RUBCN Cancer Research Results

RUBCN, Rubicon Autophagy Regulator: Click to Expand ⟱
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RUBCN - Rubicon Autophagy Regulator

Abbreviation: RUBCN, Rubicon

Alternative Names: RUN Domain Beclin-1-Interacting and Cysteine-Rich Domain-Containing Protein

Type: Autophagy regulator / Beclin 1-VPS34 complex regulator / noncanonical autophagy protein

Function: Rubicon is a negative regulator of canonical autophagy that inhibits autophagosome maturation and autophagosome-lysosome fusion through interactions with the Beclin 1-VPS34-UVRAG machinery and related fusion components. In contrast, Rubicon is required for LC3-associated phagocytosis (LAP) and other noncanonical ATG8/LC3 conjugation pathways.

Cancer: ↑ Rubicon expression is increased in several cancers and can promote tumor progression by suppressing canonical autophagic flux and by supporting Rubicon-dependent noncanonical pathways such as LAP that may reduce antitumor immune activity. High RUBCN expression has been associated with poor prognosis in some tumor types.

Favorable Direction in Cancer: ↓ RUBCN may be favorable in cancers where Rubicon promotes tumor progression or immunosuppressive LAP. However, effects can depend on tumor type, immune context, and Rubicon isoform.

Interpretation Note: Rubicon has opposite functional roles in different autophagy pathways: it inhibits canonical autophagy but is required for LC3-associated phagocytosis. Therefore, RUBCN ↑ should not automatically be interpreted simply as autophagy ↓ without identifying which pathway is being measured.
Scientific Papers found: Click to Expand⟱
8235- LCA,    Anticancer effects of licochalcones: A review of the mechanisms
- Review, Var, NA
mt-Apoptosis↑, licochalcones can activate the mitochondrial apoptosis pathway and the death receptor pathway, promote autophagy-related protein expression, inhibit cell cycle protein expression,
TumAuto↑,
TumCMig↓, regulate cancer migration-related protein expression via multiple signaling pathways, including EGFR/ERK, PI3K/Akt/mTOR, p38/JNK, JAK2/STAT3, MEK/ERK, Wnt/β-catenin, and MKK4/JNK signaling pathways.
LC3‑Ⅱ/LC3‑Ⅰ↑, increasing the LC3-II/LC3-I ratio, as well as the levels of the autophagy-related proteins ATG5, ATG7, and P62.
ATG5↑,
ATG7↑,
p62↑,
CHOP/DDIT3↑, LA-induced increases in CHOP expression also promote autophagy
ER Stress↑, LA-induced autophagy in lung cancer cells is associated with the induction of endoplasmic reticulum stress
UPR↑, LA (10 μM) enhances the expression of miR-144-3p, causes unfolded protein response,
ATG3↑, triggers autophagy by promoting the accumulation and expression of ATG1, ATG3, ATG6, and ATG16 via activation of the PERK/ATF4/CHOP signaling pathway
Beclin-1/ATG6↑,
ATG16L1↑,
PERK↑,
ATF4↑,
ATP↓, LA (2.5–25 μM) inhibited ATP production and caused mitochondrial dysfunction in H1299 and H322 lung cancer cells by inhibiting hypoxia-induced HIF-1α accumulation and the expression of target genes GLUT1 and PDK1
Hif1a↓,
GLUT1↓,
PDK1 / PDPK1↓,
Bcl-xL↓, induce apoptosis in H460 and A549 lung cancer cells by decreasing the levels of Bcl-xL and Bcl-2 while increasing the levels of Bad, Bax, cleaved PARP, and caspase-3
Bcl-2↓,
BAD↑,
BAX↑,
Casp3↑,
survivin↓, LA (5–50 μM) downregulated the expression of survivin by inhibiting the EGFR signaling pathway and its downstream kinases ERK1/2 and AKT in H3255, HCC827, H1975, and A549 lung cancer cells
EGFR↓,
ERK↓,
Akt↓,
mtDam↑, LB (5–15 μM) inhibited the EGFR and MET signaling pathways and induced mitochondrial dysfunction and endoplasmic reticulum stress in HCC827 lung cancer cells, which induced the loss of MMP, release of cytochrome c, and increased expression of casp
MMP↓,
Cyt‑c↑,
Casp↑,
MDM2↓, By inhibiting the expression of MDM2, cyclin B1, CDC2, and CDC25C, LA (10–15 μM) led to cell cycle arrest of H460 and A549 lung cancer cells at the G2/M phase
CycB/CCNB1↓,
CDC2↓,
CDC25↓,
TumCCA↑,
TumCP↓, decreases in the proliferation of lung cancer cells by LA were related to the inhibition of the Wnt/β-catenin signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
Sp1/3/4↓, LA (2–20 μM) inhibited the AKT signaling pathway and the expression of the downstream transcription factor Sp1, which reduced the levels of MMP-1 and MMP-3 and inhibited the migration and invasion of A549 and H460 lung cancer cells
MMP-10↓,
MMP3↓,
TumCI↓,
Imm↑, Activation of the immune system
PD-L1↓, LA (10–50 μM) inhibited the expression of PD-L1 and thereby induced the production of reactive oxygen species (ROS) in A549 lung cancer cells, which inhibited the phosphorylation of 4EBP1, activated the PERK/eIF2α pathway,
ROS↑,
4E-BP1↓,
eIF2α↓,
PI3K↓, By inhibiting the PI3K/Akt/mTOR signaling pathway, LA (5–20 μM) activated the mitochondrial apoptosis pathway
mTOR↓,
p‑cMET↑, LA (1–50 μM) induced endoplasmic reticulum stress in HepG2 cells by inducing phosphorylation of VEGFR2, c-Met receptor, and PLCγ1 and enhancing the cytosolic Ca2+ release from the endoplasmic reticulum, which subsequently induced ROS accumulation
Ca+2↑,
RUBCN↓, LA-induced (5–50 μM) downregulation of PDK1 and rubicon by activating the ULK1/Atg13 signaling pathway and increasing the expression of TSC1/2, PRAS40, CTMP, and PP2A.
ATG13↑,
TSC1↑,
TSC2↑,
PRAS40↑,
PP2A↑,
ULK1/ATG1↑,
THEM4/CTMP↑,
DR5↑, LA activates the death receptor pathway and caspase cascade by increasing the expression of DR3, DR5, and Fas.
Fas↑,
TNFRSF25/DR3/APO3/LARD/TRAMP/WSL1↑,
PKCδ↓, LA also decreases the expression of the survival factor PKCε, p70S6K, and Akt.
P70S6K↓,
VEGF↓, Via downregulation of VEGF-A, LE (7–14 mg/kg) inhibited angiogenesis in cancer tissue in a xenograft mouse model using MDA-MB 231 breast cancer cells
angioG↓,
HK2↓, Moreover, the inhibitory effect of LA (10–50 μM) on the AKT signaling pathway can downregulate the expression of hexokinase 2A and inhibit glycolysis, thereby inducing apoptosis of MKN45 and SGC7901 cells
Glycolysis↓,
TrxR1↓, LA (10–40 μM) can enhance the production of intracellular ROS by inhibiting the expression of thioredoxin reductase-1, which activates the mitochondrial apoptosis pathway and induces apoptosis in HCT-116 cells
APAF1↑, By increasing intracellular Ca2+ and ROS levels, decreasing mitochondrial membrane potential, upregulating Apaf-1, caspase-9, caspase-3, and cleaved PARP levels, and elevating the Bax/Bcl-2 ratio, LA (10–80 μM) induced T24 cells apoptosis
cl‑PARP↑,
Bax:Bcl2↑,
ABCG2↓, By reducing the expression of BCRP, LA (10–100 μM) reduced the BCRP-mediated efflux of doxorubicin and temozolomide in BCRP-MDCKII cells.
BioEnh↑, Inhibition of BCRP expression can promote increased intestinal (re)uptake of antineoplastic drugs and decrease their hepatic metabolization, thereby enhancing their bioavailability.


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:


NA, unassigned(tgid=0) ⓘ

ATG13↑, 1,   ATG16L1↑, 1,   RUBCN↓, 1,   THEM4/CTMP↑, 1,   TNFRSF25/DR3/APO3/LARD/TRAMP/WSL1↑, 1,   ULK1/ATG1↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,   TrxR1↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

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

Core Metabolism/Glycolysis(tgid=4) ⓘ

ATG7↑, 1,   Glycolysis↓, 1,   HK2↓, 1,   PDK1 / PDPK1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   APAF1↑, 1,   mt-Apoptosis↑, 1,   BAD↑, 1,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↑, 1,   Cyt‑c↑, 1,   DR5↑, 1,   Fas↑, 1,   MDM2↓, 1,   survivin↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Sp1/3/4↓, 1,   TSC2↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   eIF2α↓, 1,   ER Stress↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG3↑, 1,   ATG5↑, 1,   Beclin-1/ATG6↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CycB/CCNB1↓, 1,   TumCCA↑, 1,  

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

4E-BP1↓, 1,   p‑cMET↑, 1,   ERK↓, 1,   mTOR↓, 1,   P70S6K↓, 1,   PI3K↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   MMP-10↓, 1,   MMP3↓, 1,   PKCδ↓, 1,   TSC1↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

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

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,   PD-L1↓, 1,  

Protein Aggregation(tgid=19) ⓘ

PP2A↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABCG2↓, 1,   BioEnh↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   PD-L1↓, 1,  

Functional Outcomes(tgid=23) ⓘ

PRAS40↑, 1,  
Total Targets: 78

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: RUBCN, Rubicon Autophagy Regulator
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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