 can restore the mitochondrial membrane potential and inhibit mitochondrial depolarization caused by 6-OHDA.
*ROS↓, vitamin K2 can effectively remove the ROS generated by 6-OHDA and relieve cellular oxidative stress.
*p62↓, vitamin K2 treatments downregulated the expression level of p62 and upregulated the expression level of LC3A
*LC3A↑,
*Dose↝, vitamin K2 inhibited the toxic effect of 6-OHDA, and that the inhibitory effect was the best at a concentration of 30 µM
*Apoptosis↓, However, after vitamin K2 post-treatment, the apoptosis rate was significantly reduced to 11.44%.
*PINK1↑, Vitamin K2 Regulates Mitochondrial Quality-Control System by Activating Pink1/Parkin Signaling Pathway
*PARK2↑,


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

PARK2↑, 4,   ROS↑, 2,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 3,   mtDam↑, 1,   PINK1↑, 4,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   AMPK↑, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 2,   Bcl-2↓, 2,   Bcl-xL↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   proCasp8↑, 1,   p‑MAPK↑, 1,   Mcl-1↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,   LC3B↑, 1,   LC3II↑, 1,   MitoP↑, 1,   p62↓, 2,   TumAuto↑, 2,   TumAuto⇅, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 2,   TP53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   CycD3↓, 1,   cycE/CCNE↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

BMI1↓, 1,   HDAC↓, 1,   mTOR↓, 1,   mTOR↑, 1,   p‑PI3K↓, 1,   STAT6↓, 1,   TumCG↓, 1,   tyrosinase↓, 1,  

Migration(tgid=13) ⓘ

E-cadherin↑, 1,   Ki-67↓, 1,   miR-139-5p↑, 1,   MMP9↓, 1,   MMPs↓, 1,   N-cadherin↓, 1,   Snail↓, 1,   TumCI?, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 1,   TumMeta↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

JAK2↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   Dose↝, 2,   eff↓, 2,   eff↑, 3,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   Ki-67↓, 1,   TP53↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,  
Total Targets: 70

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   H2O2↓, 1,   lipid-P↓, 1,   Nrf1↑, 1,   NRF2↑, 2,   PARK2↑, 4,   ROS↓, 2,   ROS↑, 1,   SIRT3↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mt-ATP↑, 1,   mitResp↑, 1,   MMP↓, 1,   MMP↑, 1,   PINK1↑, 4,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-2↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

TFAM↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3A↑, 1,   LC3B↑, 1,   MitoP↓, 1,   MitoP↑, 1,   p62↓, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

neuroG↑, 1,  

Migration(tgid=13) ⓘ

Cartilage↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 3,   NF-kB↓, 1,   TNF-α↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 2,   eff↑, 1,   Half-Life↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   memory↑, 2,   motorD↑, 1,   neuroP↑, 1,   NP/CIPN↓, 1,   OS↑, 1,   Pain↓, 1,   RenoP↑, 1,   Strength↑, 1,  
Total Targets: 52

Scientific Paper Hit Count for: PINK1, PTEN-induced kinase 1
2 Urolithin
1 Beta-Caryophyllene
1 Cannabidiol
1 Butyrate
1 Cynaropicrin
1 Ferulic acid
1 Magnetic Fields
1 EGCG (Epigallocatechin Gallate)
1 Vitamin K2
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#:1239  State#:%  Dir#:2
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