LC3s Cancer Research Results

LC3s, Autophagosome Proteins: Click to Expand ⟱
Source:
Type:
LC3s (MAP1-LC3A, B and C) are structural proteins of autophagosomal membranes, widely used as biomarkers of autophagy. Whether these three LC3 proteins have a similar biological role in autophagy remains obscure.
Protumorigenic: In many cases, especially in advanced cancers, increased autophagy (reflected by high LC3 levels) can support tumor growth by providing nutrients and promoting cell survival under stress conditions.
Antitumorigenic: Conversely, in early-stage tumors or in response to certain therapies, autophagy can act as a tumor suppressor by preventing the accumulation of damaged organelles and proteins.
Scientific Papers found: Click to Expand⟱
357- AgNPs,    Hypoxia-mediated autophagic flux inhibits silver nanoparticle-triggered apoptosis in human lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Lung, L132
mtDam↑,
ROS↑,
Hif1a↑, HIF-1α expression was upregulated after AgNPs treatment under both hypoxic and normoxic conditions HIF-1α knockdown enhances hypoxia induced decrease in cell viability
LC3s↑,
p62↑,
eff↓, Hypoxia decreases the effects of anticancer drugs in solid tumor cells through the regulation of HIF-1α

387- AgNPs,    Silver nanoparticles induce mitochondria-dependent apoptosis and late non-canonical autophagy in HT-29 colon cancer cells
- in-vitro, Colon, HT-29
Cyt‑c↑,
P53↑,
BAX↑,
Casp3↑,
Casp9↑,
Casp12↑,
Beclin-1↑,
CHOP↑,
LC3s↑, LC3-II
XBP-1↑,

2681- BBR,  PDT,    Berberine-photodynamic induced apoptosis by activating endoplasmic reticulum stress-autophagy pathway involving CHOP in human malignant melanoma cells
- in-vitro, Melanoma, NA
Apoptosis↑, BBR-PDT induced apoptosis via up-regulating the expression of cleaved caspase-3 protein.
cl‑Casp3↑,
LC3s↑, LC3-related autophagy level was upregulated in MMCs with BBR-PDT.
ER Stress↑, BBR-PDT activated endoplasmic reticulum (ER) stress, involving a dramatic increase in reactive oxygen species (ROS).
ROS↑,
CHOP↑, knockdown of CHOP protein expression inhibited apoptosis, autophagy and ER stress levels caused by BBR-PDT, suggesting that CHOP protein may be related to apoptosis, autophagy and ER stress in MMCs with BBR-PDT

4776- CoQ10,    Antitumor properties of Coenzyme Q0 against human ovarian carcinoma cells via induction of ROS-mediated apoptosis and cytoprotective autophagy
- vitro+vivo, Ovarian, SKOV3
ROS↑, CoQ0 triggered intracellular ROS production, whereas antioxidant N-acetylcysteine prevented CoQ0-induced apoptosis, but not autophagy
eff↓, whereas antioxidant NAC N-acetylcysteine prevented CoQ0-induced apoptosis, but not autophagy
AntiCan↑, Furthermore, CoQ0 treatment to SKOV-3 xenografted nude mice reduced tumor incidence and burden
Apoptosis↑, Our findings emphasize that CoQ0 triggered ROS-mediated apoptosis and cytoprotective autophagy.
tumCV↓, CoQ0 inhibits viability and growth of human ovarian carcinoma cells
TumCG↓, CoQ0 suppresses tumor growth in SKOV-3 xenografted nude mice
TumCCA↑, CoQ0 induces G2/M cell-cycle arrest and reduces cell-cycle proteins in SKOV-3 cells
LC3s↑, CoQ0 promotes LC3 accumulation and AVOs formation in SKOV-3 cells
ERStress↑, CoQ0 triggers apoptotic death of SKOV-3 cells via mitochondrial and ER-stress signals
Beclin-1↑, CoQ0 increases Beclin-1/Bcl-2 and Bax/Bcl-2, and inhibits HER-2/neu/AKT/mTOR signalling in SKOV-3 cells
Bax:Bcl2↑,
HER2/EBBR2↓,
Akt↓,
mTOR↓,

404- CUR,    Curcumin induces ferroptosis in non-small-cell lung cancer via activating autophagy
- vitro+vivo, Lung, A549 - vitro+vivo, Lung, H1299
TumAuto↑,
TumCG↓,
TumCP↓,
Iron↑, iron overload
GSH↓, GSH depletion
lipid-P↑, accumulation of intracellular iron and lipid‐reactive oxygen species (ROS), lipid peroxidation
GPx↓, GPX4
mtDam↑, mitochondrial membrane rupture
autolysosome↑,
Beclin-1↑,
LC3s↑,
p62↓,
Ferroptosis↑, via activating autophagy

2827- FIS,    The Potential Role of Fisetin, a Flavonoid in Cancer Prevention and Treatment
- Review, Var, NA
*antiOx↑, effective antioxidant, anti-inflammatory
*Inflam↓,
neuroP↑, neuro-protective, anti-diabetic, hepato-protective and reno-protective potential.
hepatoP↑,
RenoP↑,
cycD1/CCND1↓, Figure 3
TumCCA↑,
MMPs↓,
VEGF↓,
MAPK↓,
NF-kB↓,
angioG↓,
Beclin-1↑,
LC3s↑,
ATG5↑,
Bcl-2↓,
BAX↑,
Casp↑,
TNF-α↓,
Half-Life↓, Fisetin was given at an effective dosage of 223 mg/kilogram intraperitoneally in mice. The plasma concentration declined biophysically, with a rapid half-life of 0.09 h and a terminal half-life of 3.1 h,
MMP↓, Fisetin powerfully improved apoptotic cells and caused the depolarization of the mitochondrial membrane.
mt-ROS↑, Fisetin played a role in the induction of apoptosis, independently of p53, and increased mitochondrial ROS generation.
cl‑PARP↑, fisetin-induced sub-G1 population as well as PARP cleavage.
CDK2↓, Moreover, the activities of cyclin-dependent kinases (CDK) 2 as well as CDK4 were decreased by fisetin and also inhibited CDK4 activity in a cell-free system, demonstrating that it might directly inhibit the activity of CDK4
CDK4↓,
Cyt‑c↑, Moreover, release of cytochrome c and Smac/Diablo was induced by fisetin
Diablo↑,
DR5↑, Fisetin caused an increase in the protein levels of cleaved caspase-8, DR5, Fas ligand, and TNF-related apoptosis-inducing ligand
Fas↑,
PCNA↓, Fisetin decreased proliferation-related proteins such as PCNA, Ki67 and phosphorylated histone H3 (p-H3) and decreased the expression of cell growth
Ki-67↓,
p‑H3↓,
chemoP↑, Paclitaxel treatment only showed more toxicity to normal cells than the combination of flavonoids with paclitaxel, suggesting that fisetin might bring some safety against paclitaxel-facilitated cytotoxicity.
Ca+2↑, Fisetin encouraged apoptotic cell death via increased ROS and Ca2+, while it increased caspase-8, -9 and -3 activities and reduced the mitochondrial membrane potential in HSC3 cells.
Dose↝, After fisetin treatment at 40 µM, invasion was reduced by 87.2% and 92.4%, whereas after fisetin treatment at 20 µM, invasion was decreased by 52.4% and 59.4% in SiHa and CaSki cells, respectively
CDC25↓, This study proposes that fisetin caused the arrest of the G2/M cell cycle via deactivating Cdc25c as well Cdc2 via the activation of Chk1, 2 and ATM
CDC2↓,
CHK1↑,
Chk2↑,
ATM↑,
PCK1↓, fisetin decreases the levels of SOS-1, pEGFR, GRB2, PKC, Ras, p-p-38, p-ERK1/2, p-JNK, VEGF, FAK, PI3K, RhoA, p-AKT, uPA, NF-ĸB, MMP-7,-9 and -13, whereas it increases GSK3β as well as E-cadherin in U-2 OS
RAS↓,
p‑p38↓,
Rho↓,
uPA↓,
MMP7↓,
MMP13↓,
GSK‐3β↑,
E-cadherin↑,
survivin↓, whereas those of survivin and BCL-2 were reduced in T98G cells
VEGFR2↓, Fisetin inhibited the VEGFR expression in Y79 cells as well as the angiogenesis of a tumor.
IAP2↓, The downregulation of cIAP-2 by fisetin
STAT3↓, fisetin induced apoptosis in TPC-1 cells via the initiation of oxidative damage and enhanced caspases expression by downregulating STAT3 and JAK 1 signaling
JAK1↓,
mTORC1↓, Fisetin acts as a dual inhibitor of mTORC1/2 signaling,
mTORC2↓,
NRF2↑, Moreover, In JC cells, the Nrf2 expression was gradually increased by fisetin from 8 h to 24 h

1018- SSE,    Selenite-induced autophagy antagonizes apoptosis in colorectal cancer cells in vitro and in vivo
- vitro+vivo, CRC, HCT116 - vitro+vivo, CRC, SW480
TumAuto↑,
LC3s↑, expression of autophagy marker LC3 was increased
TumW↓,
Weight∅, no obvious effect on the body weight of the mice
Beclin-1↑,
p62↓,
ROS↑, concluded that selenite-induced apoptosis and autophagy may be caused by ROS


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx↓, 1,   GSH↓, 1,   Iron↑, 1,   lipid-P↑, 1,   NRF2↑, 1,   ROS↑, 4,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 1,   CDC25↓, 1,   MMP↓, 1,   mtDam↑, 2,  

Core Metabolism/Glycolysis ⓘ

PCK1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Casp12↑, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp9↑, 1,   Chk2↑, 1,   Cyt‑c↑, 2,   Diablo↑, 1,   DR5↑, 1,   Fas↑, 1,   Ferroptosis↑, 1,   IAP2↓, 1,   MAPK↓, 1,   p‑p38↓, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

p‑H3↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   ER Stress↑, 1,   ERStress↑, 1,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   autolysosome↑, 1,   Beclin-1↑, 5,   LC3s↑, 7,   p62↓, 2,   p62↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

ATM↑, 1,   CHK1↑, 1,   P53↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↑, 1,   mTOR↓, 1,   mTORC1↓, 1,   mTORC2↓, 1,   RAS↓, 1,   STAT3↓, 1,   TumCG↓, 2,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↑, 1,   Ki-67↓, 1,   MMP13↓, 1,   MMP7↓, 1,   MMPs↓, 1,   Rho↓, 1,   TumCP↓, 1,   uPA↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↑, 1,   VEGF↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

JAK1↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,   eff↓, 2,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

HER2/EBBR2↓, 1,   Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   RenoP↑, 1,   TumW↓, 1,   Weight∅, 1,  
Total Targets: 91

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  
Total Targets: 2

Scientific Paper Hit Count for: LC3s, Autophagosome Proteins
2 Silver-NanoParticles
1 Berberine
1 Photodynamic Therapy
1 Coenzyme Q10
1 Curcumin
1 Fisetin
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

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