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Written By THT Editorial Team

Dr. Prakash Paudel

Reviewed by Dr. Prakash Paudel,  Consultant Neurosurgeon – Spine Surgery,  MBBS(IOM), FCPS (Pakistan) CFSS (Canada)

Introduction:

Tumor growth is a complex process influenced by various genetic and environmental factors. Epigenetic modifications, including DNA methylation, histone modifications, and non-coding RNA molecules, play a crucial role in the regulation of gene expression and can contribute to abnormal cell growth and the development of tumors. The ketogenic diet, a high-fat, low-carbohydrate eating plan, has been studied for its potential impact on gene regulation and its influence on tumor growth. This article aims to provide an overview of the factors inducing tumor growth, the role of epigenetics in abnormal growth, and the emerging research on the ketogenic diet’s effects on gene regulation and cell growth.

Factors Inducing Tumor Growth:

Tumor growth is influenced by a combination of genetic and environmental factors. Genetic mutations can lead to the activation of oncogenes and the inactivation of tumor suppressor genes, disrupting normal cellular processes and promoting uncontrolled cell growth. Environmental factors, such as exposure to carcinogens, chronic inflammation, hormonal imbalances, and metabolic dysregulation, can also contribute to tumor initiation and progression.

Epigenetics and Abnormal Growth:

Epigenetic modifications can have a profound impact on gene expression and contribute to abnormal cell growth and tumor development. Altered DNA methylation patterns, histone modifications, and dysregulated non-coding RNA molecules can lead to the activation or silencing of genes involved in cell proliferation, differentiation, and apoptosis. Aberrant epigenetic marks can promote oncogenic pathways and inhibit tumor-suppressive mechanisms, thereby driving tumor growth.

The Role of Epigenetics in Tumor Growth:

DNA Methylation: Hypermethylation of CpG islands within promoter regions of tumor suppressor genes can lead to their silencing, allowing uncontrolled cell growth. Hypomethylation in other regions of the genome can activate oncogenes, promoting cell proliferation. A study by Li et al. (2020) demonstrated global DNA hypomethylation in tumor tissues compared to adjacent normal tissues in colorectal cancer patients.

Histone Modifications: Abnormal histone modifications can alter chromatin structure and gene accessibility, impacting gene expression. Histone acetylation, methylation, and phosphorylation patterns can regulate oncogenic signaling pathways. Research by Rasmussen and Helin (2016) highlighted the dysregulation of histone-modifying enzymes in cancer and their potential as therapeutic targets.

Non-coding RNA: Non-coding RNAs, such as microRNAs and long non-coding RNAs, can modulate gene expression by binding to messenger RNA molecules. Dysregulated expression of these non-coding RNAs has been associated with tumor growth and metastasis. A study by Wu et al. (2021) identified specific microRNAs involved in promoting glioblastoma cell growth and invasion.

The Impact of the Ketogenic Diet on Gene Regulation and Tumor Growth:

The ketogenic diet has gained attention for its potential impact on gene regulation and its effects on tumor growth. The diet’s ability to alter cellular metabolism and induce a state of ketosis may influence gene expression patterns and cellular processes relevant to tumor growth.

Metabolic Effects: The ketogenic diet alters cellular metabolism by promoting the production of ketone bodies as an alternative energy source. Ketone bodies can affect signaling pathways involved in cell growth and survival. A study by Elgendy et al. (2021) demonstrated that ketone bodies derived from a ketogenic diet inhibited the growth of lung cancer cells in vitro.

Epigenetic Modifications: Recent research has suggested that the ketogenic diet may induce epigenetic modifications that impact gene expression. For instance, a study by Tan-Shalaby et al. (2016) showed that a ketogenic diet altered the expression of genes involved in metabolism and inflammation in a mouse model of glioblastoma, potentially impacting tumor progression.

Conclusion:

Tumor growth is a multifactorial process influenced by genetic and environmental factors. Epigenetic modifications play a critical role in the regulation of gene expression and can contribute to abnormal cell growth and tumor development. The ketogenic diet shows promise in altering gene regulation and metabolic processes relevant to tumor growth. However, further research is needed to elucidate the underlying mechanisms and assess the clinical implications of the ketogenic diet in cancer treatment.

Understanding the interplay between epigenetics, nutrition, and tumor growth opens up new avenues for targeted therapies and personalized approaches in cancer management.

REFERENCES

  • Li M, et al. DNA methylation alterations as therapeutic prospects in colorectal cancer. Front Oncol. 2020;10: 578816.
  • Rasmussen KD, Helin K. Role of TET enzymes in DNA methylation, development, and cancer. Genes Dev. 2016;30(7): 733-750.
  • Wu D, et al. microRNA involvement in glioblastoma pathogenesis. J Neurosci Res. 2021;99(2): 269-283.
  • Elgendy M, et al. Ketone bodies attenuate oxidative stress and radioresistance in lung cancer stem cells by regulating the Nrf2-ARE pathway. Life Sci. 2021;278: 119526.
  • Tan-Shalaby JL, et al. A ketogenic diet suppresses glioma tumor growth in mice. Neuro-oncology. 2016;18(7): 981-990.