Interplay Between Glucose Metabolism Reprogramming and Growth Suppressor

Interplay Between Glucose Metabolism Reprogramming and Growth Suppressor

In addition to the need for sustained proliferative signaling for tumor initiation and progression, cancer cells also need to escape growth inhibition. There are three factors that regulate the evasion of growth inhibition by cancer cells, including loss of tumor suppressor genes, contact inhibition of cancer cells, and disruption of the TGF-β signaling pathway. The above three factors are closely related to the reprogramming of glucose metabolism in cancer. The control mechanism of contact inhibition involves two genes, neurofibromatosis type 2 and liver kinase B1. Liver Kinase B1 exhibits a significant role in the regulation of glucose metabolism reprogramming. Therefore, CD BioGlyco can provide an analysis of the relationship between glucose metabolism reprogramming and tumor suppressor genes, contact inhibition, and TGF-β signaling pathways, respectively, thereby advancing the understanding of cancer cell glucose metabolism reprogramming and its evasion of growth inhibition.

LKB1 in glucose metabolic reprogramming Fig. 1 LKB1 in glucose metabolic reprogramming (Zhang Y, et al., 2021)

What We Do

  • Analysis of tumor suppressors regulating glucose metabolism

The analysis services that we can provide for tumor suppressor genes regulating glucose metabolism in cancer cells have been introduced in detail before. If you want to know the details, please click to learn more.

  • Analysis of the relationship between cell contact inhibition and glucose metabolism

Cell contact inhibition is a key regulator of cell proliferation, differentiation, and motility. Normal cells undergo contact inhibition to maintain a relative balance of cell numbers, however, cancer cells are generally resistant to contact inhibition. We provide analysis services for the regulation of glucose metabolism by liver kinase B1, hoping to help customers find potential therapeutic targets in the glucose metabolism pathways regulated by liver kinase B1.

We can provide the following analysis services based on the MOPCGM platform, including but not limited to:

  • Analysis of the effect of LKB1 on the expression of glycolysis-related enzymes
  • Analysis of the effect of LKB1 on the rate of extracellular acidification
  • Crosstalk analysis between TGF-β signaling and glucose metabolism

A positive feedback loop exists between TGF-β signaling and reprogramming of glucose metabolism. TGF-β signaling regulates the expression of glycolysis-related enzymes, and in turn, glycolytic metabolites modulate TGF-β signaling. Therefore, in response to this positive feedback loop, we provide the following specific analysis services:

  • Analysis of the effect of TGF-β signaling on the expression of glycolysis-related enzymes
  • Analysis of the effects of sugar metabolites on TGF-β signaling
  • Personalized analysis services

Our Advantages

  • Based on the MOPCGM platform, we are able to provide expression analysis of all glucose metabolism-related enzymes closely related to tumor growth inhibition evasion behavior.
  • We focused on the relationship between glucose metabolism reprogramming and contact inhibition.

CD BioGlyco can provide analysis of the relationship between glucose metabolism reprogramming and tumor suppressor genes, contact inhibition, and TGF-β signaling pathways, respectively. Our experienced teams of scientists, researchers, and technicians provide a fast turnaround, and high-quality services at competitive prices for worldwide customers. Our customers have direct access to our staff and prompt feedback on their inquiries. If you are interested in our services, please contact us for more details.

Reference:

  1. Zhang Y, et al. LKB1 deficiency-induced metabolic reprogramming in tumorigenesis and non-neoplastic diseases. Mol Metab. 2021 Feb; 44: 101131.
This service is for Research Use Only, not intended for any clinical use.

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