LC3B Cancer Research Results

LC3B, microtubule-associated protein 1 light chain 3 beta: Click to Expand ⟱

Source:

Type:

LC3B (microtubule-associated protein 1 light chain 3 beta) is a key protein involved in the autophagy pathway and is widely used as a marker to assess autophagic activity in cells. While not a classical immunogenic cell death (ICD) marker, its expression in tumors has been linked with several prognostic implications, often reflecting the balance between autophagy’s tumor-suppressive and tumor-promoting roles.

• LC3B plays a central role in autophagosome formation.
• Its conversion from LC3BI (cytosolic form) to LC3BII (lipidated, membrane-bound form) is a key indicator of autophagy activation.
• LC3B is sometimes evaluated together with other autophagy-related proteins (such as Beclin-1) to generate an overall picture of autophagic activity in the tumor.

– In several cancers (e.g., pancreatic, colorectal, and breast cancers), elevated LC3B levels have been associated with enhanced autophagy, which can promote tumor cell survival under stress conditions (such as hypoxia or chemotherapy).
– Certain studies, particularly in early-stage tumors or specific subtypes, have found that higher LC3B correlates with improved outcomes.

Scientific Papers found: Click to Expand⟱

5146-

AgNPs,

Silver Nanoparticle-Induced Autophagic-Lysosomal Disruption and NLRP3-Inflammasome Activation in HepG2 Cells Is Size-Dependent

in-vitro,

Liver,

HepG2

TumAuto↑, Overall, 10-nm AgNPs showed the highest cellular responses compared with 50- and 100-nm AgNPs . autophagy-lysosomal system
EPR↑, 10-nm AgNPs exhibited the highest uptake and accumulation.
LC3B↑, Subcytotoxic concentrations of AgNPs enhanced expression of LC3B, a pro-autophagic protein, and CHOP, an apoptosis inducing ER-stress protein, and activation of NLRP3-inflammasome (caspase-1, IL-1β).
CHOP↑,
ER Stress↑,
NLRP3↑,
Casp1↓,

1563-

Api,

MET,

Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells

in-vitro,

Nor,

HDFa

metformin (5 mM), apigenin (1 or 20 µM),

in-vitro,

PC,

AsPC-1

in-vitro,

PC,

MIA PaCa-2

in-vitro,

Pca,

DU145

in-vitro,

Pca,

LNCaP

in-vivo,

NA,

mice

selectivity↑, Metformin increased cellular ROS levels in AsPC-1 pancreatic cancer cells, with minimal effect in HDF, human primary dermal fibroblasts.
selectivity↑, Metformin reduced cellular ATP levels in HDF, but not in AsPC-1 cells
selectivity↓, Metformin increased AMPK, p-AMPK (Thr172), FOXO3a, p-FOXO3a (Ser413), and MnSOD levels in HDF, but not in AsPC-1 cells
ROS↑,
eff↑, Metformin combined with apigenin increased ROS levels dramatically and decreased cell viability in various cancer cells including AsPC-1 cells, with each drug used singly having a minimal effect.
tumCV↓,
MMP↓, Metformin/apigenin combination synergistically decreased mitochondrial membrane potential in AsPC-1 cells but to a lesser extent in HDF cells
Dose∅, co-treatment with metformin (0.05, 0.5 or 5 mM) and apigenin (20 µM) dramatically increased cellular ROS levels in AsPC-1 cells
eff↓, NAC blocked the metformin/apigenin co-treatment-induced cell death in AsPC-1 cells
DNAdam↑, Combination of metformin and apigenin leads to DNA damage-induced apoptosis, autophagy and necroptosis in AsPC-1 cells but not in HDF cells
Apoptosis↑,
TumAuto↑,
Necroptosis↑,
p‑P53↑, p-p53, Bim, Bid, Bax, cleaved PARP, caspase 3, caspase 8, and caspase 9 were also significantly increased by combination of metformin and apigenin in AsPC-1
BIM↑,
BAX↑,
p‑PARP↑,
Casp3↑,
Casp8↑,
Casp9↑,
Cyt‑c↑, Cytochrome C was also released from mitochondria in AsPC-1 cell
Bcl-2↓,
AIF↑, Interestingly, autophagy-related proteins (AIF, P62 and LC3B) and necroptosis-related proteins (MLKL, p-MLKL, RIP3 and p-RIP3) were also increased by combination of metformin and apigenin
p62↑,
LC3B↑,
MLKL↑,
p‑MLKL↓,
RIP3↑,
p‑RIP3↑,
TumCG↑, in vivo
TumW↓, metformin (125 mg/kg) or apigenin (40 mg/kg) caused a reduction of tumor size compared to the control group (Fig. 7D). However, oral administration of combination of metformin and apigenin decreased tumor weight profoundly

1363-

Ash,

doxoR,

Withaferin A Synergizes the Therapeutic Effect of Doxorubicin through ROS-Mediated Autophagy in Ovarian Cancer

in-vitro,

Ovarian,

A2780S

in-vitro,

Ovarian,

CaOV3

in-vivo,

NA,

in vivo xenograft model of ovarian cancer.

ChemoSen↑, thus reducing the dosage requirement of Dox
ROS↑,
DNAdam↑, immense DNA damage
TumCCA↑,
LC3B↑,
TumCG↓, 70 to 80% reduction in tumor growth
cl‑Casp3↑,

1387-

BBR,

Antitumor Activity of Berberine by Activating Autophagy and Apoptosis in CAL-62 and BHT-101 Anaplastic Thyroid Carcinoma Cell Lines

in-vitro,

Thyroid,

CAL-62

TumCG↓,
Apoptosis↑,
LC3B↑, LC3B-II
ROS↑,
PI3K↓,
Akt↓,
mTOR↓,

3679-

BBR,

Berberine alleviates Alzheimer's disease by activating autophagy and inhibiting ferroptosis through the JNK-p38MAPK signaling pathway

in-vivo,

AD,

5xFAD mice

*Beclin-1↑, autophagy-related markers Beclin1 and LC3B were upregulated and P62 was downregulated after BBR treatment.
*LC3B↑,
*p62↓,
*ROS↓, ROS and lipid peroxide MDA decreased significantly after BBR treatment.
*lipid-P↓,
*MDA↓,
*Ferroptosis↓, expression levels of ferroptosis-related genes TFR1, ASCL4, DMT1, and IREB2 were decreased, while the expression levels of FTH1 and SLC7A11 increased after BBR treatment.
*TfR1/CD71↓,
*FTH1↑,
*memory↑, BBR treatment enhanced spatial memory impairment in 5xFAD mice.
*JNK↓, inhibited ferroptosis by inhibiting the JNK-P38MAPK signaling pathway.
*p38↓,
*Aβ↓, further reducing Aβ plaque deposition, inhibiting inflammatory response,
*Inflam↓,

5068-

dietSTF,

mTOR-autophagy axis regulation by intermittent fasting promotes skeletal muscle growth and differentiation

in-vivo,

Nor,

*glucose↓, Following short-term fasting, blood glucose levels in the sMF and sSF groups were significantly lower than those in the ND group
ROS↑, reactive oxygen species (ROS) levels were significantly higher in the sSF group compared to the sMF and ND groups
LC3B↑, sSF groups exhibited a significant upregulation of LC3B protein levels
p62↓, Conversely, p62 levels (1.00 ± 0.08, 0.58 ± 0.09 & 0.28 ± 0.05, P < 0.01) and the phosphorylation ratio of mTOR (p-mTOR/mTOR) (1.00 ± 0.04, 0.70 ± 0.10 & 0.35 ± 0.03, P < 0.01) were significantly reduced.
p‑mTOR↓,
p‑AMPK↑, IMF group exhibited a significant increase in the LC3B-II/I ratio and the phosphorylation ratio of AMPK (p-AMPK/AMPK)

3205-

EGCG,

The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas

Review,

Var,

Review,

AD,

Beclin-1↑, EGCG not only regulates autophagy via increasing Beclin-1 expression and reactive oxygen species generation,
ROS↑,
Apoptosis↑, Apoptosis is a common cell function in biology and is induced by endoplasmic reticulum stress (ERS)
ER Stress↑,
*Inflam↓, EGCG has health benefits including anti-tumor [15], anti-inflammatory [16], anti-diabetes [17], anti-myocardial infarction [18], anti-cardiac hypertrophy [19], anti-atherosclerosis [20], and antioxidant
*cardioP↑,
*antiOx↑,
*LDL↓, These effects are mainly related to (LDL) cholesterol inhibition, NF-κB inhibition, MPO activity inhibition, decreased levels of glucose and glycated hemoglobin in plasma, decreased inflammatory markers, and reduced ROS generation
*NF-kB↓,
*MPO↓,
*glucose↓,
*ROS↓,
ATG5↑, EGCG induced autophagy by enhancing Beclin-1, ATG5, and LC3B and promoted mitochondrial depolarization in breast cancer cells.
LC3B↑,
MMP↑,
lactateProd↓, 20 mg kg−1 EGCG significantly decreased glucose, lactic acid, and vascular endothelial growth factor (VEGF) levels
VEGF↓,
Zeb1↑, (20 uM) inhibited the proliferation through activating autophagy via upregulating ZEB1, WNT11, IGF1R, FAS, BAK, and BAD genes and inhibiting TP53, MYC, and CASP8 genes in SSC-4 human oral squamous cells [
Wnt↑,
IGF-1R↑,
Fas↑,
Bak↑,
BAD↑,
TP53↓,
Myc↓,
Casp8↓,
LC3II↑, increasing the LC3-II expression levels and induced apoptosis via inducing ROS in mesothelioma cell lines,
NOTCH3↓, but also could reduce partially Notch3/DLL3 to reduce drug-resistance and the stemness of tumor cells
eff↑, In combination therapies, low-intensity pulsed electric field (PEF) can improve EGCG to affect tumor cells; ultrasound (US) with tumor cells is the application of physical stimulation in cancer therapy.
p‑Akt↓, 20 μM EGCG increased intracellular ROS levels and LC3-II, and inhibited p-Akt in PANC-1 cells
PARP↑, 100 μM EGCG increased LC3-II, activated caspase-3 and PARP, and reduced p-Akt in HepG2
*Cyt‑c↓, EGCG protected neuronal cells against human viruses by inhibiting cytochrome c and Bax translocations, and reducing autophagy with increased LC3-II expression and decreased p62 expression
*BAX↓,
*memory↑, EGCG restored autophagy in the mTOR/p70S6K pathway to weaken memory and learning disorders induced by CUMS
*neuroP↑, Finally, EGCG increased the neurological scores through inhibiting cell death
*Ca+2?, EGCG treatment, [Ca2+]m and [Ca2+]i expressions were reduced and oxyhemoglobin-induced mitochondrial dysfunction lessened.
GRP78/BiP↑, MMe cells with EGCG treatment improved GRP78 expression in the endoplasmic reticulum, and induced EDEM, CHOP, XBP1, and ATF4 expressions, and increased the activity of caspase-3 and caspase-8.
CHOP↑, GRP78 accumulation converted UPR of MMe cells into pro-apoptotic ERS
ATF4↑,
Casp3↑,
Casp8↑,
UPR↑,

2177-

itraC,

Itraconazole improves survival outcomes in patients with colon cancer by inducing autophagic cell death and inhibiting transketolase expression

Study,

Colon,

present study analyzed extensive data from patients diagnosed with colon cancer using itraconazole between January 2011 and December 2015

in-vitro,

CRC,

COLO205

in-vitro,

CRC,

HCT116

OS↑, Itraconazole increases the 5-year survival rate in patients with late-stage colon cancer who receive chemotherapy
tumCV↓, itraconazole decreased the viability and cell colony formation, and induced cleaved caspase-3 expression and G1 cell cycle arrest of COLO 205 and HCT 116 cells.
Casp3↑,
TumCCA↑,
HH↓, Itraconazole can induce autophagic cell death by activating the hedgehog pathway to inhibit breast cancer cell proliferation (25).
TumAuto↑, expression levels of the autophagy-related proteins, LC3B and p62, significantly increased in COLO 205 and HCT 116 cells following treatment with itraconazole for 24 h
LC3B↑,
p62↑,
TKT↓, TKT expression was decreased following treatment with itraconazole in a time-dependent manner

2076-

PB,

Sodium Butyrate Induces Endoplasmic Reticulum Stress and Autophagy in Colorectal Cells: Implications for Apoptosis

in-vitro,

CRC,

HCT116

0-5mM

in-vitro,

CRC,

HT29

TumCP↓, Sodium butyrate suppressed colorectal cancer cell proliferation, induced autophagy, and resulted in apoptotic cell death
TumAuto↑,
Apoptosis↑,
ER Stress↑, sodium butyrate treatment markedly enhanced the expression of endoplasmic reticulum stress-associated proteins, including BIP, CHOP, PDI, and IRE-1a.
BID↑,
CHOP↑,
PDI↑,
IRE1↓,
LC3‑Ⅱ/LC3‑Ⅰ↑, A marked conversion of free LC3-I to heavier lipid bound LC3-II was detected after exposing HCT-116 (Fig 3A) and HT-29 (Fig 3B) cells to 2mM sodium butyrate for 24 h
LC3B↑, mRNA levels of Beclin 1 and LC3B, but not ATG3, significantly increased with increasing doses of NaBu
Beclin-1↑,
other↝, These results strongly suggested that NaB induced autophagy was mediated by ER stress in CRC cells.
other↝, Inhibition of autophagy enhanced NaB-induced apoptotic cell death

1483-

SFN,

Targeting p62 by sulforaphane promotes autolysosomal degradation of SLC7A11, inducing ferroptosis for osteosarcoma treatment

in-vitro,

OS,

143B

0-10uM

in-vitro,

Nor,

HEK293

in-vivo,

OS,

25-50mg/kg

subcutaneous tumor-bearing nude mouse model

AntiCan↑, has shown potential anti-cancer effects with negligible toxicity
*toxicity∅, (liver, kidney, heart, spleen, and lung) showed no evidence of toxicity associated with SFN treatment
Ferroptosis↑, results demonstrate the dependency of downregulation of SLC7A11 in SFN-induced ferroptosis in OS cells
ROS↑, elevated ROS levels, lipid peroxidation, and GSH depletion
lipid-P↑,
GSH↓, which was dependent on decreased levels of SLC7A11
p62↑, enhanced p62/SLC7A11 protein-protein interaction, thereby promoting the lysosomal degradation of SLC7A11 and triggering ferroptosis
SLC12A5↓, SFN induces ferroptosis of OS cells through downregulation of SLC7A11
eff↓, ferroptosis inhibitors Fer-1 (ferrostatin-1), DFO (deferoxamine), and Lip-1 (liproxstatin-1) substantially rescued the cells from SFN-induced cell death
GPx4↓, SFN treatment markedly reduced the expression levels of ferroptosis markers GPX4 and SLC7A11 in OS cells
i-Iron↑, validated the intracellular Fe2+ accumulation by SFN
eff↓, SLC7A11 overexpression notably reversed SFN-induced changes in the ROS level, GSH level, and lipid peroxidation
MDA↑, SFN treatment reduced GSH levels and increased MDA production, indicating the induction of ferroptosis
TumVol↓,
TumW↓,
Ki-67↓, subcutaneous tumors revealed significantly lower expression levels of Ki67, SLC7A11, and GPX4, along with upregulated LC3B in the SFN-treated group
LC3B↑,
*Weight∅, no significant difference in body weight was observed between the control and SFN-treated groups

2416-

SK,

Shikonin induces cell death by inhibiting glycolysis in human testicular cancer I-10 and seminoma TCAM-2 cells

in-vitro,

Testi,

TCAM-2

MMP↓, Shikonin treatment significantly reduced mitochondrial membrane potential, increased ROS levels and lower the level of lactic acid in both I-10 and TCAM-2 cells
ROS↑,
lactateProd↓,
Bcl-2↓, shikonin treatment significantly down- regulated the expressions of Bax, Bcl-2, cleaved caspase-3, PKM2, GLUT1 and HK2, and up-regulated the expression of autophagy-related protein LC3B
cl‑Casp3↓,
PKM2↓,
GLUT1↓,
HK2↓,
LC3B↑,

Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

AntiCan↑, 1, OS↑, 1, TumVol↓, 1, TumW↓, 2,
Total Targets: 93

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Ferroptosis↓, 1, lipid-P↓, 1, MDA↓, 1, MPO↓, 1, ROS↓, 2,

Metal & Cofactor Biology ⓘ

FTH1↑, 1, TfR1/CD71↓, 1,

Core Metabolism/Glycolysis ⓘ

glucose↓, 2, LDL↓, 1,

Cell Death ⓘ

BAX↓, 1, Cyt‑c↓, 1, Ferroptosis↓, 1, JNK↓, 1, p38↓, 1,

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1, LC3B↑, 1, p62↓, 1,

Migration ⓘ

Ca+2?, 1,

Immune & Inflammatory Signaling ⓘ

Inflam↓, 2, NF-kB↓, 1,

Protein Aggregation ⓘ

Aβ↓, 1,

Functional Outcomes ⓘ

cardioP↑, 1, memory↑, 2, neuroP↑, 1, toxicity∅, 1, Weight∅, 1,
Total Targets: 27

Scientific Paper Hit Count for: LC3B, microtubule-associated protein 1 light chain 3 beta

2 Berberine
1 Silver-NanoParticles
1 Apigenin (mainly Parsley)
1 Metformin
1 Ashwagandha(Withaferin A)
1 doxorubicin
1 diet Short Term Fasting
1 EGCG (Epigallocatechin Gallate)
1 itraconazole
1 Phenylbutyrate
1 Sulforaphane (mainly Broccoli)
1 Shikonin

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#:1081  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

LC3B Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Autophagy & Lysosomes ⓘ

Migration ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Functional Outcomes ⓘ

Home Page