LC3‑Ⅱ/LC3‑Ⅰ Cancer Research Results

LC3‑Ⅱ/LC3‑Ⅰ, ratio of LC3‑Ⅱ/LC3‑Ⅰ: Click to Expand ⟱
Source:
Type: marker
The ratio of LC3-II to LC3-I is often used as a marker for autophagy, a cellular process in which cells recycle their damaged or dysfunctional components. In cancer, autophagy can play a complex role, and the LC3-II/LC3-I ratio can be used to assess autophagic activity.
Many cancers, have an increased LC3-II/LC3-I ratio indicating 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.
Cell Survival: Increased autophagy, as indicated by a higher LC3-II/LC3-I ratio, can help cancer cells survive in adverse conditions, contributing to tumor growth and metastasis.
Therapeutic Resistance: Elevated autophagy can lead to resistance against chemotherapy and targeted therapies, as cancer cells may utilize autophagy to survive treatment-induced stress.
Metabolic Adaptation: Autophagy allows cancer cells to adapt to metabolic stress by recycling cellular components, which can support continued proliferation and survival.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
1580- Citrate,    Citrate activates autophagic death of prostate cancer cells via downregulation CaMKII/AKT/mTOR pathway
- in-vitro, Pca, PC3 - in-vivo, PC, NA - in-vitro, Pca, LNCaP - in-vitro, Pca, WPMY-1
Apoptosis↑, Ca+2↓, Akt↓, mTOR↓, selectivity↑, TumCP↓, cl‑Casp3↑, cl‑PARP↑, LC3‑Ⅱ/LC3‑Ⅰ↑, p62↓, ATG5↑, ATG7↑, Beclin-1↑, TumAuto↑, CaMKII ↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Core Metabolism/Glycolysis ⓘ

ATG7↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   cl‑Casp3↑, 1,  

Kinase & Signal Transduction ⓘ

CaMKII ↓, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,  

Migration ⓘ

Ca+2↓, 1,   TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: LC3‑Ⅱ/LC3‑Ⅰ, ratio of LC3‑Ⅱ/LC3‑Ⅰ
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:22  Cells:%  prod#:%  Target#:685  State#:%  Dir#:2
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