LC3II Cancer Research Results

LC3II, Microtubule-associated protein 1A/1B light chain 3: Click to Expand ⟱
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Type:
LC3II (Microtubule-associated protein 1A/1B light chain 3, also known as LC3) is a protein that plays a crucial role in the process of autophagy. Autophagy is a cellular process in which cells recycle and remove damaged or dysfunctional components.
LC3II is often used as a marker for autophagy, as its levels increase during autophagic activity.
LC3II is overexpressed in certain types of cancer, including breast, lung, and colon cancer.
LC3II is also known by other names, including:
    MAP1LC3B (Microtubule-associated protein 1 light chain 3 beta)
    LC3B (Microtubule-associated protein 1 light chain 3 beta)
    ATG8F (Autophagy-related protein 8F)
: In many cancers, increased LC3-II expression indicates enhanced autophagy, which can support tumor cell survival, especially under stress conditions (e.g., nutrient deprivation, hypoxia). This is often associated with poor prognosis and treatment resistance.
Scientific Papers found: Click to Expand⟱
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↑,

6819- EMD,    Recent advances in the therapeutic potential of emodin for human health
- Review, Nor, NA
AntiCan↑, It has therapeutic effects in cancer, diabetes, neurodegenerative diseases or chronic inflammatory diseases.
*AntiDiabetic↑, anticancer, neuroprotective, antidiabetic, antioxidant and anti-inflammatory.
*neuroP↑,
*Inflam↓,
*antiOx↑,
*BioAv↓, Because its bioavailability is low, there are limitations in clinical therapeutic use.
*BioAv↑, combined administration of emodin and piperine has been observed to clinically improve emodin pharmacokinetics, increasing 221 % of the area under the curve (AUC), 258 % the maximum concentration (Cmax), and decreasing 230 % the clearance related to
*SOD↑, fig 2 antioxidant
*GPx↑,
*GSH↑,
*NRF2↑,
*ROS↓,
*lipid-P↓,
*Cyt‑c↓,
*BAX↓, fig 2 antiinflammatory
*Bcl-2↓,
*iNOS↓,
*NO↓,
*IL6↓,
*IL10↓,
*IL17↓,
*IFN-γ↓,
*NF-kB↓,
*LC3II↓,
*Akt↓,
*Beclin-1↓,
*AMPK↓, fig 2 neuroprotective
*TNF-α↓,
*PGE2↓,
*Apoptosis↓,
*Casp3↓,
*Casp9↓,
*P53↓,
*P21↓,
*NAD↓, neuronal oxidative stress
*ATP↓,
*CHOP↓,
*GADD34↓,
*ATF4↓,
tumCV↓, fig 2 anticancer
Apoptosis↑,
TumCG↓,
TumCI↓,
TumMeta↓,
CSCs↓, glioma stem cells ↓b-catenin, ↓Notch-1, ↓STAT3
NOTCH1↓,
STAT3↓,
eff↑, emodin combined with curcumin ↓proliferation, ↑miR-34a
miR-34a↓,
*neuroP↑, Neuroprotective LPS-stimulated mouse ↓Nrf-2, NQO1, ↓TNF-α,↓↓ IL-6, ↓NO, ↓PGE2
*BDNF↓, model of chronic stress mice in vivo ↓progression of behavioral impairments in mice ↓consumption of sucrose, ↓plasmatic corticosterone, ↓mRNA, ↓BDNF,
*hepatoP↑, Hepatoprotective rats in vivo ↓ethanol-mediated liver steatosis ↓ ALT, ↓AST, ↓ TGL
*ALAT↓,
*AST↓,
TG/TAG↓,
ROS↑, However, at higher concentrations, emodin significantly increased ROS generation and reduced cell viability.
Slug↓, expression levels of Slug (a transcription factor) were also suppressed with emodin treatment.
EMT↓, results suggested that emodin suppressed the epithelial-mesenchymal transition of cancer cells through the ILK/GSK-3β/Slug signaling pathway
Glycolysis↓, In addition, emodin inhibited glycolysis via ROS-induced inactivation of the PI3K/AKT signaling pathway.
ChemoSen↑, The study by Peng et al. [130] also showed chemosensitizing effects of emodin to cisplatin in A549 (2–20 µM, for 48 h) and H460 (0.5–10 µM) non-small cell lung cancer cells.
P-gp↓, The sensitization mechanism was mediated by the inhibition of P-glycoprotein (Pgp), a drug-resistant protein related to the efflux pump mechanism.
Ki-67↓, The significant reduction of Ki-67 and proliferating cell nuclear antigen (PCNA) protein levels supported the antiproliferative effect of emodin in animal models.
PCNA↓,
ER Stress↑, findings suggested that emodin exerts its apoptotic effects in a process mediated by ER stress and the activation of the TRIB3/NF-κB pathway in lung cancer cells.
TRIB3↑,
NF-kB↑,
TumMeta↑, Emodin (40 mg/kg for 7 days) significantly decreased the metastatic recurrence of breast cancer after surgery in the lungs by reducing the formation of epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC).
*Imm↓, emodin may be developed as an immunosuppressive agent in case of immune activation, autoimmune disorders even in organ transplantation
*toxicity↝, An excess of emodin due to its laxative effects causes intestinal pain and severe diarrhea with subsequent electrolyte imbalance and dehydration [157]. Therefore, treatment should begin when symptoms appear, with special attention to electrolyte leve

6824- EMD,    Neuroprotective, Anti-Inflammatory and Antifibrillogenic Offerings by Emodin against Alzheimer’s Dementia: A Systematic Review
- Review, AD, NA
*Inflam?, Emodin is a bioactive phytochemical with potent multimodal anti-inflammatory, antioxidant, and antifibrillogenic properties.
*antiOx↑,
*tau↓, While emodin effectively prevents tau and amyloid-beta (Aβ) oligomerization, it also mitigates their neurotoxicity by attenuating neuroinflammatory, oxidative, and bioenergetic defects.
*Aβ↓,
*neuroP↑, In recent years, several studies have advocated for a robust neuroprotective function of emodin
*ROS↓,
*memory↑, Evidences for emodin-mediated enhancements in memory, learning, and cognition were also found in the literature
*cognitive↑,
*other↝, Well-known sources of emodin include Rheum palmatum,10Polygonum cuspidatum,11Aloe vera,12Polygonum multifarum,13 and Casia obtusofolia.
*AChE↓, potent in vitro inhibition of AChE (IC50 of 21.8 μM), in addition to amelioration of H2O2-induced oxidative damage in PC12 cells
*BACE↓, potent inhibition of the activities of BACE-1 (IC50 of 4.5 μM) and AChE (IC50 of 9.7 μM); and strong and mixed-type inhibition for BACE-1 (Ki of 20 μM) in kinetic studies
*LC3II↓, Inhibition of autophagic (LC3-II and beclin-1)
*Beclin-1↓,
*p‑tau↓, 80 mg/kg/day for 2 weeks (intragastric administration) repression of the levels of BACE-1, Aβ species and phosphorylated-tau, stimulation of CREB signaling
*CREB↑,
*HNE↓, downregulation of Aβ and phosphorylated-tau levels, reduced oxidative damage and 4-HNE levels
*BioAv↓, Bioavailability of exogenously administered emodin suffers from some issues, including its weak intestinal absorption, high rate of elimination, and first-pass metabolism
*BioAv↝, bioavailability of orally supplemented emodin may show appreciable dependence on gender, given that there are four times higher plasma levels of emodin in male rats, compared to females after a single oral dosing of emodin at 8 mg/kg body weight.
*BioAv↑, pretreatment with stilbene glucosides from Radix Polygoni Multiflori prevents glucuronidation of emodin, and increases its plasma concentration upon oral administration
*BioAv↑, cotreatment with piperine was also found to inhibit glucuronide formation of orally administered emodin, while increasing the bioavailability of its free form
*BioAv↑, Nanoemulsification may also decreses the clearance of orally administered emodin, while increasing its brain distribution and bioavailability.
*BioAv↑, Lastly, treatment of emodin with sodium hydroxide to form its sodium salt may represent another strategy for improving the solubility and bioavailability of emodin
BioAv↑, ultrasound-sensitive emodin-containing lecithin-based nanoformulations squamous cell carcinoma FaDu and CAL-27 cells neck squamous cell carcinoma sonodynamic therapy-based beneficial actions
*HO-1↑, figure 3, neuroproctive
*PKCδ↑,
*Akt↑,
*NLRP3↓,
*NF-kB↓,
*TLR3↓,

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↓,


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   GPx↓, 1,   HO-1↑, 1,   lipid-P↑, 1,   NQO1↑, 1,   ROS↑, 3,   SOD↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↓, 1,   FGFR1↓, 2,   mtDam↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   cMyc↓, 1,   Glycolysis↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Akt↑, 1,   Apoptosis↑, 2,   BAX↓, 1,   Bcl-2↓, 2,   Casp3↑, 2,   Casp9↑, 1,   CK2↓, 1,   Fas↑, 1,   NOXA↑, 1,   PUMA↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

SOX9?, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

EZH2↓, 1,   miR-21↓, 1,   miR-27a-3p↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,   Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↓, 1,   LC3II↓, 2,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 2,   DNMT1↓, 1,   p16↑, 1,   P53↑, 1,   PARP↑, 1,   PCNA↓, 1,   TP53↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

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

CSCs↓, 2,   EMT↓, 3,   FGF↓, 1,   FGFR2↓, 1,   miR-34a↓, 1,   Nanog↓, 1,   NOTCH1↓, 2,   OCT4↓, 1,   PI3K↓, 1,   PTEN↑, 2,   SOX2↓, 1,   STAT3↓, 2,   p‑STAT3↓, 1,   TumCG↓, 1,   tyrosinase↓, 1,  

Migration(tgid=13) ⓘ

CXCL12↓, 1,   E-cadherin↓, 1,   Ki-67↓, 1,   LAMs↓, 1,   MMP2↓, 2,   MMP9↓, 2,   PDGF↓, 1,   Slug↓, 1,   TGF-β↓, 1,   TIMP1↑, 1,   TRIB3↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 1,   TumMeta↑, 1,   Vim↓, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,   VEGF↓, 3,   ZBTB10↑, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   IL6↓, 1,   JAK2↓, 1,   NF-kB↓, 1,   NF-kB↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 2,   ChemoSen↑, 3,   eff↑, 2,   RadioS↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   EZH2↓, 1,   IL6↓, 1,   Ki-67↓, 1,   TG/TAG↓, 1,   TP53↑, 1,   TRIB3↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,  
Total Targets: 105

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   GPx↑, 1,   GSH↑, 1,   HNE↓, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 4,   SOD↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   AMPK↓, 1,   CREB↑, 1,   NAD↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Akt↑, 1,   Apoptosis↓, 1,   BAX↓, 1,   Bcl-2↓, 1,   Casp3↓, 1,   Casp9↓, 1,   Cyt‑c↓, 1,   GADD34↓, 1,   iNOS↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 2,   LC3II↓, 2,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,  

Migration(tgid=13) ⓘ

PKCδ↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 1,   NO↓, 1,   NO↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IFN-γ↓, 1,   IL10↓, 1,   IL17↓, 1,   IL6↓, 1,   Imm↓, 1,   Inflam?, 1,   Inflam↓, 2,   NF-kB↓, 2,   PGE2↓, 1,   TLR3↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   BDNF↓, 1,   tau↓, 1,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   BACE↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 3,   BioAv↑, 5,   BioAv↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 1,   cognitive↑, 2,   hepatoP↑, 1,   memory↑, 2,   neuroP↑, 3,   toxicity↝, 1,  
Total Targets: 65

Scientific Paper Hit Count for: LC3II, Microtubule-associated protein 1A/1B light chain 3
2 Emodin
1 Curcumin
1 Ferulic acid
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#:721  State#:%  Dir#:1
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