UPR Cancer Research Results

UPR, Unfolded Protein Response: Click to Expand ⟱
Source:
Type:
Cellular stress response related to the endoplasmic reticulum (ER) stress, which involves protein folding, quality control, and signaling pathways. The unfolded protein response (UPR) is the cells' way of maintaining the balance of protein folding in the endoplasmic reticulum. (UPR) is triggered by the presence of misfolded proteins in the endoplasmic reticulum.
The UPR is a cellular stress response activated by the accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER).
- It is primarily mediated by three ER-resident sensors: IRE1α, PERK, and ATF6.

Cancer cells often experience high levels of protein synthesis, hypoxia, nutrient deprivation, and oxidative stress, all of which can activate the UPR.
– Numerous studies have reported that key UPR components (e.g., GRP78/BiP, IRE1α, PERK, CHOP) are overexpressed in various malignancies such as breast, pancreatic, lung, and prostate cancers.

Unfolded Protein Response is typically upregulated in cancers and is associated with poorer prognosis due to its role in promoting cell survival, adaptation to stress, and therapeutic resistance. Although the UPR harbors the potential for tumor-suppressive (apoptotic) effects under severe stress conditions, its predominant activation in tumors supports an adaptive, protumorigenic state that facilitates cancer progression. Targeting UPR components and modulating this balance remain promising therapeutic strategies.
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
2288- AgNPs,    Silver Nanoparticle-Mediated Cellular Responses in Various Cell Lines: An in Vitro Model
- Review, Var, NA
*ROS↑, Akt↓, ERK↓, DNAdam↑, Ca+2↑, ROS↑, MMP↓, Cyt‑c↑, TumCCA↑, DNAdam↑, Apoptosis↑, P53↑, p‑ERK↑, ER Stress↑, cl‑ATF6↑, GRP78/BiP↑, CHOP↑, UPR↑,
5862- carbop,  Cisplatin,    Molecular Mechanisms of Resistance and Toxicity Associated with Platinating Agents
- Review, Var, NA
DNAdam↑, ER Stress↑, UPR↑, ATF4↑, ATF6↑, XBP-1↑, GRP78/BiP↑, NP/CIPN↝, toxicity↝, eff↑, TrxR1⇅,
2782- CHr,    Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives
- Review, Var, NA - Review, Stroke, NA - Review, Park, NA
*antiOx↑, *Inflam↓, *hepatoP↑, *neuroP↑, *BioAv↓, *cardioP↑, *lipidLev↓, *RenoP↑, *TNF-α↓, *IL2↓, *PI3K↓, *Akt↓, *ROS↓, *cognitive↑, eff↑, cycD1/CCND1↓, hTERT/TERT↓, VEGF↓, p‑STAT3↓, TumMeta↓, TumCP↓, eff↑, eff↑, IL1β↓, IL6↓, NF-kB↓, ROS↑, MMP↓, Cyt‑c↑, Apoptosis↑, ER Stress↑, Ca+2↑, TET1↑, Let-7↑, Twist↓, EMT↓, TumCCA↑, Casp3↑, Casp9↑, BAX↑, HK2↓, GlucoseCon↓, lactateProd↓, Glycolysis↓, SHP1↑, N-cadherin↓, E-cadherin↑, UPR↑, PERK↑, ATF4↑, eIF2α↑, RadioS↑, NOTCH1↑, NRF2↓, BioAv↑, eff↑,
2785- CHr,    Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin
- Review, Var, NA
*NF-kB↓, *COX2↓, *iNOS↓, angioG↓, TOP1↓, HDAC↓, TNF-α↓, IL1β↓, cardioP↑, RenoP↑, neuroP↑, LDL↓, BioAv↑, eff↑, cycD1/CCND1↓, hTERT/TERT↓, MMP-10↓, Akt↓, STAT3↓, VEGF↓, EGFR↓, Snail↓, Slug↓, Vim↓, E-cadherin↑, eff↑, TET1↑, ROS↑, mTOR↓, PPARα↓, ER Stress↑, Ca+2↑, ERK↓, MMP↑, Cyt‑c↑, Casp3↑, HK2↓, NRF2↓, HO-1↓, MMP2↓, MMP9↓, Fibronectin↓, GRP78/BiP↑, XBP-1↓, p‑eIF2α↑, *AST↓, ALAT↓, ALP↓, LDH↓, COX2↑, Bcl-xL↓, IL6↓, PGE2↓, iNOS↓, DNAdam↑, UPR↑, Hif1a↓, EMT↓, Twist↓, lipid-P↑, CLDN1↓, PDK1↓, IL10↓, TLR4↓, NOTCH1↑, PARP↑, Mcl-1↓, XIAP↓,
2790- CHr,    Chrysin: Pharmacological and therapeutic properties
- Review, Var, NA
*hepatoP↑, *neuroP↓, *ROS↓, *cardioP↑, *Inflam↓, eff↑, hTERT/TERT↓, cycD1/CCND1↓, MMP9↓, MMP2↓, TIMP1↑, TIMP2↑, BioAv↑, HK2↓, ROS↑, MMP↓, Casp3↑, ADP:ATP↑, Apoptosis↑, ER Stress↑, UPR↑, GRP78/BiP↝, eff↑, Ca+2↑,
5070- dietSTF,    A review of fasting effects on the response of cancer to chemotherapy
- Review, Var, NA
chemoP↑, ChemoSen↑, *DNArepair↑, *Apoptosis↓, *CD8+↑, UPR↑, eff↝, TumAuto↑,
3204- EGCG,    The Role of ER Stress and the Unfolded Protein Response in Cancer
- Review, Var, NA
BID↓, UPR↑, ER Stress↑,
3205- EGCG,    The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas
- Review, Var, NA - Review, AD, NA
Beclin-1↑, ROS↑, Apoptosis↑, ER Stress↑, *Inflam↓, *cardioP↑, *antiOx↑, *LDL↓, *NF-kB↓, *MPO↓, *glucose↓, *ROS↓, ATG5↑, LC3B↑, MMP↑, lactateProd↓, VEGF↓, Zeb1↑, Wnt↑, IGF-1R↑, Fas↑, Bak↑, BAD↑, TP53↓, Myc↓, Casp8↓, LC3II↑, NOTCH3↓, eff↑, p‑Akt↓, PARP↑, *Cyt‑c↓, *BAX↓, *memory↑, *neuroP↑, *Ca+2?, GRP78/BiP↑, CHOP↑, ATF4↑, Casp3↑, Casp8↑, UPR↑,
5519- EP,    Nanosecond Pulsed Electric Fields (nsPEFs) for Precision Intracellular Oncotherapy: Recent Advances and Emerging Directions
- Review, Var, NA
MMP↓, Ca+2↑, eff↑, ER Stress↑, selectivity↑, CSCs↓, CD44↓, CD133↓, ROS↑, Imm↑, DNAdam↑, MOMP↑, Cyt‑c↑, Casp9↑, Casp3↑, Casp9↑, TumCD↑, Fas↑, UPR↑, Dose↝, Dose↝, Dose↓, Dose↑, HMGB1↓, eff↑, EPR↑, ChemoSen↑, ETC↝, *AntiAge↑, *Hif1a↑, *SIRT1↑,
2517- H2,    Molecular Hydrogen Enhances Proliferation of Cancer Cells That Exhibit Potent Mitochondrial Unfolded Protein Response
- in-vitro, Var, A549 - in-vitro, NA, HCT116 - in-vitro, NA, HeLa - in-vitro, NA, HepG2 - in-vitro, NA, HT1080 - in-vitro, NA, PC3 - in-vitro, NA, SH-SY5Y
TumCP↓, other↝, eff↝, mt-UPR↑,
3457- MF,    Cellular stress response to extremely low‐frequency electromagnetic fields (ELF‐EMF): An explanation for controversial effects of ELF‐EMF on apoptosis
- Review, Var, NA
Apoptosis↑, H2O2↑, ROS↑, eff↑, eff↑, Ca+2↑, MAPK↑, *Catalase↑, *SOD1↑, *GPx1↑, *GPx4↑, *NRF2↑, TumAuto↑, ER Stress↑, HSPs↑, SIRT3↑, ChemoSen↑, UPR↑, other↑, PI3K↓, JNK↑, p38↑, eff↓, *toxicity?,
4643- OLE,  HT,    Use of Oleuropein and Hydroxytyrosol for Cancer Prevention and Treatment: Considerations about How Bioavailability and Metabolism Impact Their Adoption in Clinical Routine
- Review, Var, NA
TumCCA↑, Apoptosis↑, ER Stress↑, UPR↑, CHOP↑, ROS↑, Bcl-2↓, NOX4↑, Hif1a↓, MMP2↓, MMP↓, VEGF↓, Akt↓, NF-kB↓, p65↓, SIRT3↓, mTOR↓, Catalase↓, SOD2↓, FASN↓, STAT3↓, HDAC2↓, HDAC3↓, BAD↑, BAX↑, Bak↑, Casp3↑, Casp9↑, PARP↑, P53↑, P21↑, p27↑, Half-Life↝, BioAv↓, BioAv↓, selectivity↑, RadioS↑, *ROS↓, *GSH↑, *MDA↓, *SOD↑, *Catalase↑, *NRF2↑, *chemoP↑, *Inflam↓, PPARγ↑,
1664- PBG,    Anticancer Activity of Propolis and Its Compounds
- Review, Var, NA
Apoptosis↑, TumCMig↓, TumCCA↑, TumCP↓, angioG↓, P21↑, p27↑, CDK1↓, p‑CDK1↓, cycA1/CCNA1↓, CycB/CCNB1↓, P70S6K↓, CLDN2↓, HK2↓, PFK↓, PKM2↓, LDHA↓, TLR4↓, H3↓, α-tubulin↓, ROS↑, Akt↓, GSK‐3β↓, FOXO3↓, NF-kB↓, cycD1/CCND1↓, MMP↓, ROS↑, i-Ca+2↑, lipid-P↑, ER Stress↑, UPR↑, PERK↑, eIF2α↑, GRP78/BiP↑, BAX↑, PUMA↑, ROS↑, MMP↓, Cyt‑c↑, cl‑Casp8↑, cl‑Casp8↑, cl‑Casp3↑, cl‑PARP↑, eff↑, eff↑, RadioS↑, ChemoSen↑, eff↑,
3002- RosA,    Anticancer Effects of Rosemary (Rosmarinus officinalis L.) Extract and Rosemary Extract Polyphenols
- Review, Var, NA
TumCG↓, TumCP↓, TumCCA↑, ChemoSen↑, NRF2↑, PERK↑, SESN2↑, HO-1↑, cl‑Casp3↑, ROS↑, UPR↑, ER Stress↑, CHOP↑, HER2/EBBR2↓, ER-α36↓, PSA↓, BAX↑, AR↓, P-gp↓, Cyt‑c↑, HSP70/HSPA5↑, eff↑, p‑Akt↓, p‑mTOR↓, p‑P70S6K↓, cl‑PARP↑, eff↑,
3180- SFN,    Exploring the therapeutic effects of sulforaphane: an in-depth review on endoplasmic reticulum stress modulation across different disease contexts
- Review, Var, NA
*cardioP↑, *ER Stress↓, GRP78/BiP↑, XBP-1↑, Apoptosis↑, *NRF2↑, UPR↑,

Showing Research Papers: 1 to 15 of 15

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   H2O2↑, 1,   HO-1↓, 1,   HO-1↑, 1,   lipid-P↑, 2,   NOX4↑, 1,   NRF2↓, 2,   NRF2↑, 1,   ROS↑, 12,   SIRT3↓, 1,   SIRT3↑, 1,   SOD2↓, 1,   TrxR1⇅, 1,  

Mitochondria & Bioenergetics ⓘ

ADP:ATP↑, 1,   ETC↝, 1,   MMP↓, 7,   MMP↑, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   FASN↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 4,   lactateProd↓, 2,   LDH↓, 1,   LDHA↓, 1,   LDL↓, 1,   PDK1↓, 1,   PFK↓, 1,   PKM2↓, 1,   PPARα↓, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 2,   Apoptosis↑, 8,   BAD↑, 2,   Bak↑, 2,   BAX↑, 4,   Bcl-2↓, 1,   Bcl-xL↓, 1,   BID↓, 1,   Casp3↑, 6,   cl‑Casp3↑, 2,   Casp8↓, 1,   Casp8↑, 1,   cl‑Casp8↑, 2,   Casp9↑, 4,   Cyt‑c↑, 6,   Fas↑, 2,   hTERT/TERT↓, 3,   iNOS↓, 1,   JNK↑, 1,   MAPK↑, 1,   Mcl-1↓, 1,   MOMP↑, 1,   Myc↓, 1,   p27↑, 2,   p38↑, 1,   PUMA↑, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

H3↓, 1,   other↑, 1,   other↝, 1,  

Protein Folding & ER Stress ⓘ

ATF6↑, 1,   cl‑ATF6↑, 1,   CHOP↑, 4,   eIF2α↑, 2,   p‑eIF2α↑, 1,   ER Stress↑, 12,   GRP78/BiP↑, 6,   GRP78/BiP↝, 1,   HSP70/HSPA5↑, 1,   HSPs↑, 1,   PERK↑, 3,   UPR↑, 14,   mt-UPR↑, 1,   XBP-1↓, 1,   XBP-1↑, 2,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3B↑, 1,   LC3II↑, 1,   SESN2↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 5,   P53↑, 2,   PARP↑, 3,   cl‑PARP↑, 2,   TP53↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   p‑CDK1↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 4,   P21↑, 2,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CD44↓, 1,   CSCs↓, 1,   EMT↓, 2,   ERK↓, 2,   p‑ERK↑, 1,   FOXO3↓, 1,   GSK‐3β↓, 1,   HDAC↓, 1,   HDAC2↓, 1,   HDAC3↓, 1,   IGF-1R↑, 1,   Let-7↑, 1,   mTOR↓, 2,   p‑mTOR↓, 1,   NOTCH1↑, 2,   NOTCH3↓, 1,   P70S6K↓, 1,   p‑P70S6K↓, 1,   PI3K↓, 1,   SHP1↑, 1,   STAT3↓, 2,   p‑STAT3↓, 1,   TOP1↓, 1,   TumCG↓, 1,   Wnt↑, 1,  

Migration ⓘ

Ca+2↑, 6,   i-Ca+2↑, 1,   CLDN1↓, 1,   CLDN2↓, 1,   E-cadherin↑, 2,   ER-α36↓, 1,   Fibronectin↓, 1,   MMP-10↓, 1,   MMP2↓, 3,   MMP9↓, 2,   N-cadherin↓, 1,   Slug↓, 1,   Snail↓, 1,   TET1↑, 2,   TIMP1↑, 1,   TIMP2↑, 1,   TumCMig↓, 1,   TumCP↓, 4,   TumMeta↓, 1,   Twist↓, 2,   Vim↓, 1,   Zeb1↑, 1,   α-tubulin↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   ATF4↑, 3,   EGFR↓, 1,   EPR↑, 1,   Hif1a↓, 2,   VEGF↓, 4,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↑, 1,   HMGB1↓, 1,   IL10↓, 1,   IL1β↓, 2,   IL6↓, 2,   Imm↑, 1,   NF-kB↓, 3,   p65↓, 1,   PGE2↓, 1,   PSA↓, 1,   TLR4↓, 2,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 3,   ChemoSen↑, 5,   Dose↓, 1,   Dose↑, 1,   Dose↝, 2,   eff↓, 1,   eff↑, 19,   eff↝, 2,   Half-Life↝, 1,   RadioS↑, 3,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AR↓, 1,   EGFR↓, 1,   HER2/EBBR2↓, 1,   hTERT/TERT↓, 3,   IL6↓, 2,   LDH↓, 1,   Myc↓, 1,   PSA↓, 1,   TP53↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   chemoP↑, 1,   neuroP↑, 1,   NP/CIPN↝, 1,   RenoP↑, 1,   toxicity↝, 1,  
Total Targets: 195

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↑, 2,   GPx1↑, 1,   GPx4↑, 1,   GSH↑, 1,   MDA↓, 1,   MPO↓, 1,   NRF2↑, 3,   ROS↓, 4,   ROS↑, 1,   SOD↑, 1,   SOD1↑, 1,  

Core Metabolism/Glycolysis ⓘ

glucose↓, 1,   LDL↓, 1,   lipidLev↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↓, 1,   BAX↓, 1,   Cyt‑c↓, 1,   iNOS↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,  

DNA Damage & Repair ⓘ

DNArepair↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,  

Migration ⓘ

Ca+2?, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL2↓, 1,   Inflam↓, 4,   NF-kB↓, 2,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Clinical Biomarkers ⓘ

AST↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cardioP↑, 4,   chemoP↑, 1,   cognitive↑, 1,   hepatoP↑, 2,   memory↑, 1,   neuroP↓, 1,   neuroP↑, 2,   RenoP↑, 1,   toxicity?, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 44

Scientific Paper Hit Count for: UPR, Unfolded Protein Response
3 Chrysin
2 EGCG (Epigallocatechin Gallate)
1 Silver-NanoParticles
1 carboplatin
1 Cisplatin
1 diet Short Term Fasting
1 Electrical Pulses
1 Hydrogen Gas
1 Magnetic Fields
1 Oleuropein
1 HydroxyTyrosol
1 Propolis -bee glue
1 Rosmarinic acid
1 Sulforaphane (mainly Broccoli)
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:26  Cells:%  prod#:%  Target#:459  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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