PAK1 Cancer Research Results

PAK1, : Click to Expand ⟱
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PAK1 (p21-activated kinase 1) is a serine/threonine kinase that plays a significant role in various cellular processes, including cell motility, proliferation, and survival.
PAK1 is often found to be overexpressed in several types of cancers, including breast cancer, prostate cancer, colorectal cancer, and pancreatic cancer.
PAK1 expression can be regulated by various oncogenic signaling pathways, including those involving RAS, PI3K/Akt, and MAPK. These pathways can lead to the activation of PAK1, further promoting cancer cell survival and proliferation.
In many cancer types, PAK1 expression and/or activity is frequently upregulated.
Overexpression and/or hyperactivation of PAK1 has been reported in breast, ovarian, colorectal, lung, and other cancers.
Scientific Papers found: Click to Expand⟱
6342- DRE,    Mechanistic Study on the Inhibitory Effect of Dandelion Extract on Breast Cancer Cell Proliferation and Its Induction of Apoptosis
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
eff↑, MTT assays revealed that the ethyl acetate fraction exhibited the strongest inhibitory effect on cell proliferation.
selectivity↑, 12 potential active compounds, including sesquiterpenes such as Isoalantolactone and Artemisinin, which showed significantly lower toxicity toward normal mammary epithelial MCF-10A cells compared to tumor cells (
Apoptosis↑, the extract induced apoptosis in a dose-dependent manner, with an apoptosis rate as high as 85.04%, and significantly arrested the cell cycle at the S and G2/M phases
TumCCA↑,
PI3K↓, antitumor effects were primarily mediated through the regulation of PI3K-Akt (hsa04151), JAK-STAT (hsa04630), and PPAR (hsa03320) signaling pathways.
Akt↓, these active compounds exhibited strong binding affinities with key target proteins such as PI3K and JAK1
JAK1↓,
STAT↓,
PPARγ↑, EA-2 may remodel tumor cell lipid metabolism by activating the PPARγ pathway
TumCP↓, EA-2 Inhibits the Proliferation of MDA-MB-231 Breast Cancer Cells In Vitro
SIRT6↓, PI3K, AKT1S1, SIRT6, JAK1, SCD, STAT3, CASP8, STAT6, PAK1, and FABP4—were significantly downregulated.
SCD1↓,
STAT3↓,
Casp8↓,
STAT6↓,
PAK1↓,
FABP4↓,

8020- IVM,    Ivermectin induces PAK1-mediated cytostatic autophagy in breast cancer
- vitro+vivo, BC, NA
AntiP↑, Ivermectin is a broad-spectrum antiparasitic drug that has recently been demonstrated to exhibit potent anticancer activity against colon cancer, ovarian cancer, melanoma and leukemia.
TumAuto↑, We recently found that ivermectin markedly inhibits the growth of breast cancer cells by stimulating cytostatic macroautophagy/autophagy in vitro and in vivo.
Akt↓, inhibits the AKT-MTOR signaling pathway by promoting ubiquitination-mediated degradation of PAK1 (p21 [RAC1] activated kinase 1), leading to increased autophagic flux.
mTOR↓,
PAK1↓,
selectivity↑, marked growth inhibition after 24-h treatment with ivermectin in a range of breast cancer cell lines, with no obvious effects on nontumorigenic human breast cells.

8049- IVM,    Ivermectin Induces Cytostatic Autophagy by Blocking the PAK1/Akt Axis in Breast Cancer
- vitro+vivo, BC, NA
*AntiP↑, Ivermectin, a broad-spectrum antiparasitic drug, has recently been characterized as a potential anticancer agent due to observed antitumor effects.
AntiCan↑,
AntiTum↑,
PAK1↓, decreased P21-activated kinase 1 (PAK1) expression via the ubiquitination-mediated degradation pathway.
p‑Akt↓, decreases the phosphorylation level of Akt, resulting in the blockade of the Akt/mTOR signaling pathway.
Akt↓,
mTOR↓,
TumCG↓, In breast cancer xenografts, the ivermectin-induced cytostatic autophagy leads to suppression of tumor growth.

8047- IVM,    The multitargeted drug ivermectin: from an antiparasitic agent to a repositioned cancer drug
- Review, Var, NA
Half-Life↝, it has a mean peak plasma level of ~4 h after oral administration with a second peak at 6-12 h because of enterohepatic recycling. its half-life is approximately 19 h
MDR1↓, Ivermectin as an inhibitor of the multi-drug resistance (MDR) phenotype
P-gp/ABCB1↓, concluding that ivermectin is also a substrate and an inhibitor of P-glycoprotein
mtDam↑, Ivermectin as an inductor of mitochondrial dysfunction and oxidative damage
ROS↑,
OCR↓, ivermectin inhibits in a dose-dependent manner the basal and maximum oxygen consumption rate (OCR), most likely by decreasing the enzyme activity of respiratory complex I but not II, IV or V,
compI↓,
MMP↓, both the membrane potential and electrochemical proton gradient decrease while a significant increase in mitochondrial superoxide and decreased ATP are observed.
mt-SOD↑,
ATP↓,
p‑Akt↓, Results showed that ivermectin decreases phosphorylation of Akt (S473), mTOR (S2481)
p‑mTOR↓,
eff↓, abolition of the inhibitory effect of ivermectin in these renal cancer cell lines when co-treated with acetyl-L-carnitine (ALCAR) or N-acetyl-L-cysteine (NAC)
ICD↑, Ivermectin as an inductor of immunogenic cell death (ICD)
TumAuto↑, Ivermectin as an inductor of autophagy
PAK1↓, Ivermectin in ovarian and glioblastoma cancer cell lines promotes ubiquitination-mediated degradation of the oncogenic kinase PAK1
Wnt↓, Ivermectin as an inhibitor of the WNT-TCF pathway
TCF↓,
Nanog↓, 0.5 µM it reduces NANOG and SOX2 gene expression by 80%,
SOX2↓,
CSCs↓, Ivermectin as a stem-cell cancer inhibitor
CD44↓, ivermectin preferentially inhibits the viability of CSCs-enriched populations (CD44+/CD24-) and cells growing in spheroids,
CD24↓,
Dose↝, Thus, the in vitro and in vivo results with ivermectin strongly suggest that its antitumor effects in cancer patients can be achieved at feasible doses.

8043- IVM,    Ivermectin suppresses tumour growth and metastasis through degradation of PAK1 in oesophageal squamous cell carcinoma
- vitro+vivo, ESCC, KYSE-30 - in-vitro, ESCC, KYSE70 - in-vitro, ESCC, KYSE150
tumCV↓, We demonstrated that ivermectin significantly inhibited cell viability and colony formation, and induced apoptosis through a mitochondrial‐dependent manner in ESCC cells.
Apoptosis↑,
TumCMig↓, Ivermectin also abrogated ESCC cell migration, invasion, as well as the protein levels of MMP‐2 and MMP‐9.
TumCI↓,
MMP2↓,
MMP9↓,
PAK1↓, ivermectin promoted PAK1 degradation through the proteasome‐dependent pathway.
ChemoSen↑, ivermectin synergized with chemotherapeutic drugs including cisplatin and 5‐fluorouracil to induce apoptosis of ESCC cells.
cl‑PARP↑, increase of the cleavage of PARP and activation of Caspase‐3
Casp3↑,
TumMeta↓, in vivo results indicate that ivermectin effectively diminishes the tumour metastasis of ESCC

8040- IVM,    Ivermectin, a potential anticancer drug derived from an antiparasitic drug
- Review, Var, NA
Akt↓, inhibition by IVM of the Akt/mTOR pathway to induce autophagy and p-21-activated kinase 1(PAK1)was the target of IVM for breast cancer
mTOR↓,
TumAuto↑,
TumCP↓, IVM could inhibit the proliferation of the canine breast tumor cell lines CMT7364 and CIPp by blocking the cell cycle without increasing apoptosis, and the mechanism of IVM may be related to the inhibition of the Wnt pathway
TumCCA↑,
Wnt↓,
YAP/TEAD↓,
MMP↓, IVM could significantly reduce the mitochondrial membrane potential and inhibit mitochondrial respiration and ATP production.
mitResp↓,
ATP↓,
eff↓, acetyl-L-cysteine (NAC), could reverse IVM-induced inhibition
eff↑, it was found that IVM could enhance the drug activity of the anti-androgen drug enzalutamide in the prostate cancer cell line LNCaP and reverse the resistance of the prostate cancer cell line PC3 to docetaxel
ROS↑, induction of reactive oxygen species (ROS) production.
ChemoSen↑, IVM can enhance the efficacy of cisplatin to improve the treatment of epithelial ovarian cancer, and the mechanism is related to the inhibition of the Akt/mTOR pathway
PAK1↓, IVM also had a cytotoxic effect on a variety of nasopharyngeal cancer cells in vitro, and the mechanism is related to the reduction of PAK1 kinase activity to inhibit the MAPK pathway.
MAPK↓,
EMT↓, IVM could reduce the metastasis of lung cancer cells by inhibiting EMT.
Beclin-1/ATG6↑, IVM in the breast cancer cell lines MCF-7 and MDA-MB-231 significantly increased intracellular autophagic flux and the expression of key autophagy proteins such as LC3, Bclin1, Atg5
ATG5↑,
CSCs↓, Further studies showed that IVM could inhibit CSCs by regulating the PAK1-STAT3 axis
STAT3↝,
P-gp/ABCB1↓, Several studies have confirmed that IVM could reverse drug resistance by inhibiting P-gp and MDR-associated proteins
MDR1↓,
HSP27↓, Inhibit HSP27 Prostate cancer, Lung cancer Colorectal cancer
Chl↑, Activate chloride channels Leukemia
TFE3↑, Increase TFE3 Activity Melanoma

1676- PBG,    Use of Stingless Bee Propolis and Geopropolis against Cancer—A Literature Review of Preclinical Studies
- Review, Var, NA
ROS↑, evidenced in the accumulation of reactive oxygen species (ROS)
MMP↓, reduction of mitochondrial membrane potential (Δψm)
Bcl-2↓, decreased levels of Bcl-2 proteins (antiapoptotic proteins) and AKT-3
eff↑, combination of the extract (30 µg/mL) with the antineoplastic vemurafenib (15 μM) against melanoma cells demonstrated a synergistic effect
tumCV↓, decreased cell viability for 23% of the colon cancer cells (SW620) treated with the aqueous propolis extract produced by Trigona laeviceps
TumCCA↑, antitumor activity of artepillin C is mediated by one of the following mechanisms: induction of cell cycle arrest in cancer cells, inhibition of angiogenesis, and inhibition of the oncogenic PAK1 signaling cascade
angioG↓,
PAK1↓,
HDAC1↓, negatively regulated expression of histone deacetylases (HDAC) 1 and 2
HDAC2↓,
P53↑, positive regulation of acetyl-p53 expression at the protein level
PCNA↓, negative regulation of cell-cycle-related gene expression, i.e., proliferating cell nuclear antigen (PCNA) and cyclin D1 and E1
cycD1/CCND1↓,
cycE/CCNE↓,
P21?, positively regulating the expression of the cell cycle arrest gene p21
BAX↑, Bax, Bcl-2, cleaved caspase-3, and poly(ADP-ribose) polymerase
cl‑Casp3↑,
cl‑PARP↑,
ChemoSen↑, apigenin significantly down-regulates Mcl-1 transcription and translation levels in SKOV3 and SKOV3/DDP cells, which is responsible for its cytotoxic functions and chemosensitizing effects

1662- PBG,    The immunomodulatory and anticancer properties of propolis
- Review, Var, NA
IL6↓, suppressing the proinflammatory cytokines IL-6 and IL-12 but overexpressing the immune-tolerant cytokine IL-10.
IL12↓,
IL10↑,
CSCs↓, Propolis may Decrease Cancer Stem Cells Population
PAK1↓, artepillin C, a major component in Brazilian green propolis extract, can completely suppress the growth of human neurofibromatosis-associated tumor xenografts in mice through the blocking of oncogenic PAK1 signaling
VEGF↓, royal jelly and Chinese red propolis suppressed both VEGF-induced HUVEC proliferation and migration,
MMP2↓, CAPE from propolis could effectively suppress the adhesion and invasion potential of human hepatocellular carcinoma cells (SK-Hep1) by totally abolishing the expression of MMP-2 and MMP-9.
MMP9↓,
NF-kB↓, It was postulated that such action was related to the inhibition of the NFκB pathway
Hif1a↓, Brazilian green propolis and found that some compounds significantly inhibited the expression of the HIF-1α protein and HIF-1 downstream target genes such as glucose transporter 1, hexokinase 2, and VEGF-A
ChemoSen↑, the group with combined usage of paclitaxel and propolis achieved the lowest tumor weight compared to those with paclitaxel alone, propolis alone, or untreated controls
RadioS↑, complementary therapy to mainstream anticancer chemotherapies or radiotherapies.

1073- SK,  Chemo,    Natural Compound Shikonin Is a Novel PAK1 Inhibitor and Enhances Efficacy of Chemotherapy against Pancreatic Cancer Cells
- in-vitro, PC, PANC1 - in-vitro, PC, Bxpc-3
PAK1↓, significantly inhibited the activity of PAK1 kinase
TumCP↓,
Apoptosis↑,
ChemoSen↑, shikonin sensitized pancreatic cancer cells to chemotherapeutic
ROS↑, Moreover, shikonin has been shown to trigger ROS-based mitochondria-mediated apoptosis and significantly inhibited tumor growth in a human colon cancer SW480 xenograft mouse model [18]


Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

AntiP↑, 1,   TFE3↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

compI↓, 1,   ICD↑, 1,   ROS↑, 4,   mt-SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 2,   mitResp↓, 1,   MMP↓, 3,   mtDam↑, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

FABP4↓, 1,   PPARγ↑, 1,   SCD1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 4,   p‑Akt↓, 2,   Apoptosis↑, 3,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp8↓, 1,   MAPK↓, 1,   YAP/TEAD↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP27↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 1,   TumAuto↑, 3,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   cl‑PARP↑, 2,   PCNA↓, 1,   SIRT6↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21?, 1,   TumCCA↑, 3,  

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

CD24↓, 1,   CD44↓, 1,   CSCs↓, 3,   EMT↓, 1,   HDAC1↓, 1,   HDAC2↓, 1,   mTOR↓, 3,   p‑mTOR↓, 1,   Nanog↓, 1,   PI3K↓, 1,   SOX2↓, 1,   STAT↓, 1,   STAT3↓, 1,   STAT3↝, 1,   STAT6↓, 1,   TCF↓, 1,   TumCG↓, 1,   Wnt↓, 2,  

Migration(tgid=13) ⓘ

Chl↑, 1,   MMP2↓, 2,   MMP9↓, 2,   PAK1↓, 9,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 3,   TumMeta↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL10↑, 1,   IL12↓, 1,   IL6↓, 1,   JAK1↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 5,   Dose↝, 1,   eff↓, 2,   eff↑, 3,   Half-Life↝, 1,   MDR1↓, 2,   RadioS↑, 1,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   AntiTum↑, 1,  
Total Targets: 83

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiP↑, 1,  
Total Targets: 1

Scientific Paper Hit Count for: PAK1,
5 Ivermectin
2 Propolis -bee glue
1 Dandelion Root
1 Shikonin
1 Chemotherapy
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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