CXCL12 Cancer Research Results

CXCL12, SDF–1: Click to Expand ⟱
Source:
Type:
SDF–1, also known as CXCL12, is a chemokine with key roles in cell signaling, migration, angiogenesis, and the regulation of the tumor microenvironment.

-SDF–1 is widely recognized for its role in tumor progression and metastasis. In many cancers—including breast, colorectal, lung, liver, and pancreatic cancers—increased expression of SDF–1 or hyperactivation of its receptor-mediated signaling is associated with more aggressive disease features and poorer patient outcomes.
Scientific Papers found: Click to Expand⟱
3169- Ash,    Withaferin A blocks formation of IFN-γ-induced metastatic cancer stem cells through inhibition of the CXCR4/CXCL12 pathway in the UP-LN1 carcinoma cell model
- in-vitro, GC, NA
CXCR4↓, inhibition of the CXCR4/CXCL12 pathway in the UP-LN1 carcinoma cell model
CXCL12↓,

2688- CUR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Var, NA - Review, AD, NA
*ROS↓, CUR reduced the production of ROS
*SOD↑, CUR also upregulated the expression of superoxide dismutase (SOD) genes
p16↑, The effects of CUR on gene expression in cancer-associated fibroblasts obtained from breast cancer patients has been examined. CUR increased the expression of the p16INK4A and other tumor suppressor proteins
JAK2↓, CUR decreased the activity of the JAK2/STAT3 pathway
STAT3↓,
CXCL12↓, and many molecules involved in cellular growth and metastasis including: stromal cell-derived factor-1 (SDF-1), IL-6, MMP2, MMP9 and TGF-beta
IL6↓,
MMP2↓,
MMP9↓,
TGF-β↓,
α-SMA↓, These effects reduced the levels of alpha-smooth muscle actin (alpha-SMA) which was attributed to decreased migration and invasion of the cells.
LAMs↓, CUR suppressed Lamin B1 and
DNAdam↑, induced DNA damage-independent senescence in proliferating but not quiescent breast stromal fibroblasts in a p16INK4A-dependent manner.
*memory↑, CUR has recently been shown to suppress memory decline by suppressing beta-site amyloid precursor protein cleaving enzyme 1 (BACE1= Beta-secretase 1, an important gene in AD) expression which is implicated in beta-amyoid pathology in 5xFAD transgenic
*cognitive↑, CUR was found to decrease adiposity and improve cognitive function in a similar fashion as CR in 15-month-old mice.
*Inflam↓, The effects of CUR and CR were positively linked with anti-inflammatory or antioxidant actions
*antiOx↑,
*NO↑, CUR treatment increased nNOS expression, acidity and NO concentration
*MDA↓, CUR treatment resulted in decreased levels of MDA
*ROS↓, CUR treatment was determined to cause reduction of ROS in the AMD-RPEs and protected the cells from H2O2-induced cell death by reduction of ROS levels.
DNMT1↓, CUR has been shown to downregulate the expression of DNA methyl transferase I (DNMT1)
ROS↑, induction of ROS and caspase-3-mediated apoptosis
Casp3↑,
Apoptosis↑,
miR-21↓, CUR was determined to decrease both miR-21 and anti-apoptotic protein expression.
LC3II↓, CUR also induced proteins associated with cell death such as LC3-II and other proteins in U251 cells
ChemoSen↑, The combined CUR and temozolomide treatment resulted in enhanced toxicity in U-87 glioblastoma cells.
NF-kB↓, suppression of NF-kappaB activity
CSCs↓, Dendrosomal curcumin increased the expression of miR-145 and decreased the expression of stemness genes including: NANOG, OCT4A, OCT4B1, and SOX2 [113]
Nanog↓,
OCT4↓,
SOX2↓,
eff↑, A synergistic interaction was observed when emodin and CUR were combined in terms of inhibition of cell growth, survival and invasion.
Sp1/3/4↓, CUR inducing ROS which results in suppression of specificity protein expression (SP1, SP3 and SP4) as well as miR-27a.
miR-27a-3p↓,
ZBTB10↑, downregulation of miR-27a by CUR, increased expression of ZBTB10 occurred
SOX9?, This resulted in decreased SOX9 expression.
ChemoSen↑, CUR used in combination with cisplatin resulted in a synergistic cytotoxic effect, while the effects were additive or sub-additive in combination with doxorubicin
VEGF↓, Some of the effects of CUR treatment are inhibition of NF-κB activity and downstream effector proteins, including: VEGF, MMP-9, XIAP, BCL-2 and Cyclin-D1.
XIAP↓,
Bcl-2↓,
cycD1/CCND1↓,
BioAv↑, Piperine is an alkaloid found in the seeds of black pepper (Piper nigrum) and is known to enhance the bioavailability of several therapeutic agents, including CUR
Hif1a↓, CUR inhibits HIF-1 in certain HCC cell lines and in vivo studies with tumor xenografts. CUR also inhibited EMT by suppressing HIF-1alpha activity in HepG2 cells
EMT↓,
BioAv↓, CUR has a poor solubility in aqueous enviroment, and consequently it has a low bioavailability and therefore low concentrations at the target sites.
PTEN↑, CUR treatment has been shown to result in activation of PTEN, which is a target of miR-21.
VEGF↓, CUR treatment resulted in a decrease of VEGF and activated Akt.
Akt↑,
EZH2↓, CUR also suppressed EZH2 expression by induction of miR-let 7c and miR-101.
NOTCH1↓, The expression of NOTCH1 was inhibited upon EZH2 suppression [
TP53↑, CUR has been shown to activate the TP53/miR-192-5p/miR-215/XIAP pathway in NSCLC.
NQO1↑, CUR can also induce the demethylation of the nuclear factor erythroid-2 (NF-E2) related factor-2 (NRT2) gene which in turn activates (NQO1), heme oxygenase-1 (HO1) and an antioxidant stress pathway which can prevent growth in mouse TRAMP-C1 prostate
HO-1↑,

220- MFrot,  MF,    Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation
- in-vitro, Melanoma, B16-F10
OS↑, prolonged the mouse survival rate
DCells↑,
T-Cell↑,
Apoptosis↑,
IL1↑,
IFN-γ↓, most of cytokines were decreased
IL10↑,
TumCG↓, grow slowed
ROS↑, Phagocyte activity, ROS release and interleukin-1β (IL-1β) production were significantly promoted after continuous exposure to 50 Hz LF-MF (1mT)
TumCP↓, LF-MF inhibits the proliferation of B16-F10 cells
TumCCA↑, the S-phase rate was significantly decreased from 40.76% to 37.24% and the G2/M-phase rate was significantly increased from 8.9% to 11.6%
ChrMod↑, Compared with control cells, the treated cells were characterized by the breaking down of chromatin (white arrow) and black granule accumulation (black arrow).
CXCL9↓, in tumor-bearing mice groups, most of cytokines were decreased after LF-MF exposure, including KC, CCL1, IFN-γ, CXCL9, CXCL12, TREM-1, CCL12, IL-1rα and IL-16.
CXCL12↓,
CD4+↑, After LF-MF exposure, the proportions of CD3+, CD3 + CD4+ and CD3 + CD8+ T cells in tumor-bearing mice were increased to 24.0%, 13.28% and 7.46%, respectively
CD8+↑,

3368- QC,    The potential anti-cancer effects of quercetin on blood, prostate and lung cancers: An update
- Review, Var, NA
*Inflam↓, quercetin is known for its anti-inflammatory, antioxidant, and anticancer properties.
*antiOx↑,
*AntiCan↑,
Casp3↓, Quercetin increases apoptosis and autophagy in cancer by activating caspase-3, inhibiting the phosphorylation of Akt, mTOR, and ERK, lessening β-catenin, and stabilizing the stabilization of HIF-1α.
p‑Akt↓,
p‑mTOR↓,
p‑ERK↓,
β-catenin/ZEB1↓,
Hif1a↓,
AntiAg↓, Quercetin have revealed an anti-tumor effect by reducing development of blood vessels. I
VEGFR2↓, decrease tumor growth through targeting VEGFR-2-mediated angiogenesis pathway and suppressing the downstream regulatory component AKT in prostate and breast malignancies.
EMT↓, effects of quercetin on inhibition of EMT, angiogenesis, and invasiveness through the epidermal growth factor receptor (EGFR)/VEGFR-2-mediated pathway in breast cancer
EGFR↓,
MMP2↓, MMP2 and MMP9 are two remarkable compounds in metastatic breast cancer (28–30). quercetin on breast cancer cell lines (MDA-MB-231) and showed that after treatment with this flavonoid, the expression of these two proteinases decreased
MMP↓,
TumMeta↓, head and neck (HNSCC), the inhibitory effect of quercetin on the migration of tumor cells has been shown by regulating the expression of MMPs
MMPs↓,
Akt↓, quercetin by inhibiting the Akt activation pathway dependent on Snail, diminishing the expression of N-cadherin, vimentin, and ADAM9 and raising the expression of E-cadherin and proteins
Snail↓,
N-cadherin↓,
Vim↓,
E-cadherin↑,
STAT3↓, inhibiting STAT3 signaling
TGF-β↓, reducing the expression of TGF-β caused by vimentin and N-cadherin, Twist, Snail, and Slug and increasing the expression of E-cadherin in PC-3 cells.
ROS↓, quercetin exerted an anti-proliferative role on HCC cells by lessening intracellular ROS independently of p53 expression
P53↑, increasing the expression of p53 and BAX in hepatocellular carcinoma (HepG2) cell lines through the reduction of PKC, PI3K, and cyclooxygenase (COX-2)
BAX↑,
PKCδ↓,
PI3K↓,
COX2↓,
cFLIP↓, quercetin by inhibiting PI3K/AKT/mTOR and STAT3 pathways, decreasing the expression of cellular proteins such as c-FLIP, cyclin D1, and c-Myc, as well as reducing the production of IL-6 and IL-10 cytokines, leads to the death of PEL cells
cycD1/CCND1↓,
cMyc↓,
IL6↓,
IL10↓,
Cyt‑c↑, In addition, quercetin induced c-cytochrome-dependent apoptosis and caspase-3 almost exclusively in the HSB2 cell line
TumCCA↑, Exposure of K562 cells to quercetin also significantly raised the cells in the G2/M phase, which reached a maximum peak in 24 hours
DNMTs↓, pathway through DNA demethylation activity, histone deacetylase (HDAC) repression, and H3ac and H4ac enrichment
HDAC↓,
ac‑H3↑,
ac‑H4↑,
Diablo↑, SMAC/DIABLO exhibited activation
Casp3↑, enhanced levels of activated caspase 3, cleaved caspase 9, and PARP1
Casp9↑,
PARP1↑,
eff↑, green tea and quercetin as monotherapy caused the reduction of levels of anti-apoptotic proteins, CDK6, CDK2, CYCLIN D/E/A, BCL-2, BCL-XL, and MCL-1 and an increase in expression of BAX.
PTEN↑, Quercetin upregulates the level of PTEN as a tumor suppressor, which inhibits AKT signaling
VEGF↓, Quercetin had anti-inflammatory and anti-angiogenesis effects, decreasing VGEF-A, NO, iNOS, and COX-2 levels
NO↓,
iNOS↓,
ChemoSen↑, quercetin and chemotherapy can potentiate their effect on the malignant cell
eff↑, combination with hyperthermia, Shen et al. Quercetin is a method used in cancer treatment by heating, and it was found to reduce Doxorubicin hydrochloride resistance in leukemia cell line K562
eff↑, treatment with ellagic acid, luteolin, and curcumin alone showed excellent anticancer effects.
eff↑, co-treatment with quercetin and curcumin led to a reduction of mitochondrial membrane integrity, promotion of cytochrome C release, and apoptosis induction in CML cells
uPA↓, A-549 cells were shown to have reduced mRNA expressions of urokinase plasminogen activator (uPA), Upar, protein expression of CXCR-4, CXCL-12, SDF-1 when quercetin was applied at 20 and 40 mM/ml by real-time PCR.
CXCR4↓,
CXCL12↓,
CLDN2↓, A-549 cells, indicated that quercetin could reduce mRNA and protein expression of Claudin-2 in A-549 cell lines without involving Akt and ERK1/2,
CDK6↓, CDK6, which supports the growth and viability of various cancer cells, was hampered by the dose-dependent manner of quercetin (IC50 dose of QR for A-549 cells is 52.35 ± 2.44 μM).
MMP9↓, quercetin up-regulated the rates of G1 phase cell cycle and cellular apoptotic in both examined cell lines compared with the control group, while it declined the expressions of the PI3K, AKT, MMP-2, and MMP-9 proteins
TSP-1↑, quercetin increased TSP-1 mRNA and protein expression to inhibit angiogenesis,
Ki-67↓, significant reductions in Ki67 and PCNA proliferation markers and cell survival markers in response to quercetin and/or resveratrol.
PCNA↓,
ROS↑, Also, quercetin effectively causes intracellular ROS production and ER stress
ER Stress↑,

3373- QC,    The Effect of Quercetin in the Yishen Tongluo Jiedu Recipe on the Development of Prostate Cancer through the Akt1-related CXCL12/ CXCR4 Pathway
- in-vitro, Pca, DU145
TumCP↓, Quercetin inhibited the proliferation of DU145 cells by upregulating caspase-3 and downregulating Bcl-2 expression, promoting apoptosis and reducing invasion and migration abilities.
Casp3↑,
Bcl-2↓,
Apoptosis↑,
TumCI↓,
TumCMig↓,
CXCL12↓, In vivo, quercetin downregulated CXCL12 and CXCR4 expressions and inhibited PCa development by the Akt1-related CXCL12/CXCR4 pathway.
CXCR4↓,

3082- RES,    Resveratrol Ameliorates the Malignant Progression of Pancreatic Cancer by Inhibiting Hypoxia-induced Pancreatic Stellate Cell Activation
- in-vitro, PC, PANC1 - in-vitro, PC, MIA PaCa-2 - in-vivo, NA, NA
VEGF↓, Furthermore, our in vivo studies revealed that the administration of RSV to LSL-KrasG12D/+, Trp53fl/+, and Pdx1-Cre (KPC) mice by gastric perfusion could significantly suppress VEGF-A, SDF-1, IL-6, alpha-smooth muscle actin (α-SMA), and HIF-1α expres
CXCL12↓,
IL6↓,
α-SMA↓,
Hif1a↓,
TumCI↓, RSV Suppresses Pancreatic Cancer Cell Invasion and EMT Induced by Hypoxia
EMT↓,


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   NQO1↑, 1,   ROS↓, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   p‑Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 1,   Bcl-2↓, 2,   Casp3↓, 1,   Casp3↑, 3,   Casp9↑, 1,   cFLIP↓, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   iNOS↓, 1,  

Kinase & Signal Transduction ⓘ

SOX9?, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

ChrMod↑, 1,   EZH2↓, 1,   ac‑H3↑, 1,   ac‑H4↑, 1,   miR-21↓, 1,   miR-27a-3p↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↓, 1,   DNMTs↓, 1,   p16↑, 1,   P53↑, 1,   PARP1↑, 1,   PCNA↓, 1,   TP53↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 2,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 3,   p‑ERK↓, 1,   HDAC↓, 1,   p‑mTOR↓, 1,   Nanog↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   PI3K↓, 1,   PTEN↑, 2,   SOX2↓, 1,   STAT3↓, 2,   TumCG↓, 1,  

Migration ⓘ

AntiAg↓, 1,   CLDN2↓, 1,   CXCL12↓, 6,   E-cadherin↑, 1,   Ki-67↓, 1,   LAMs↓, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 1,   N-cadherin↓, 1,   PKCδ↓, 1,   Snail↓, 1,   TGF-β↓, 2,   TSP-1↑, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   uPA↓, 1,   Vim↓, 1,   α-SMA↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   Hif1a↓, 3,   NO↓, 1,   VEGF↓, 4,   VEGFR2↓, 1,   ZBTB10↑, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2↓, 1,   CXCL9↓, 1,   CXCR4↓, 3,   DCells↑, 1,   IFN-γ↓, 1,   IL1↑, 1,   IL10↓, 1,   IL10↑, 1,   IL6↓, 3,   JAK2↓, 1,   NF-kB↓, 1,   T-Cell↑, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 3,   eff↑, 5,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   EZH2↓, 1,   IL6↓, 3,   Ki-67↓, 1,   TP53↑, 1,  

Functional Outcomes ⓘ

OS↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 106

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   MDA↓, 1,   ROS↓, 2,   SOD↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cognitive↑, 1,   memory↑, 1,  
Total Targets: 9

Scientific Paper Hit Count for: CXCL12, SDF–1
2 Quercetin
1 Ashwagandha(Withaferin A)
1 Curcumin
1 Magnetic Field Rotating
1 Magnetic Fields
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#:1247  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

Home Page