Cancer is a multifaceted disease with alterations at genomic, transcriptomic, proteomic or metabolomic level. Tumor cells are known to possess altered energy metabolism, known as metabolic reprogramming. Under conditions of limited oxygen availability, for example in the hypoxic microenvironment of tumor tissues, glycolysis becomes the obligatory pathway of energy production. Besides glucose, cancer cells use additional nutrients to support their biosynthetic needs and in this context glutamine is a key nutrient that provides carbon for acetyl-CoA, citrate production and lipogenesis; nitrogen for purine, pyrimidine and DNA synthesis; and reducing power in the form of NADPH to support cell proliferation.
The mitochondria are a common site for multiple metabolic reactions in order to meet energy and biomolecule demands, thus controlling and integrating the diverse metabolic pathways taking place in these organelles. As such, mitochondria enable cancer cells to modulate their metabolism under various stress conditions providing metabolic flexibility. Mitochondrial proteins and genes have been partially recognized as biomarkers, indicative that mitochondria are organelles with an enigmatic role in disease pathogenesis, especially in cancers. Mitochondria have therefore been identified as a target organ site for investigation. They have also been linked to the endoplasmic reticulum in some of the pathogenic mechanisms.
Endoplasmic reticular stress (ERS) is one of the contributors in promoting diseases like inflammation mediated cancer. Controversial literature has stated that ERS aids in attenuating cancer as ER stress initiates apoptosis by activating transcription factor 4 (ATF4)-dependent C/EBP homologous transcription factor (CHOP), apoptosis signal-regulating kinase 1 (ASK1), and caspase-12. On the other hand, the physiological environments of solid tumors differ from that of normal tissues in many ways: it is hypoxic, low in pH and low in nutrients. These environmental factors all contribute to the activation of ER stress and as a result, cancerous cells must possess ways to adapt and prevent the fate of ER stress-induced apoptosis. Recent studies have shown methods by which cancerous cells utilize altered states of ER stress responses in order to perturb ER associated cell death signaling. This has led to the belief that cellular organelles like mitochondria and ER are a key link to cancer progression.
This Topic will focus on the involvement and role of the mitochondria and ER in cancer initiation and progression as well as how they orchestrate the underlying disease pathogenesis, with possible contribution to therapeutic and mechanistic avenues. It will also aid in defining the active role of the mitochondria and endoplasmic reticulum in cancer progression and how potential therapeutics could be developed through understanding the signaling pathways. Recent advancements in cellular research have immensely helped in deciphering novel sub cellular mechanisms that participate and orchestrate oncogenesis. Scientists are utilizing these clues to corner carcinogenesis. The current topic therefore will address all such principal mechanisms that can be used as a therapeutic target.
We welcome submissions covering but not limited to:
1. Deciphering ER stress mediated mechanisms in cancer
2. Role of mitochondria in cancer progression
3. Energy metabolism in cancer
4. Unfolded protein response as therapeutic target
5. ER stress mediated apoptosis 6. ER stress modulators and small molecule inhibitors
7. Dissecting mitophagy, mitostress, mitoCPR in cancer
8. Deeper knowledge about mitochondrial dynamics, fission and fusion
9. Enumeration of mitochondrial role in cancer metastasis and progression
Cancer is a multifaceted disease with alterations at genomic, transcriptomic, proteomic or metabolomic level. Tumor cells are known to possess altered energy metabolism, known as metabolic reprogramming. Under conditions of limited oxygen availability, for example in the hypoxic microenvironment of tumor tissues, glycolysis becomes the obligatory pathway of energy production. Besides glucose, cancer cells use additional nutrients to support their biosynthetic needs and in this context glutamine is a key nutrient that provides carbon for acetyl-CoA, citrate production and lipogenesis; nitrogen for purine, pyrimidine and DNA synthesis; and reducing power in the form of NADPH to support cell proliferation.
The mitochondria are a common site for multiple metabolic reactions in order to meet energy and biomolecule demands, thus controlling and integrating the diverse metabolic pathways taking place in these organelles. As such, mitochondria enable cancer cells to modulate their metabolism under various stress conditions providing metabolic flexibility. Mitochondrial proteins and genes have been partially recognized as biomarkers, indicative that mitochondria are organelles with an enigmatic role in disease pathogenesis, especially in cancers. Mitochondria have therefore been identified as a target organ site for investigation. They have also been linked to the endoplasmic reticulum in some of the pathogenic mechanisms.
Endoplasmic reticular stress (ERS) is one of the contributors in promoting diseases like inflammation mediated cancer. Controversial literature has stated that ERS aids in attenuating cancer as ER stress initiates apoptosis by activating transcription factor 4 (ATF4)-dependent C/EBP homologous transcription factor (CHOP), apoptosis signal-regulating kinase 1 (ASK1), and caspase-12. On the other hand, the physiological environments of solid tumors differ from that of normal tissues in many ways: it is hypoxic, low in pH and low in nutrients. These environmental factors all contribute to the activation of ER stress and as a result, cancerous cells must possess ways to adapt and prevent the fate of ER stress-induced apoptosis. Recent studies have shown methods by which cancerous cells utilize altered states of ER stress responses in order to perturb ER associated cell death signaling. This has led to the belief that cellular organelles like mitochondria and ER are a key link to cancer progression.
This Topic will focus on the involvement and role of the mitochondria and ER in cancer initiation and progression as well as how they orchestrate the underlying disease pathogenesis, with possible contribution to therapeutic and mechanistic avenues. It will also aid in defining the active role of the mitochondria and endoplasmic reticulum in cancer progression and how potential therapeutics could be developed through understanding the signaling pathways. Recent advancements in cellular research have immensely helped in deciphering novel sub cellular mechanisms that participate and orchestrate oncogenesis. Scientists are utilizing these clues to corner carcinogenesis. The current topic therefore will address all such principal mechanisms that can be used as a therapeutic target.
We welcome submissions covering but not limited to:
1. Deciphering ER stress mediated mechanisms in cancer
2. Role of mitochondria in cancer progression
3. Energy metabolism in cancer
4. Unfolded protein response as therapeutic target
5. ER stress mediated apoptosis 6. ER stress modulators and small molecule inhibitors
7. Dissecting mitophagy, mitostress, mitoCPR in cancer
8. Deeper knowledge about mitochondrial dynamics, fission and fusion
9. Enumeration of mitochondrial role in cancer metastasis and progression
