GLUT2 Cancer Research Results

GLUT2, Glucose Transporter 2: Click to Expand ⟱
Source:
Type:
GLUT2 is a member of the facilitative glucose transporter family, primarily responsible for the uptake of glucose and other hexoses into cells.

– In cancers like HCC, lower GLUT2 expression sometimes correlates with poorer differentiation and a more aggressive phenotype. As cancer cells shift toward a more glycolytic metabolism, they may rely less on the regulated glucose uptake observed in normal cells, and decreased GLUT2 expression can serve as a marker of this metabolic reprogramming.


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⟱
5069- dietSTF,    The Role of Intermittent Fasting in the Activation of Autophagy Processes in the Context of Cancer Diseases
- Review, Var, NA
Risk↓, ChemoSen↑, RadioS↑, *Dose↝, *Dose↝, *Dose↝, *LDL↓, *CRP↓, *TNF-α↓, TumAuto↓, GLUT1↓, GLUT2↓, glucose↓, IGF-1↓, Insulin↓, mTOR↓, mTORC1↓, AMPK↑, Warburg↓, OXPHOS↑, ROS↑, DNAdam↑, JAK1↓, STAT↓, TumCP↓, QoL↑,
2380- PBG,    Potential Strategies for Overcoming Drug Resistance Pathways Using Propolis and Its Polyphenolic/Flavonoid Compounds in Combination with Chemotherapy and Radiotherapy
- Review, Var, NA
Hif1a↓, Glycolysis↓, PKM2↓, LDHA↓, GLUT2↓, HK2↓, PFK1↓, PDK1↓, chemoP↓, radioP↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

OXPHOS↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics

Insulin↓, 1,  

Core Metabolism/Glycolysis

AMPK↑, 1,   glucose↓, 1,   GLUT2↓, 2,   Glycolysis↓, 1,   HK2↓, 1,   LDHA↓, 1,   PDK1↓, 1,   PFK1↓, 1,   PKM2↓, 1,   Warburg↓, 1,  

Autophagy & Lysosomes

TumAuto↓, 1,  

DNA Damage & Repair

DNAdam↑, 1,  

Proliferation, Differentiation & Cell State

IGF-1↓, 1,   mTOR↓, 1,   mTORC1↓, 1,   STAT↓, 1,  

Migration

TumCP↓, 1,  

Angiogenesis & Vasculature

Hif1a↓, 1,  

Barriers & Transport

GLUT1↓, 1,  

Immune & Inflammatory Signaling

JAK1↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 1,   RadioS↑, 1,  

Functional Outcomes

chemoP↓, 1,   QoL↑, 1,   radioP↑, 1,   Risk↓, 1,  
Total Targets: 29

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis

LDL↓, 1,  

Immune & Inflammatory Signaling

CRP↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance

Dose↝, 3,  

Clinical Biomarkers

CRP↓, 1,  
Total Targets: 5

Scientific Paper Hit Count for: GLUT2, Glucose Transporter 2
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#:1198  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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