EMT Cancer Research Results

EMT, Epithelial-Mesenchymal Transition: Click to Expand ⟱
Source:
Type:
Biological process in which epithelial cells lose their cell polarity and cell-cell adhesion properties and gain mesenchymal traits, such as increased motility and invasiveness. This process is pivotal during embryogenesis and wound healing. Hh signaling pathway is able to regulate the EMT. Snail, E-cadherin and N-cadherin, key components of EMT; EMT-related factors, E-cadherin, N-cadherin, vimentin; The hallmark of EMT is the upregulation of N-cadherin followed by the downregulation of E-cadherin.
EMT is regulated by various signaling pathways, including TGF-β, Wnt, Notch, and Hedgehog pathways. Transcription factors such as Snail, Slug, Twist, and ZEB play critical roles in repressing epithelial markers (like E-cadherin) and promoting mesenchymal markers (like N-cadherin and vimentin).
EMT is associated with increased tumor aggressiveness, enhanced migratory and invasive capabilities, and resistance to apoptosis.
Scientific Papers found: Click to Expand⟱
1123- aLinA,    Linoleic acid induces an EMT-like process in mammary epithelial cells MCF10A
- in-vitro, BC, NA - in-vitro, NA, MCF10
TumCP↑, Linoleic acid (LA) induces proliferation and invasion in breast cancer cells.
E-cadherin↓,
Snail↑, increase of Snail1, Snail2, Twist1, Twist2 and Sip1 expressions.
Twist↑,
ZEB2↑,
FAK↑,
NF-kB↑,
MMP2↓, Furthermore, LA induces FAK and NFκB activation, MMP-2 and -9 secretions, migration and invasion.
MMP9↓,
*EMT↑, LA promotes an EMT-like process in MCF10A
TumCI↑,

3155- Ash,    Overview of the anticancer activity of withaferin A, an active constituent of the Indian ginseng Withania somnifera
- Review, Var, NA
Half-Life↝, The pharmacokinetic study demonstrates that a dose of 4 mg/kg in mice results in 2 μM concentration in plasma (with a half-life of 1.3 h, in the breast cancer model of mice),
Inflam↓, WA has many biological activities: anti-inflammatory (Dubey et al. 2018), immunomodulatory (Davis and Girija 2000), antistress (Singh et al. 2016), antioxidant (Sumathi et al. 2007) and anti-angiogenesis
antiOx↓,
angioG↓,
ROS↑, WA induces oxidative stress (ROS) determining mitochondrial dysfunction as well as apoptosis in leukaemia cells
BAX↑, withaferin mediates apoptosis by ROS generation and activation of Bax/Bak.
Bak↑,
E6↓, The results of the study show that withaferin treatment downregulates the HPV E6 and E7 oncoprotein and induces accumulation of p53 result in the activation of various apoptotic markers (e.g. Bcl2, Bax, caspase-3 and cleaved PARP).
E7↓,
P53↑,
Casp3↑,
cl‑PARP↑,
STAT3↓, WA treatment also decreases the level of STAT3
eff↑, This study concludes that combination of DOX with WA can reduce the doses and side effects of the treatment which gives valuable possibilities for future research.
HSP90↓, by inhibiting the HSP90
TGF-β↓, WA inhibited TGFβ1 and TNFα- induced EMT;
TNF-α↓,
EMT↑,
mTOR↓, by downregulation of mTOR/STAT3 signalling.
NOTCH1↓, WA showed inhibition of pro-survival signalling markers (Notch1, pAKT and NFκB)
p‑Akt↓,
NF-kB↓,
Dose↝, WA dose escalation sets consisted of 72, 108, 144 and 216 mg, fractioned in 2-4 doses/day.

2693- BBR,    Antitumor Effects of Berberine on Gliomas via Inactivation of Caspase-1-Mediated IL-1β and IL-18 Release
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG
Casp1↓, berberine significantly inhibits inflammatory cytokine Caspase-1 activation via ERK1/2 signaling and subsequent production of IL-1β and IL-18 by glioma cells.
ERK↓, berberine induces senescence of human glioma cells by downregulating the extracellular kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway
IL1β↓, Berberine Exhibit Inhibitory Effects on Caspase-1, IL-18, and IL-1β Proteins
IL18↓,
EMT↑, berberine can reverse the process of epithelial-mesenchymal transition. aken together, these results suggest that berberine can inhibit the process of EMT

2674- BBR,    Berberine: A novel therapeutic strategy for cancer
- Review, Var, NA - Review, IBD, NA
Inflam↓, anti-inflammatory, antidiabetic, antibacterial, antiparasitic, antidiarrheal, antihypertensive, hypolipidemic, and fungicide.
AntiCan↑, elaborated on the anticancer effects of BBR through the regulation of different molecular pathways such as: inducing apoptosis, autophagy, arresting cell cycle, and inhibiting metastasis and invasion.
Apoptosis↑,
TumAuto↑,
TumCCA↑,
TumMeta↓,
TumCI↓,
eff↑, BBR is shown to have beneficial effects on cancer immunotherapy.
eff↑, BBR inhibited the release of Interleukin 1 beta (IL-1β), Interferon gamma (IFN-γ), Interleukin 6 (IL-6), and Tumor Necrosis Factor-alpha (TNF-α) from LPS stimulated lymphocytes by acting as a dopamine receptor antagonist
CD4+↓, BBR inhibited the proliferation of CD4+ T cells and down-regulated TNF-α and IL-1 and thus, improved autoimmune neuropathy.
TNF-α↓,
IL1↓,
BioAv↓, On the other hand, P-Glycoprotein (P-gp), a secretive pump located in the epithelial cell membrane, restricts the oral bioavailability of a variety of medications, such as BBR. The use of P-gp inhibitors is a common and effective way to prevent this
BioAv↓, Regardless of its low bioavailability, BBR has shown great therapeutic efficacy in the treatment of a number of diseases.
other↓, BBR has been also used as an effective therapeutic agent for Inflammatory Bowel Disease (IBD) for several years
AMPK↑, inhibitory effects on inflammation by regulating different mechanisms such as 5′ Adenosine Monophosphate-Activated Protein Kinase (AMPK. Increase of AMPK
MAPK↓, Mitogen-Activated Protein Kinase (MAPK), and NF-κB signaling pathways
NF-kB↓,
IL6↓, inhibiting the expression of proinflammatory genes such as IL-1, IL-6, Monocyte Chemoattractant Protein 1 (MCP1), TNF-α, Prostaglandin E2 (PGE2), and Cyclooxygenase-2 (COX-2)
MCP1↓,
PGE2↓,
COX2↓,
*ROS↓, BBR protected PC-12 cells (normal) from oxidative damage by suppressing ROS through PI3K/AKT/mTOR signaling pathways
*antiOx↑, BBR therapy improved the antioxidant function of mice intestinal tissue by enhancing the levels of glutathione peroxidase and catalase enzymes.
*GPx↑,
*Catalase↑,
AntiTum↑, Besides, BBR leaves great antitumor effects on multiple types of cancer such as breast cancer,69 bladder cancer,70 hepatocarcinoma,71 and colon cancer.72
TumCP↓, BBR exerts its antitumor activity by inhibiting proliferation, inducing apoptosis and autophagy, and suppressing angiogenesis and metastasis
angioG↓,
Fas↑, by increasing the amounts of Fas receptor (death receptor)/FasL (Fas ligand), ROS, ATM, p53, Retinoblastoma protein (Rb), caspase-9,8,3, TNF-α, Bcl2-associated X protein (Bax), BID
FasL↑,
ROS↑,
ATM↑,
P53↑,
RB1↑,
Casp9↑,
Casp8↑,
Casp3↓,
BAX↑,
Bcl-2↓, and declining Bcl2, Bcl-X, c-IAP1 (inhibitor of apoptosis protein), X-linked inhibitor of apoptosis protein (XIAP), and Survivin levels
Bcl-xL↓,
IAP1↓,
XIAP↓,
survivin↓,
MMP2↓, Furthermore, BBR suppressed Matrix Metalloproteinase-2 (MMP-2), and MMP-9 expression.
MMP9↓,
CycB/CCNB1↓, Inhibition of cyclin B1, cdc2, cdc25c
CDC25↓,
CDC25↓,
Cyt‑c↑, BBR inhibited tumor cell proliferation and migration and induced mitochondria-mediated apoptosis pathway in Triple Negative Breast Cancer (TNBC) by: stimulating cytochrome c release from mitochondria to cytosol
MMP↓, decreased the mitochondrial membrane potential, and enabled cytochrome c release from mitochondria to cytosol
RenoP↑, BBR significantly reduced the destructive effects of cisplatin on the kidney by inhibiting autophagy, and exerted nephroprotective effects.
mTOR↓, U87 cell, Inhibition of m-TOR signaling
MDM2↓, Downregulation of MDM2
LC3II↑, Increase of LC3-II and beclin-1
ERK↓, BBR stimulated AMPK signaling, resulting in reduced extracellular signal–regulated kinase (ERK) activity and COX-2 expression in B16F-10 lung melanoma cells
COX2↓,
MMP3↓, reducing MMP-3 in SGC7901 GC and AGS cells
TGF-β↓, BBR suppressed the invasion and migration of prostate cancer PC-3 cells by inhibiting TGF-β-related signaling molecules which induced Epithelial-Mesenchymal Transition (EMT) such as Bone morphogenetic protein 7 (BMP7),
EMT↑,
ROCK1↓, inhibiting metastasis-associated proteins such as ROCK1, FAK, Ras Homolog Family Member A (RhoA), NF-κB and u-PA, leading to in vitro inhibition of MMP-1 and MMP-13.
FAK↓,
RAS↓,
Rho↓,
NF-kB↓,
uPA↓,
MMP1↓,
MMP13↓,
ChemoSen↑, recent studies have indicated that it can be used in combination with chemotherapy agents

5204- CAP,    Low-concentration capsaicin promotes colorectal cancer metastasis by triggering ROS production and modulating Akt/mTOR and STAT-3 pathways
- in-vitro, Colon, SW480 - in-vitro, Colon, CT26
TumCP↓, high-concentration of capsaicin (≥ 200 µM for SW480 and CT-26 cell lines; ≥ 25 µM for HCT116 cell line) inhibited CRC cell proliferation in a dose-dependent manner
TumCMig↑, low-concentration of capsaicin (100 µM for SW480 and CT-26 cell lines; 12.5 µM for HCT116 cell line) enhanced both migratory and invasive capability of these cells
TumCI↑,
EMT↑, 100 µM capsaicin induced epithelial-to-mesenchymal (EMT), up-regulated expression of MMP-2 and MMP-9, and activated Akt/mTOR and STAT-3 pathways in SW480 cells.
MMP2↓,
MMP9↑,
STAT3↑,
TumMeta↑, capsaicin-induced metastasis of CRC cells was mediated by modulating reactive oxygen species (ROS) production.
ROS↑,

5115- JG,    Natural Products to Fight Cancer: A Focus on Juglans regia
- Review, Var, NA
Casp3↑, In LNCaP cells, it triggered apoptosis through the intrinsic pathway, promoting the activation of caspases 3 and 9, and decreasing mitochondrial potential (ΔΨ)
Casp9↑,
MMP↓,
AR↓, At sub-toxic concentrations, it downregulated ARs and PSA expression
PSA↓,
E-cadherin↑, Juglone upregulated the expression of the epithelial marker E-cadherin while reducing the mesenchymal factors N-caderin and vimentin.
N-cadherin↓,
Vim↓,
Akt↓, Furthermore, it synergistically inhibited the Akt/glycogen synthase kinase-3β (GSK-3β)/Snail axis that would physiologically promote E-cadherin repression and EMT induction
GSK‐3β↓,
EMT↑,
TumCI↓, decreased cell invasions by 56% and 80%, respectively, on BxPC-3 and PANC-1 cell lines.
MMP9↓, Juglone significantly dropped the protein level of MMP-9 and the vascular endothelial growth factor (VEGF) reporter Phactr-1 in both cell lines, while a drop of MMP-2 was evident only on BxPC-3
VEGF↓,
MMP2↓,
TumCCA↑, juglone promoted G1 cell-cycle arrest [94,95] and ROS-driven apoptosis
ROS↑,
Apoptosis↑,
GSH↓, Glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase protein levels diminished
Catalase↓,
SOD↓,
GPx↓,
DNAdam↑, juglone cytotoxicity is, at least partially, ascribed to DNA damage
γH2AX↑, high levels of γ-H2AX were registered when juglone was tested in combination with ascorbate.
eff↑, juglone’s anticancer profile (in terms of proliferation inhibition, cytotoxicity, and ROS induction) was highly improved by ascorbate [115], revealing an interesting synergistic activity between these two compounds
BAX↑, upregulation of many proteins involved in the intrinsic and extrinsic pathway, such as Bax, Cyt-c, Fas cell surface death receptor (Fas), Fas-ligand.
Fas↑,
Pin1↓, On U251 glioblastoma cells, juglone arrested cell growth by promoting apoptosis with the involvement of peptidyl-prolyl cis/trans isomerase (Pin1) inhibition [111]. Juglone is a well-known Pin1 inhibitor

1135- Selenate,    Selenate induces epithelial-mesenchymal transition in a colorectal carcinoma cell line by AKT activation
- in-vitro, CRC, DLD1
EMT↑, deleterious effects of EMT induction should be taken into careful consideration
Akt↑,
Twist↑, increased expression of the EMT-inducing transcription factor TWIST1
Vim↑,
E-cadherin↓,

2196- SK,    Research progress in mechanism of anticancer action of shikonin targeting reactive oxygen species
- Review, Var, NA
*ALAT↓, shikonin was found to mitigate the rise in ALT and AST levels triggered by LPS/GalN
*AST↓,
*Inflam?, demonstrated the anti-inflammatory properties of shikonin within two traditional mouse models frequently employed in pharmacological research to assess anti-inflammatory activities
*EMT↑, Shikonin stimulates EMT by weakening the nuclear translocation of NF-κB p65
ROS?, naphthoquinone framework possesses the capacity to produce ROS, which in turn modulate cellular oxidative stress levels
TrxR1↓, Duan and colleagues demonstrated that shikonin specifically inhibits the physiological function of TrxR1 by targeting its Sec residue
PERK↑, In vivo Western blot of HCT-15(colon cancer) xenografts showed shikonin upregulated PERK/eIF2α/ATF4/CHOP and IRE1α/JNK pathways.
eIF2α↑,
ATF4↑,
CHOP↑,
IRE1↑,
JNK↑,
eff↝, oral shikonin did not demonstrate anti-tumor effects in the colorectal cancer model, intraperitoneal injection significantly inhibited tumor growth.
DR5↑, upregulation of Death Receptor 5 (DR5) in cholangiocarcinoma cells through ROS-induced activation of the JNK signaling cascade.
Glycolysis↓, inhibited glycolysis in HepG2 cells by suppressing the activity of PKM2, a critical enzyme within the glycolytic pathway
PKM2↓,
ChemoSen↑, The combination of shikonin with drugs can reverse drug resistance and enhance therapeutic efficacy
GPx4↓, shikonin conjunction with cisplatin overcame drug resistance in cancer cells, downregulated GPX4, and upregulated haemoglobin oxygenase 1 (HMOX1) inducing iron death in cells.
HO-1↑,

1222- Z,    Zinc regulates primary ovarian tumor growth and metastasis through the epithelial to mesenchymal transition
- in-vitro, Ovarian, NA
EMT↑, zinc contributes to ovarian tumor metastasis by promoting EMT through a MTF-1 dependent pathway
TumCMig↑,
TumCI↑,
ERK↑,
Akt↑, .


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:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   Catalase↓, 1,   GPx↓, 1,   GPx4↓, 1,   GSH↓, 1,   HO-1↑, 1,   ROS?, 1,   ROS↑, 4,   SOD↓, 1,   TrxR1↓, 1,  

Mitochondria & Bioenergetics ⓘ

CDC25↓, 2,   MMP↓, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   Glycolysis↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 2,   p‑Akt↓, 1,   Apoptosis↑, 2,   Bak↑, 1,   BAX↑, 3,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp1↓, 1,   Casp3↓, 1,   Casp3↑, 2,   Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 1,   DR5↑, 1,   Fas↑, 2,   FasL↑, 1,   IAP1↓, 1,   JNK↑, 1,   MAPK↓, 1,   MDM2↓, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↑, 1,   HSP90↓, 1,   IRE1↑, 1,   PERK↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

ATM↑, 1,   DNAdam↑, 1,   P53↑, 2,   cl‑PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CycB/CCNB1↓, 1,   RB1↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

EMT↑, 7,   ERK↓, 2,   ERK↑, 1,   GSK‐3β↓, 1,   mTOR↓, 2,   NOTCH1↓, 1,   RAS↓, 1,   STAT3↓, 1,   STAT3↑, 1,  

Migration ⓘ

E-cadherin↓, 2,   E-cadherin↑, 1,   FAK↓, 1,   FAK↑, 1,   MMP1↓, 1,   MMP13↓, 1,   MMP2↓, 4,   MMP3↓, 1,   MMP9↓, 3,   MMP9↑, 1,   N-cadherin↓, 1,   Rho↓, 1,   ROCK1↓, 1,   Snail↑, 1,   TGF-β↓, 2,   TumCI↓, 2,   TumCI↑, 3,   TumCMig↑, 2,   TumCP↓, 2,   TumCP↑, 1,   TumMeta↓, 1,   TumMeta↑, 1,   Twist↑, 2,   uPA↓, 1,   Vim↓, 1,   Vim↑, 1,   ZEB2↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   ATF4↑, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↓, 1,   COX2↓, 2,   IL1↓, 1,   IL18↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 2,   MCP1↓, 1,   NF-kB↓, 3,   NF-kB↑, 1,   PGE2↓, 1,   PSA↓, 1,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   ChemoSen↑, 2,   Dose↝, 1,   eff↑, 4,   eff↝, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   E6↓, 1,   E7↓, 1,   IL6↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   Pin1↓, 1,   RenoP↑, 1,  
Total Targets: 122

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↑, 2,  

Immune & Inflammatory Signaling ⓘ

Inflam?, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,  
Total Targets: 9

Scientific Paper Hit Count for: EMT, Epithelial-Mesenchymal Transition
2 Berberine
1 alpha Linolenic acid
1 Ashwagandha(Withaferin A)
1 Capsaicin
1 Juglone
1 Selenate
1 Shikonin
1 Zinc
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#:96  State#:%  Dir#:2
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