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Interplay Between Metabolism and Oncogenic Process: Role of microRNAs.

Arora A, Singh S, Bhatt AN, Pandey S, Sandhir R, Dwarakanath BS - Transl Oncogenomics (2015)

Bottom Line: Cancer is a complex disease that arises from the alterations in the composition and regulation of several genes leading to the disturbances in signaling pathways, resulting in the dysregulation of cell proliferation and death as well as the ability of transformed cells to invade the host tissue and metastasize.The process of metabolic reprograming is linked to the activation of oncogenes and/or suppression of tumor suppressor genes, which are further regulated by microRNAs (miRNAs) that play important roles in the interplay between oncogenic process and metabolic reprograming.Looking at the advances made in the recent past, it appears that the translation of knowledge from research in the areas of metabolism, miRNA, and therapeutic response will lead to paradigm shift in the management of this disease.

View Article: PubMed Central - PubMed

Affiliation: Division of Radiation Biosciences, Institute of Nuclear Medicine and Allied Sciences, Delhi, India.; Department of Biochemistry, Panjab University, Chandigarh, India.

ABSTRACT
Cancer is a complex disease that arises from the alterations in the composition and regulation of several genes leading to the disturbances in signaling pathways, resulting in the dysregulation of cell proliferation and death as well as the ability of transformed cells to invade the host tissue and metastasize. It is increasingly becoming clear that metabolic reprograming plays a critical role in tumorigenesis and metastasis. Therefore, targeting this phenotype is considered as a promising approach for the development of therapeutics and adjuvants. The process of metabolic reprograming is linked to the activation of oncogenes and/or suppression of tumor suppressor genes, which are further regulated by microRNAs (miRNAs) that play important roles in the interplay between oncogenic process and metabolic reprograming. Looking at the advances made in the recent past, it appears that the translation of knowledge from research in the areas of metabolism, miRNA, and therapeutic response will lead to paradigm shift in the management of this disease.

No MeSH data available.


Related in: MedlinePlus

Warburg phenotype (enhanced aerobic glycolysis) in cancer cells showing alterations in enzymes and glutaminolysis.
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f2-tog-7-2015-011: Warburg phenotype (enhanced aerobic glycolysis) in cancer cells showing alterations in enzymes and glutaminolysis.

Mentions: Glycolysis, glutaminolysis, and de novo lipid biosynthesis form a stereotypic platform supporting cancer cell proliferation (Fig. 2).36 Cancer cell proliferation can only proceed as metabolites accumulate to ensure an ample supply of building blocks such as reduced nicotinamide adenine dinucleotide phosphate (NADPH), acetyl-CoA, and ribose for DNA, RNA, protein, lipid, and complex carbohydrates to prepare for mitosis.37 The emerging cancer cell rewires its metabolic program to support growth, evade death (through apoptosis), and maintain favorable redox balance. Metabolic reprograming of cancer cells is a complex interplay of regulatory networks involving phosphoinositide 3-kinase (PI3K), mechanistic target of rapamycin (mTOR), Akt, phosphatase and tensin homolog (PTEN), and adenosine monophosphate-activated protein kinase (AMPK) and can be traced to a “triad” of transcription factors: hypoxia-inducible factor-1 (HIF-1), c-MYC, and p53. The underlying mechanisms leading to the Warburg phenomenon/aerobic glycolysis include mitochondrial changes, upregulation of rate-limiting enzymes/proteins involved in glycolysis and intracellular pH regulation, hypoxia-induced switch to anaerobic metabolism, and metabolic reprograming associated with loss of p53 function.38Figure 3 provides an overview of the miRNAs involved in the regulation of metabolism achieved by targeting key metabolic enzymes and multiple oncogenic signaling pathways.


Interplay Between Metabolism and Oncogenic Process: Role of microRNAs.

Arora A, Singh S, Bhatt AN, Pandey S, Sandhir R, Dwarakanath BS - Transl Oncogenomics (2015)

Warburg phenotype (enhanced aerobic glycolysis) in cancer cells showing alterations in enzymes and glutaminolysis.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4696840&req=5

f2-tog-7-2015-011: Warburg phenotype (enhanced aerobic glycolysis) in cancer cells showing alterations in enzymes and glutaminolysis.
Mentions: Glycolysis, glutaminolysis, and de novo lipid biosynthesis form a stereotypic platform supporting cancer cell proliferation (Fig. 2).36 Cancer cell proliferation can only proceed as metabolites accumulate to ensure an ample supply of building blocks such as reduced nicotinamide adenine dinucleotide phosphate (NADPH), acetyl-CoA, and ribose for DNA, RNA, protein, lipid, and complex carbohydrates to prepare for mitosis.37 The emerging cancer cell rewires its metabolic program to support growth, evade death (through apoptosis), and maintain favorable redox balance. Metabolic reprograming of cancer cells is a complex interplay of regulatory networks involving phosphoinositide 3-kinase (PI3K), mechanistic target of rapamycin (mTOR), Akt, phosphatase and tensin homolog (PTEN), and adenosine monophosphate-activated protein kinase (AMPK) and can be traced to a “triad” of transcription factors: hypoxia-inducible factor-1 (HIF-1), c-MYC, and p53. The underlying mechanisms leading to the Warburg phenomenon/aerobic glycolysis include mitochondrial changes, upregulation of rate-limiting enzymes/proteins involved in glycolysis and intracellular pH regulation, hypoxia-induced switch to anaerobic metabolism, and metabolic reprograming associated with loss of p53 function.38Figure 3 provides an overview of the miRNAs involved in the regulation of metabolism achieved by targeting key metabolic enzymes and multiple oncogenic signaling pathways.

Bottom Line: Cancer is a complex disease that arises from the alterations in the composition and regulation of several genes leading to the disturbances in signaling pathways, resulting in the dysregulation of cell proliferation and death as well as the ability of transformed cells to invade the host tissue and metastasize.The process of metabolic reprograming is linked to the activation of oncogenes and/or suppression of tumor suppressor genes, which are further regulated by microRNAs (miRNAs) that play important roles in the interplay between oncogenic process and metabolic reprograming.Looking at the advances made in the recent past, it appears that the translation of knowledge from research in the areas of metabolism, miRNA, and therapeutic response will lead to paradigm shift in the management of this disease.

View Article: PubMed Central - PubMed

Affiliation: Division of Radiation Biosciences, Institute of Nuclear Medicine and Allied Sciences, Delhi, India.; Department of Biochemistry, Panjab University, Chandigarh, India.

ABSTRACT
Cancer is a complex disease that arises from the alterations in the composition and regulation of several genes leading to the disturbances in signaling pathways, resulting in the dysregulation of cell proliferation and death as well as the ability of transformed cells to invade the host tissue and metastasize. It is increasingly becoming clear that metabolic reprograming plays a critical role in tumorigenesis and metastasis. Therefore, targeting this phenotype is considered as a promising approach for the development of therapeutics and adjuvants. The process of metabolic reprograming is linked to the activation of oncogenes and/or suppression of tumor suppressor genes, which are further regulated by microRNAs (miRNAs) that play important roles in the interplay between oncogenic process and metabolic reprograming. Looking at the advances made in the recent past, it appears that the translation of knowledge from research in the areas of metabolism, miRNA, and therapeutic response will lead to paradigm shift in the management of this disease.

No MeSH data available.


Related in: MedlinePlus