Research Topic

Warburg Effect in Hepatobiliary and Pancreatic Cancer

About this Research Topic

Warburg effect is the best characterized metabolic phenotype in tumor cells. To meet the increased anabolic needs of proliferation, cancer cells require both sufficient energy and biosynthetic precursors as cellular building blocks to support cell survival and growth. Cancer cells metabolize glucose by aerobic glycolysis (Warburg effect) rather than through the more energetically efficient oxidative phosphorylation (OXPHOS) even in the presence of oxygen. With relatively poor efficiency of generating ATP, Warburg effect still allows the switch of glycolytic intermediates into various biosynthetic pathways, which in turn facilitate the biosynthesis of macromolecules that are required for assembling new cells. Accumulated evidence reveals that Warburg effect contributes to the progression of hepatobiliary and pancreatic cancer. However, exact role and molecular mechanisms of Warburg effect in hepatobiliary and pancreatic cancer are still unknown.

The first objective of this Research Topic is to unveil the role and mechanisms of Warburg effect in the development, growth, metastasis, and chemoresistance of hepatobiliary and pancreatic cancer. Additionally, because the complexity and interconnectedness of metabolic signalling, targeting a particular metabolic pathway may have limited anticancer effects. However, dampening metabolic flexibility of cancer cells by targeting master regulators can make them more sensitive to cytotoxic chemotherapy. As drugs that target the known master regulators such as the MAPK and PI3K-mTOR pathways and activated oncogenes (e.g., Ras, c-Myc) show limited effects in hepatobiliary and pancreatic cancer, it is necessary to explore new master regulators of Warburg effect.

We welcome Original Research articles and Reviews on the themes below:
- The role and mechanism of Warburg effect in the development, growth, metastasis, and chemoresistance of hepatobiliary and pancreatic cancer.
- New master regulators of Warburg effect in hepatobiliary and pancreatic cancer.
- The influence of Warburg effect on epigenetics.
- The influence of Warburg effect on immune evasion.
- The role of non-coding RNA in the regulation of Warburg effect in hepatobiliary and pancreatic cancer.
- The effects of Warburg effect on specific inhibitors in hepatobiliary and pancreatic cancer.


Keywords: Warburg effect, aerobic glycolysis, hepatocellular carcinoma, cholangiocarcinoma, pancreatic cancer


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Warburg effect is the best characterized metabolic phenotype in tumor cells. To meet the increased anabolic needs of proliferation, cancer cells require both sufficient energy and biosynthetic precursors as cellular building blocks to support cell survival and growth. Cancer cells metabolize glucose by aerobic glycolysis (Warburg effect) rather than through the more energetically efficient oxidative phosphorylation (OXPHOS) even in the presence of oxygen. With relatively poor efficiency of generating ATP, Warburg effect still allows the switch of glycolytic intermediates into various biosynthetic pathways, which in turn facilitate the biosynthesis of macromolecules that are required for assembling new cells. Accumulated evidence reveals that Warburg effect contributes to the progression of hepatobiliary and pancreatic cancer. However, exact role and molecular mechanisms of Warburg effect in hepatobiliary and pancreatic cancer are still unknown.

The first objective of this Research Topic is to unveil the role and mechanisms of Warburg effect in the development, growth, metastasis, and chemoresistance of hepatobiliary and pancreatic cancer. Additionally, because the complexity and interconnectedness of metabolic signalling, targeting a particular metabolic pathway may have limited anticancer effects. However, dampening metabolic flexibility of cancer cells by targeting master regulators can make them more sensitive to cytotoxic chemotherapy. As drugs that target the known master regulators such as the MAPK and PI3K-mTOR pathways and activated oncogenes (e.g., Ras, c-Myc) show limited effects in hepatobiliary and pancreatic cancer, it is necessary to explore new master regulators of Warburg effect.

We welcome Original Research articles and Reviews on the themes below:
- The role and mechanism of Warburg effect in the development, growth, metastasis, and chemoresistance of hepatobiliary and pancreatic cancer.
- New master regulators of Warburg effect in hepatobiliary and pancreatic cancer.
- The influence of Warburg effect on epigenetics.
- The influence of Warburg effect on immune evasion.
- The role of non-coding RNA in the regulation of Warburg effect in hepatobiliary and pancreatic cancer.
- The effects of Warburg effect on specific inhibitors in hepatobiliary and pancreatic cancer.


Keywords: Warburg effect, aerobic glycolysis, hepatocellular carcinoma, cholangiocarcinoma, pancreatic cancer


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

31 March 2021 Abstract
30 June 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

31 March 2021 Abstract
30 June 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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