Src Cancer Research Results

Src, Src kinase: Click to Expand ⟱
Source:
Type: Oncogene
Src family of tyrosine kinases, which are a group of proteins involved in the regulation of various cellular processes, including cell growth, differentiation, and survival.
Src is overexpressed in several types of cancer, including breast, colon, lung, and prostate cancers.


Scientific Papers found: Click to Expand⟱
238- Api,    Apigenin inhibits TGF-β-induced VEGF expression in human prostate carcinoma cells via a Smad2/3- and Src-dependent mechanism
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
VEGF↓,
TGF-β↓,
Src↓,
FAK↓,
Akt↓,
SMAD2↓,
SMAD3↓,

2016- CAP,    Capsaicin binds the N-terminus of Hsp90, induces lysosomal degradation of Hsp70, and enhances the anti-tumor effects of 17-AAG (Tanespimycin)
HSP90↓, Here, we investigated the mechanism by which capsaicin inhibits Hsp90
ATPase↓, capsaicin binds to the N-terminus of Hsp90 and inhibits its ATPase activity
eff↑, Combined treatments of capsaicin and the Hsp90 inhibitor 17-AAG improved the anti-tumor efficacy of 17-AAG in cell culture
HSP70/HSPA5↓, capsaicin triggers the lysosomal degradation of Hsp70 in various cancer cell lines
other↝, The mechanism by which capsaicin induces apoptosis in cancer cells is not well understood, but it appears to be independent of the TRPV1 receptor as neither capsazepine, a TRPV1 antagonist, nor intracellular Ca2+ chelators have been found to inhibit
NF-kB↓, capsaicin can block the activity of many oncogenic signaling proteins including NF-κB, ER, EGFR/HER2, CDK4, Src, VEGF, and PI3K/Akt, among others.
EGFR↓,
CDK4↓,
Src↓,
VEGF↓,
PI3K↓,
Akt↓,

5939- Cela,  Chemo,    Celastrol inhibits proliferation and induces chemosensitization through down-regulation of NF-κB and STAT3 regulated gene products in multiple myeloma cells
- in-vitro, Melanoma, U266 - in-vitro, Melanoma, RPMI-8226
TumCP↓, Celastrol inhibited the proliferation of MM cell lines regardless of whether they were sensitive or resistant to bortezomib and other conventional chemotherapeutic drugs.
ChemoSen↑, It also synergistically enhanced the apoptotic effects of thalidomide and bortezomib.
cycD1/CCND1↓, down-regulation of various proliferative and anti-apoptotic gene products including cyclin D1, Bcl-2, Bcl-xL, survivin, XIAP and Mcl-1.
Bcl-2↓,
survivin↓, Bcl-2, Bcl-xL, XIAP and survivin (BIRC5) were decreased with Hsp90 inhibition
XIAP↓,
Mcl-1↓,
NF-kB↓, suppression of constitutively active NF-κB
IL6↓, Celastrol also inhibited both the constitutive and IL6-induced activation of STAT3
STAT3↓,
Apoptosis↑, which induced apoptosis as indicated by an increase in the accumulation of cells in the sub-G1 phase, an increase in the expression of pro-apoptotic proteins and activation of caspase-3
TumCCA↑,
Casp3↑,
HSP90↓, Predictive analysis of HSP90 activity knock-down along with HO-1 induction
HO-1↑,
JAK2↓, Active phosphorylated STAT3, JAK2 and Src were all show reduced
Src↓,
Akt↑, Celastrol suppresses Akt activation and inhibits the expression of anti-apoptotic proteins in MM cells

424- CUR,    Curcumin inhibits autocrine growth hormone-mediated invasion and metastasis by targeting NF-κB signaling and polyamine metabolism in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Src↓,
p‑STAT1↓, pSTAT-1
p‑Akt↓,
p‑p44↓, p-p44
p‑p42↓, p-p42
RAS↓,
Raf↓, c-RAF
Vim↓,
β-catenin/ZEB1↓,
P53↓,
Bcl-2↓,
Mcl-1↓,
PIAS-3↑,
SOCS-3↑,
SOCS1↑,
ROS↑,
NF-kB↓, NF-kB inactivation, ROS generation and PA depletion in MCF-7, MDA-MB-453 and MDA-MB-231 breast can- cer cells
PAO↑,
SSAT↑,
P21↑,
Bak↑,

4027- FulvicA,    Mummy Induces Apoptosis Through Inhibiting of Epithelial-Mesenchymal Transition (EMT) in Human Breast Cancer Cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
tumCV↓, MDA-MB-231 showed more sensitivity than the MCF-7 cell line to the anticancer activity of mummy,
selectivity↑, while mummy did not exhibit significant cell cytotoxicity against human normal cells (MCF-10A).
TGF-β↓, gene expression profile demonstrated a significant decrease in TGF-β1, TGF-βR1, TWIST1, NOTCH1, CTNNB1, SRC along with an increase in E-cadherin mRNA levels in mummy treated cells compared to the untreated control group
Twist↓,
NOTCH1↓,
CTNNB1↓,
Src↓,
E-cadherin↑,
EMT↓, Mummy triggers inhibition of EMT and metastasis in breast cancer cells mainly through the downregulation of TGFβ1 activity
TumMeta↓,
BioAv↑, water-soluble non-toxic and inexpensive compound, can be consumed as a part of the daily diet

830- GAR,    Garcinol modulates tyrosine phosphorylation of FAK and subsequently induces apoptosis through down-regulation of Src, ERK, and Akt survival signaling in human colon cancer cells
- in-vitro, CRC, HT-29
TumCI↓,
TumCMig↓,
Apoptosis↑,
p‑FAK↓,
Src↓,
MAPK↓,
ERK↓,
PI3K/Akt↓,
Bax:Bcl2↑,
Cyt‑c↑, release of cytochrome c from the mitochondria to the cytosol
MMP7↓,

2919- LT,    Luteolin as a potential therapeutic candidate for lung cancer: Emerging preclinical evidence
- Review, Var, NA
RadioS↑, it can be used as an adjuvant to radio-chemotherapy and helps to ameliorate cancer complications
ChemoSen↑,
chemoP↑,
*lipid-P↓, ↓LPO, ↑CAT, ↑SOD, ↑GPx, ↑GST, ↑GSH, ↓TNF-α, ↓IL-1β, ↓Caspase-3, ↑IL-10
*Catalase↑,
*SOD↑,
*GPx↑,
*GSTs↑,
*GSH↑,
*TNF-α↓,
*IL1β↓,
*Casp3↓,
*IL10↑,
NRF2↓, Lung cancer model ↓Nrf2, ↓HO-1, ↓NQO1, ↓GSH
HO-1↓,
NQO1↓,
GSH↓,
MET↓, Lung cancer model ↓MET, ↓p-MET, ↓p-Akt, ↓HGF
p‑MET↓,
p‑Akt↓,
HGF/c-Met↓,
NF-kB↓, Lung cancer model ↓NF-κB, ↓Bcl-XL, ↓MnSOD, ↑Caspase-8, ↑Caspase-3, ↑PARP
Bcl-2↓,
SOD2↓,
Casp8↑,
Casp3↑,
PARP↑,
MAPK↓, LLC-induced BCP mouse model ↓p38 MAPK, ↓GFAP, ↓IBA1, ↓NLRP3, ↓ASC, ↓Caspase1, ↓IL-1β
NLRP3↓,
ASC↓,
Casp1↓,
IL6↓, Lung cancer model ↓TNF‑α, ↓IL‑6, ↓MuRF1, ↓Atrogin-1, ↓IKKβ, ↓p‑p65, ↓p-p38
IKKα↓,
p‑p65↓,
p‑p38↑,
MMP2↓, Lung cancer model ↓MMP-2, ↓ICAM-1, ↓EGFR, ↓p-PI3K, ↓p-Akt
ICAM-1↓,
EGFR↑,
p‑PI3K↓,
E-cadherin↓, Lung cancer model ↑E-cadherin, ↑ZO-1, ↓N-cadherin, ↓Claudin-1, ↓β-Catenin, ↓Snail, ↓Vimentin, ↓Integrin β1, ↓FAK
ZO-1↑,
N-cadherin↓,
CLDN1↓,
β-catenin/ZEB1↓,
Snail↓,
Vim↑,
ITGB1↓,
FAK↓,
p‑Src↓, Lung cancer model ↓p-FAK, ↓p-Src, ↓Rac1, ↓Cdc42, ↓RhoA
Rac1↓,
Cdc42↓,
Rho↓,
PCNA↓, Lung cancer model ↓Cyclin B1, ↑p21, ↑p-Cdc2, ↓Vimentin, ↓MMP9, ↑E-cadherin, ↓AIM2, ↓Pro-caspase-1, ↓Caspase-1 p10, ↓Pro-IL-1β, ↓IL-1β, ↓PCNA
Tyro3↓, Lung cancer model ↓TAM RTKs, ↓Tyro3, ↓Axl, ↓MerTK, ↑p21
AXL↓,
CEA↓, B(a)P induced lung carcinogenesis ↓CEA, ↓NSE, ↑SOD, ↑CAT, ↑GPx, ↑GR, ↑GST, ↑GSH, ↑Vitamin E, ↑Vitamin C, ↓PCNA, ↓CYP1A1, ↓NF-kB
NSE↓,
SOD↓,
Catalase↓,
GPx↓,
GSR↓,
GSTs↓,
GSH↓,
VitE↓,
VitC↓,
CYP1A1↓,
cFos↑, Lung cancer model ↓Claudin-2, ↑p-ERK1/2, ↑c-Fos
AR↓, ↓Androgen receptor
AIF↑, Lung cancer model ↑Apoptosis-inducing factor protein
p‑STAT6↓, ↓p-STAT6, ↓Arginase-1, ↓MRC1, ↓CCL2
p‑MDM2↓, Lung cancer model ↓p-PI3K, ↓p-Akt, ↓p-MDM2, ↑p-P53, ↓Bcl-2, ↑Bax
NOTCH1↓, Lung cancer model ↑Bax, ↑Cleaved-caspase 3, ↓Bcl2, ↑circ_0000190, ↓miR-130a-3p, ↓Notch-1, ↓Hes-1, ↓VEGF
VEGF↓,
H3↓, Lung cancer model ↑Caspase 3, ↑Caspase 7, ↓H3 and H4 HDAC activities
H4↓,
HDAC↓,
SIRT1↓, Lung cancer model ↑Bax/Bcl-2, ↓Sirt1
ROS↑, Lung cancer model ↓NF-kB, ↑JNK, ↑Caspase 3, ↑PARP, ↑ROS, ↓SOD
DR5↑, Lung cancer model ↑Caspase-8, ↑Caspase-3, ↑Caspase-9, ↑DR5, ↑p-Drp1, ↑Cytochrome c, ↑p-JNK
Cyt‑c↑,
p‑JNK↑,
PTEN↓, Lung cancer model 1/5/10/30/50/80/100 μmol/L ↑Cleaved caspase-3, ↑PARP, ↑Bax, ↓Bcl-2, ↓EGFR, ↓PI3K/Akt/PTEN/mTOR, ↓CD34, ↓PCNA
mTOR↓,
CD34↓,
FasL↑, Lung cancer model ↑DR 4, ↑FasL, ↑Fas receptor, ↑Bax, ↑Bad, ↓Bcl-2, ↑Cytochrome c, ↓XIAP, ↑p-eIF2α, ↑CHOP, ↑p-JNK, ↑LC3II
Fas↑,
XIAP↓,
p‑eIF2α↑,
CHOP↑,
LC3II↑,
PD-1↓, Lung cancer model ↓PD-L1, ↓STAT3, ↑IL-2
STAT3↓,
IL2↑,
EMT↓, Luteolin exerts anticancer activity by inhibiting EMT, and the possible mechanisms include the inhibition of the EGFR-PI3K-AKT and integrin β1-FAK/Src signaling pathways
cachexia↓, luteolin could be a potential safe and efficient alternative therapy for the treatment of cancer cachexi
BioAv↑, A low-energy blend of castor oil, kolliphor and polyethylene glycol 200 increases the solubility of luteolin by a factor of approximately 83
*Half-Life↝, ats administered an intraperitoneal injection of luteolin (60 mg/kg) absorbed it rapidly as well, with peak levels reached at 0.083 h (71.99 ± 11.04 μg/mL) and a prolonged half-life (3.2 ± 0.7 h)
*eff↑, Luteolin chitosan-encapsulated nano-emulsions increase trans-nasal mucosal permeation nearly 6-fold, drug half-life 10-fold, and biodistribution of luteolin in brain tissue 4.4-fold after nasal administration

4699- PTS,    Pterostilbene inhibits triple-negative breast cancer metastasis via inducing microRNA-205 expression and negatively modulates epithelial-to-mesenchymal transition
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, HS587T - in-vivo, BC, MDA-MB-231
TumCMig↓, Pterostilbene inhibited the migratory and invasive potential of triple-negative MDA-MB-231 and Hs578t cells,
TumCI↓,
E-cadherin↑, accompanied by the up-regulation of E-cadherin and down-regulation of Snail, Slug, vimentin and ZEB1.
Snail↓,
Slug↓,
Vim↓,
Zeb1↑,
miR-205↑, significant up-regulation of miR-205, which resulted in the reduction of Src expression in pterostilbene-treated breast cancer cells
Src↓,
TumCG↓, suppressed tumor growth and metastasis in MDA-MB-231-bearing NOD/SCID mice
FAK↓, by reducing Src/Fak signaling
EMT↓, Our findings provide supports for the usage of pterostilbene as an inhibitor of EMT process and potential candidate for adjuvant therapy.

3028- RosA,    Network pharmacology mechanism of Rosmarinus officinalis L.(Rosemary) to improve cell viability and reduces apoptosis in treating Alzheimer’s disease
- in-vitro, AD, HT22 - in-vivo, NA, NA
*Aβ↓, It was found that rosemary could reversed Aβ25–35 induced damage to mouse hippocampal neuron HT22 cells,
*Apoptosis↓, significantly improved the viability of damaged cells, and reduced apoptosis
*antiOx↑, main antioxidant compound in rosemary, carnosic acid, also has neuroprotective effects.
*neuroP↑,
*eff↑, main active carnosic acid, carnosol, rosmarinol, rosmadial, genkwanin, cirsimaritin, rosmarinic acid and caffeic acid in Rosmarinus officinalis L,
*IGF-1↑, rosemary could elevated expression of IGF1, MMP9 and decreased mRNA levels of SRC, MAPK14, compared with the control group.
*MMP9↑,
*Src↓,
*MAPK↓,
*MMP↑, Rosemary reduced Aβ-induced HT22 cell damage in AD models to enhance the mitochondrial membrane potential levels

2355- SK,    Pharmacological properties and derivatives of shikonin-A review in recent years
- Review, Var, NA
AntiCan↑, anticancer effects on various types of cancer by inhibiting cell proliferation and migration, inducing apoptosis, autophagy, and necroptosis.
TumCP↓,
TumCMig↓,
Apoptosis↑,
TumAuto↑,
Necroptosis↑,
ROS↑, Shikonin also triggers Reactive Oxygen Species (ROS) generation
TrxR1↓, inhibiting the activation of TrxR1, PKM2, RIP1/3, Src, and FAK
PKM2↓,
RIP1↓,
RIP3↓,
Src↓,
FAK↓,
PI3K↓, modulating the PI3K/AKT/mTOR and MAPKs signaling;
Akt↓, shikonin induced a dose-dependent reduction of miR-19a to inhibit the activity of PI3K/AKT/mTOR pathway
mTOR↓,
GRP58↓, shikonin induced apoptosis in human myeloid cell line HL-60 cells through downregulating the expression of ERS protein ERP57 (42).
MMPs↓, hikonin suppressed cell migration through inhibiting the NF-κB pathway and reducing the expression of MMP-2 and MMP-9
ATF2↓, shikonin inhibited cell proliferation and tumor growth through suppressing the ATF2 pathway
cl‑PARP↑, shikonin significantly upregulated the expression of apoptosis-related proteins cleaved PARP and caspase-3 and increased cell apoptosis through increasing the phosphorylation of p38 MAPK and JNK, and inhibiting the phosphorylation of ERK
Casp3↑,
p‑p38↑,
p‑JNK↑,
p‑ERK↓,

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.

2083- TQ,    Thymoquinone inhibits proliferation in gastric cancer via the STAT3 pathway in vivo and in vitro
- in-vitro, GC, HGC27 - in-vitro, GC, BGC-823 - in-vitro, GC, SGC-7901 - in-vivo, NA, NA
p‑STAT3↓, TQ inhibited the phosphorylation of STAT3
JAK2↓, reduction in JAK2 and c-Src activity
c-Src↓,
Bcl-2↓, TQ also downregulated the expression of STAT3-regulated genes, such as Bcl-2, cyclin D, survivin, and vascular endothelial growth factor
cycD1/CCND1↓,
survivin↓,
VEGF↓,
Casp3?, activated caspase-3,7,9
Casp7?,
Casp9?,
*toxicity∅, A phase I study reported that in adult patients with solid tumors or hematological malignancies who were treated with TQ, there were no significant systemic toxicities[10].
TumVol↓, Thymoquinone inhibits tumor growth in a gastric mouse xenograft model.

119- UA,  CUR,  RES,    Combinatorial treatment with natural compounds in prostate cancer inhibits prostate tumor growth and leads to key modulations of cancer cell metabolism
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ROS⇅, ROS↑ only with CUR alone, otherwise ↓
p‑STAT3↓, all the combination treatments decreased phosphorylation of STAT3
Src↓, All the combinations of these natural compounds also decreased phosphorylation of Src
AMPK↑,
GlutMet↑, UA in combination with both CUR or RES greatly enhanced the modulation of a number of metabolic pathways, including the “Alanine, aspartate and glutamate metabolism” and the “tricarboxylic acid (TCA) cycle”
TCA↑,
glut↓, Since the combination of CUR + UA and UA + RES decreased the uptake of glutamine


Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   CYP1A1↓, 1,   GPx↓, 1,   GSH↓, 2,   GSR↓, 1,   GSTs↓, 1,   HO-1↓, 1,   HO-1↑, 1,   NQO1↓, 1,   NRF2↓, 2,   PAO↑, 1,   ROS↑, 4,   ROS⇅, 1,   SOD↓, 1,   SOD2↓, 1,   TrxR1↓, 1,   VitC↓, 1,   VitE↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   p‑p42↓, 1,   Raf↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   glut↓, 1,   GlutMet↑, 1,   PI3K/Akt↓, 1,   PKM2↓, 2,   SIRT1↓, 1,   SSAT↑, 1,   TCA↑, 1,  

Cell Death ⓘ

Akt↓, 3,   Akt↑, 1,   p‑Akt↓, 2,   Apoptosis↑, 3,   ATF2↓, 1,   Bak↑, 1,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 5,   Casp1↓, 1,   Casp3?, 1,   Casp3↑, 4,   Casp7?, 1,   Casp7↑, 1,   Casp8↑, 1,   Casp9?, 1,   Casp9↑, 1,   Cyt‑c↑, 2,   DR5↑, 1,   Fas↑, 1,   FasL↑, 1,   GRP58↓, 1,   HGF/c-Met↓, 1,   p‑JNK↑, 2,   MAPK↓, 2,   Mcl-1↓, 2,   p‑MDM2↓, 1,   Myc↓, 1,   Necroptosis↑, 1,   p‑p38↑, 2,   RIP1↓, 1,   RIP1↑, 1,   survivin↓, 2,   TRAIL↑, 1,  

Transcription & Epigenetics ⓘ

H3↓, 1,   H4↓, 1,   miR-205↑, 1,   other↝, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   p‑eIF2α↑, 1,   HSP70/HSPA5↓, 1,   HSP90↓, 2,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DFF45↓, 1,   DNMT1↓, 1,   P53↓, 1,   P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 2,   P21↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD34↓, 1,   cFos↑, 1,   CTNNB1↓, 1,   EMT↓, 4,   ERK↓, 1,   p‑ERK↓, 1,   HDAC↓, 1,   mTOR↓, 3,   NOTCH1↓, 2,   PI3K↓, 2,   p‑PI3K↓, 1,   PIAS-3↑, 1,   PTEN↓, 1,   PTEN↑, 1,   RAS↓, 1,   Src↓, 10,   p‑Src↓, 1,   c-Src↓, 1,   p‑STAT1↓, 1,   STAT3↓, 2,   p‑STAT3↓, 2,   p‑STAT6↓, 1,   TumCG↓, 1,  

Migration ⓘ

ATPase↓, 1,   AXL↓, 1,   Ca+2↑, 1,   Cdc42↓, 1,   CEA↓, 1,   CLDN1↓, 1,   E-cadherin↓, 1,   E-cadherin↑, 2,   FAK↓, 5,   p‑FAK↓, 1,   ITGB1↓, 1,   MET↓, 1,   p‑MET↓, 1,   MMP13↓, 1,   MMP2↓, 1,   MMP7↓, 2,   MMP9↓, 1,   MMPs↓, 1,   N-cadherin↓, 1,   p‑p44↓, 1,   Rac1↓, 1,   Rho↓, 1,   RIP3↓, 1,   RIP3↑, 1,   Slug↓, 1,   SMAD2↓, 1,   SMAD3↓, 1,   Snail↓, 2,   TGF-β↓, 2,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 2,   TumMeta↓, 1,   Twist↓, 1,   Tyro3↓, 1,   uPA↓, 1,   Vim↓, 2,   Vim↑, 1,   Zeb1↑, 1,   ZO-1↑, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   EGFR↑, 1,   Hif1a↓, 1,   VEGF↓, 5,  

Immune & Inflammatory Signaling ⓘ

ASC↓, 1,   COX2↓, 1,   ICAM-1↓, 1,   IKKα↓, 1,   IL2↑, 1,   IL6↓, 2,   JAK2↓, 2,   NF-kB↓, 5,   p‑p65↓, 1,   PD-1↓, 1,   SOCS-3↑, 1,   SOCS1↑, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   ChemoSen↑, 2,   eff↑, 1,   MDR1↓, 1,   RadioS↑, 2,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 2,   CEA↓, 1,   EGFR↓, 1,   EGFR↑, 1,   IL6↓, 2,   Myc↓, 1,   NSE↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cachexia↓, 1,   chemoP↑, 1,   TumVol↓, 1,  
Total Targets: 186

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSTs↑, 1,   lipid-P↓, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   Casp3↓, 1,   MAPK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1↑, 1,   Src↓, 1,  

Migration ⓘ

MMP9↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL10↑, 1,   IL1β↓, 1,   TNF-α↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 2,   Half-Life↝, 1,  

Functional Outcomes ⓘ

neuroP↑, 1,   toxicity∅, 1,  
Total Targets: 22

Scientific Paper Hit Count for: Src, Src kinase
2 Curcumin
2 Shikonin
1 Apigenin (mainly Parsley)
1 Capsaicin
1 Celastrol
1 Chemotherapy
1 Shilajit/Fulvic Acid
1 Garcinol
1 Luteolin
1 Pterostilbene
1 Rosmarinic acid
1 Thymoquinone
1 Ursolic acid
1 Resveratrol
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#:291  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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