Beclin-1 Cancer Research Results

Beclin-1, Beclin-1 (BECN1 gene): Click to Expand ⟱
Source:
Type: Protein Coding gene
Beclin 1, an autophagy and haploinsufficient tumor-suppressor protein, is frequently monoallelically deleted in breast and ovarian cancers. However, the precise mechanisms by which Beclin 1 inhibits tumor growth remain largely unknown.
A key biomarker of autophagy is Beclin-1. Beclin-1 stimulates LC3-I’s lipidation to produce LC3-II, which localizes to the autophagosome membrane to activate the development of autophagosomes.
-BECN1 = the official gene symbol (human gene name)
-Beclin-1 = the protein name encoded by the BECN1 gene
Scientific Papers found: Click to Expand⟱
265- ALA,    Alpha-Lipoic Acid Reduces Cell Growth, Inhibits Autophagy, and Counteracts Prostate Cancer Cell Migration and Invasion: Evidence from In Vitro Studies
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
ROS↓, ALA decreased ROS production, SOD1 and GSTP1 protein expression
SOD↓, SOD1, DU145
GSTP1/GSTπ↓,
NRF2↓, significantly reduced the cytosolic and nuclear content of the transcription factor Nrf2
p62↓, du145
p62↑, LNCaP
SOD↑, LNCaP
p‑mTOR↑, revealed that in both cancer cells, ALA, by upregulating pmTOR expression, reduced the protein content of two autophagy initiation markers, Beclin-1 and MAPLC3.
Beclin-1↓,
ROS↑, Interestingly, in LNCaP cells, we observed an almost significant increase in ROS content (p = 0.06) after ALA compared to the control, concomitantly with a significant upregulation of the antioxidant enzyme SOD1 after 48 h.
SOD1↑,

2720- BetA,    Betulinic acid induces apoptosis of HeLa cells via ROS-dependent ER stress and autophagy in vitro and in vivo
- in-vitro, Cerv, HeLa
Keap1↝, The findings revealed that BA activated Keap1/Nrf2 pathway and triggered mitochondria-dependent apoptosis due to ROS production.
ROS↑,
Ca+2↑, Furthermore, BA increased the intracellular Ca2+ levels
Beclin-1↓, inhibited the expression of Beclin1 and promoted the expression of GRP78, LC3-II, and p62 associated with ERS and autophagy.
GRP78/BiP↑,
LC3II↑,
p62↑,
ERStress↑,
TumAuto↑,

1871- DAP,    Targeting PDK1 with dichloroacetophenone to inhibit acute myeloid leukemia (AML) cell growth
- in-vitro, AML, U937 - in-vivo, AML, NA
TumCP↓, DAP significantly inhibited cell proliferation, increased apoptosis induction and suppressed autophagy in AML cells in vitro
Apoptosis↑,
TumCG↓, inhibited tumor growth in an AML mouse model in vivo
PDK1↓, inhibition of PDK1 with DAP
cl‑PARP↑, increased the cleavage of pro-apoptotic proteins (PARP and Caspase 3)
Bcl-xL↓, decreased the expression of the anti-apoptotic proteins (BCL-xL and BCL-2) and autophagy regulators (ULK1, Beclin-1 and Atg).
Bcl-2↓,
Beclin-1↓,
ATG3↓,
PI3K↓, DAP inhibited the PI3K/Akt signaling pathway
Akt↓,
eff↑, Importantly, 2,2-dichloroacetophenone (DAP) is a much more potent inhibitor of PDK1(than DCA). It is effective at concentrations in the micromolar (μM) range.

1656- FA,    Ferulic Acid: A Natural Phenol That Inhibits Neoplastic Events through Modulation of Oncogenic Signaling
- Review, Var, NA
tyrosinase↓,
CK2↓,
TumCP↓,
TumCMig↓,
FGF↓,
FGFR1↓,
PI3K↓,
Akt↓,
VEGF↓,
FGFR1↓,
FGFR2↓,
PDGF↓,
ALAT↓,
AST↓,
TumCCA↑, G0/G1 phase arrest
CDK2↓,
CDK4↓,
CDK6↓,
BAX↓,
Bcl-2↓,
MMP2↓,
MMP9↓,
P53↑,
PARP↑,
PUMA↑,
NOXA↑,
Casp3↑,
Casp9↑,
TIMP1↑,
lipid-P↑,
mtDam↑,
EMT↓,
Vim↓,
E-cadherin↓,
p‑STAT3↓,
COX2↓,
CDC25↓,
RadioS↑,
ROS↑,
DNAdam↑,
γH2AX↑,
PTEN↑,
LC3II↓,
Beclin-1↓,
SOD↓,
Catalase↓,
GPx↓,
Fas↑,
*BioAv↓, ferulic acid stability and limited solubility in aqueous media continue to be key obstacles to its bioavailability, preclinical efficacy, and clinical use.
cMyc↓,
Beclin-1↑, ferulic acid by elevating the levels of the apoptosis and autophagy biomarkers, including beclin-1, Light chain (LC3-I/LC3-II), PTEN-induced putative kinase 1 (PINK-1), and Parkin
LC3‑Ⅱ/LC3‑Ⅰ↓,

2912- LT,    Luteolin: a flavonoid with a multifaceted anticancer potential
- Review, Var, NA
ROS↑, induction of oxidative stress, cell cycle arrest, upregulation of apoptotic genes, and inhibition of cell proliferation and angiogenesis in cancer cells.
TumCCA↑,
TumCP↓,
angioG↓,
ER Stress↑, Luteolin induces mitochondrial dysfunction and activates the endoplasmic reticulum stress response in glioblastoma cells, which triggers the generation of intracellular reactive oxygen species (ROS)
mtDam↑,
PERK↑, activate the expression of stress-related proteins by mediating the phosphorylation of PERK, ATF4, eIF2α, and cleaved-caspase 12.
ATF4↑,
eIF2α↑,
cl‑Casp12↑,
EMT↓, Luteolin is known to reverse epithelial-to-mesenchymal transition (EMT), which is associated with the cancer cell progression and metastasis.
E-cadherin↑, upregulating the biomarker E-cadherin expression, followed by a significant downregulation of the N-cadherin and vimentin expression
N-cadherin↓,
Vim↓,
*neuroP↑, Furthermore, luteolin holds potential to improve the spinal damage and brain trauma caused by 1-methyl-4-phenylpyridinium due to its excellent neuroprotective properties.
NF-kB↓, downregulation and suppression of cellular pathways such as nuclear factor kappa B (NF-kB), phosphatidylinositol 3’-kinase (PI3K)/Akt, and X-linked inhibitor of apoptosis protein (XIAP)
PI3K↓,
Akt↑,
XIAP↓,
MMP↓, Furthermore, the membrane action potential of mitochondria depletes in the presence of luteolin, Ca2+ levels and Bax expression upregulate, the levels of caspase-3 and caspase-9 increase, while the downregulation of Bcl-2
Ca+2↑,
BAX↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Cyt‑c↑, cause the cytosolic release of cytochrome c from mitochondria
IronCh↑, Luteolin serves as a good metal-chelating agent owing to the presence of dihydroxyl substituents on the aromatic ring framework
SOD↓, luteolin further triggered an early phase accumulation of ROS due to the suppression of the activity of cellular superoxide dismutase.
*ROS↓, Luteolin reportedly demonstrated an optimal 43.7% inhibition of the accumulation of ROS, 24.5% decrease in malondialdehyde levels, and 38.7% lowering of lactate dehydrogenase levels at a concentration of 30 µM
*LDHA↑,
*SOD↑, expression of superoxide dismutase ameliorated by 73.7%, while the activity of glutathione improved by 72.3% at the same concentration of luteolin
*GSH↑,
*BioAv↓, Poor bioavailability of luteolin limits its optimal therapeutic efficacy and bioactivity
Telomerase↓, MDA-MB-231 cells with luteolin led to dose dependent arrest of cell cycle in S phase by reducing the levels of telomerase and by inhibiting the phosphorylation of NF-kB inhibitor α along with its target gene c-Myc
cMyc↓,
hTERT/TERT↓, These events led to the suppression of the expression of human telomerase reverse transcriptase (hTERT) encoding for the catalytic subunit of telomerase
DR5↑, luteolin upregulated the expression of caspase cascades and death receptors, including DR5
Fas↑, expression of proapoptotic genes such as FAS, FADD, BAX, BAD, BOK, BID, TRADD upregulates, while the anti-apoptotic genes NAIP, BCL-2, and MCL-1 experience downregulation.
FADD↑,
BAD↑,
BOK↑,
BID↑,
NAIP↓,
Mcl-1↓,
CDK2↓, expression of cell cycle regulatory genes CDK2, CDKN2B, CCNE2, CDKN1A, and CDK4 decreased on incubation with luteolin
CDK4↓,
MAPK↓, expression of MAPK1, MAPK3, MAP3K5, MAPK14, PIK3C2A, PIK3C2B, AKT1, AKT2, and ELK1 downregulated
AKT1↓,
Akt2↓,
*Beclin-1↓, luteolin led to downregulation of the expression of hypoxia-inducible factor-1α and autophagy-associated proteins, Beclin 1, and LC3
Hif1a↓,
LC3II↑, LC3-II is upregulated following the luteolin treatment in p53 wild type HepG2 cells i
Beclin-1↑, Luteolin treatment reportedly increased the number of intracellular autophagosomes, as indicated by an increased expression of Beclin 1, and conversion of LC3B-I to LC3B-II in hepatocellular carcinoma SMMC-7721 cells.

3092- RES,    Resveratrol in breast cancer treatment: from cellular effects to molecular mechanisms of action
- Review, BC, MDA-MB-231 - Review, BC, MCF-7
TumCP↓, The anticancer mechanisms of RES in regard to breast cancer include the inhibition of cell proliferation, and reduction of cell viability, invasion, and metastasis.
tumCV↓,
TumCI↓,
TumMeta↓,
*antiOx↑, antioxidative, cardioprotective, estrogenic, antiestrogenic, anti-inflammatory, and antitumor properties it has been used against several diseases, including diabetes, neurodegenerative diseases, coronary diseases, pulmonary diseases, arthritis, and
*cardioP↑,
*Inflam↓,
*neuroP↑,
*Keap1↓, RES administration resulted in a downregulation of Keap1 expression, therefore, inducing Nrf2 signaling, and leading to a decrease in oxidative damage
*NRF2↑,
*ROS↓,
p62↓, decrease the severity of rheumatoid arthritis by inducing autophagy via p62 downregulation, decreasing the levels of interleukin-1β (IL-1β) and C-reactive protein as well as mitigating angiopoietin-1 and vascular endothelial growth factor (VEGF) path
IL1β↓,
CRP↓,
VEGF↓,
Bcl-2↓, RES downregulates the levels of Bcl-2, MMP-2, and MMP-9, and induces the phosphorylation of extracellular-signal-regulated kinase (ERK)/p-38 and FOXO4
MMP2↓,
MMP9↓,
FOXO4↓,
POLD1↓, The in vivo experiment involving a xenograft model confirmed the ability of RES to reduce tumor growth via POLD1 downregulation
CK2↓, RES reduces the expression of casein kinase 2 (CK2) and diminishes the viability of MCF-7 cells.
MMP↓, Furthermore, RES impairs mitochondrial membrane potential, enhances ROS generation, and induces apoptosis, impairing BC progression
ROS↑,
Apoptosis↑,
TumCCA↑, RES has the capability of triggering cell cycle arrest at S phase and reducing the number of 4T1 BC cells in G0/G1 phase
Beclin-1↓, RES administration promotes cytotoxicity of DOX against BC cells by downregulating Beclin-1 and subsequently inhibiting autophagy
Ki-67↓, Reducing the Ki-67
ATP↓, RES’s administration is responsible for decreasing ATP production and glucose metabolism in MCF-7 cells.
GlutMet↓,
PFK↓, RES decreased PFK activity, preventing glycolysis and glucose metabolism in BC cells and decreasing cellular growth rate
TGF-β↓, RES (12.5–100 µM) inhibited TGF-β signaling and reduced the expression levels of its downstream targets that include Smad2 and Smad3 and as a result impaired the progression of BC cells.
SMAD2↓,
SMAD3↓,
Vim?, a significant decrease in the levels of vimentin, Snail1 and Slug occurred, while E-cadherin levels increased to suppress EMT and metastasis of BC cells.
Snail↓,
Slug↓,
E-cadherin↑,
EMT↓,
Zeb1↓, a significant decrease in the levels of vimentin, Snail1 and Slug occurred, while E-cadherin levels increased to suppress EMT and metastasis of BC cells.
Fibronectin↓,
IGF-1↓, RES administration (10 and 20 µM) impaired the migration and invasion of BC cells via inhibiting PI3K/Akt and therefore decreasing IGF-1 expression and preventing the upregulation of MMP-2
PI3K↓,
Akt↓,
HO-1↑, The activation of heme oxygenase-1 (HO-1) signaling by RES reduced MMP-9 expression and prevented metastasis of BC cells
eff↑, RES-loaded gold nanoparticles were found to enhance RES’s ability to reduce MMP-9 expression as compared to RES alone
PD-1↓, RES inhibited PD-1 expression to promote CD8+ T cell activity and enhance Th1 immune responses.
CD8+↑,
Th1 response↑,
CSCs↓, RES has the ability to target CSCs in various tumors
RadioS↑, RES in reversing drug resistance and radio resistance.
SIRT1↑, RES administration (12.5–200 µmol/L) promotes sensitivity of BC cells to DOX by increasing Sirtuin 1 (SIRT1) expression
Hif1a↓, downregulating HIF-1α expression, an important factor in enhancing radiosensitivity
mTOR↓, mTOR suppression

4729- Se,    Selenium regulates Nrf2 signaling to prevent hepatotoxicity induced by hexavalent chromium in broilers
*ROS↓, Studies have reported that selenium (Se), which is one of the essential trace elements of the poultry and participates in the oxidative metabolism, can alleviate Cr(Ⅵ)-induced organ damage by inhibiting oxidative stress,
*NRF2↑, levels of Nrf2, glutathione peroxidase 1 (GPx-1), NAD(P)H: quinone oxidoreductase 1 (NQO1), and mechanistic target of rapamycin (mTOR) in the Se&Cr group was upregulated
*GPx1↑,
*NQO1↑,
*mTOR↑,
*Beclin-1↓, along with decreased expression of Beclin 1, ATG5 and LC3 compared to the Cr group.
*ATG5↓,
*LC3s↓,
*hepatoP↑,

5108- SSE,    Activation of p53 by sodium selenite switched human leukemia NB4 cells from autophagy to apoptosis
- in-vitro, AML, U937
p‑P53↑, Selenite induced phosphorylation of p53 at the vital site Ser15 via p38MAPK and ERK.
Beclin-1↓, The active p53 participated in the decrease of autophagic protein Beclin-1 and LC-3, as well as activation of apoptosis-related caspases.
LC3I↓,
Apoptosis↑,
Casp↑,


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 ⓘ

Catalase↓, 1,   GPx↓, 1,   GSTP1/GSTπ↓, 1,   HO-1↑, 1,   Keap1↝, 1,   lipid-P↑, 1,   NRF2↓, 1,   ROS↓, 1,   ROS↑, 5,   SOD↓, 3,   SOD↑, 1,   SOD1↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   BOK↑, 1,   CDC25↓, 1,   FGFR1↓, 2,   MMP↓, 2,   mtDam↑, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   ALAT↓, 1,   cMyc↓, 2,   GlutMet↓, 1,   PDK1↓, 1,   PFK↓, 1,   POLD1↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 3,   Akt↑, 1,   Apoptosis↑, 3,   BAD↑, 1,   BAX↓, 1,   BAX↑, 1,   Bcl-2↓, 4,   Bcl-xL↓, 1,   BID↑, 1,   Casp↑, 1,   cl‑Casp12↑, 1,   Casp3↑, 2,   Casp9↑, 2,   CK2↓, 2,   Cyt‑c↑, 1,   DR5↑, 1,   FADD↑, 1,   Fas↑, 2,   hTERT/TERT↓, 1,   MAPK↓, 1,   Mcl-1↓, 1,   NAIP↓, 1,   NOXA↑, 1,   PUMA↑, 1,   Telomerase↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

eIF2α↑, 1,   ER Stress↑, 1,   ERStress↑, 1,   GRP78/BiP↑, 1,   PERK↑, 1,  

Autophagy & Lysosomes ⓘ

ATG3↓, 1,   Beclin-1↓, 6,   Beclin-1↑, 2,   LC3‑Ⅱ/LC3‑Ⅰ↓, 1,   LC3I↓, 1,   LC3II↓, 1,   LC3II↑, 2,   p62↓, 2,   p62↑, 2,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 2,   CDK4↓, 2,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 3,   FGF↓, 1,   FGFR2↓, 1,   FOXO4↓, 1,   IGF-1↓, 1,   mTOR↓, 1,   p‑mTOR↑, 1,   PI3K↓, 4,   PTEN↑, 1,   p‑STAT3↓, 1,   TumCG↓, 1,   tyrosinase↓, 1,  

Migration ⓘ

Akt2↓, 1,   Ca+2↑, 2,   E-cadherin↓, 1,   E-cadherin↑, 2,   Fibronectin↓, 1,   Ki-67↓, 1,   MMP2↓, 2,   MMP9↓, 2,   N-cadherin↓, 1,   PDGF↓, 1,   Slug↓, 1,   SMAD2↓, 1,   SMAD3↓, 1,   Snail↓, 1,   TGF-β↓, 1,   TIMP1↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 4,   TumMeta↓, 1,   Vim?, 1,   Vim↓, 2,   Zeb1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   ATF4↑, 1,   Hif1a↓, 2,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CRP↓, 1,   IL1β↓, 1,   NF-kB↓, 1,   PD-1↓, 1,   Th1 response↑, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 2,   RadioS↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   CRP↓, 1,   hTERT/TERT↓, 1,   Ki-67↓, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 133

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GPx1↑, 1,   GSH↑, 1,   Keap1↓, 1,   NQO1↑, 1,   NRF2↑, 2,   ROS↓, 3,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

LDHA↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↓, 1,   Beclin-1↓, 2,   LC3s↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,  

Functional Outcomes ⓘ

cardioP↑, 1,   hepatoP↑, 1,   neuroP↑, 2,  
Total Targets: 18

Scientific Paper Hit Count for: Beclin-1, Beclin-1 (BECN1 gene)
1 Alpha-Lipoic-Acid
1 Betulinic acid
1 Dichloroacetophenone(2,2-)
1 Ferulic acid
1 Luteolin
1 Resveratrol
1 Selenium
1 Selenite (Sodium)
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#:30  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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