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Published on: November 26, 2018
Metabolic and epigenetic reprogramming in the arsenic-induced cancer stem cells
Lingzhi Li1, Zhuoyue Bi2, Priya Wadgaonkar3
1Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, 259 Mack Avenue, Detroit, MI, 48201, USA; Department of Developmental and Stem Cell Biology, Beckman Research Institute of City of Hope, Duarte, CA, 91010, USA.
Abstract:
At present, the belief that genetic mutations control every aspect of tumorigenesis is still very popular. Even for the highly debated "bad luck" theory of cancers, it ascertained that random mutation of genes during the self-renewal of somatic stem cells is responsible for cancer initiation. Logically, most of the new therapeutic strategies so far, from molecular targeting to precision medicine or personalized medicine, are genome-obsessed and focused on identifying and targeting these mutated genes. Accordingly, a rather simplified therapeutic regimen was formulated: cancers with the same mutations, e.g., lung cancer, pancreatic cancer, breast cancer, ovarian cancer, etc, were managed with the same chemo or targeting medicine, whereas for a particular cancer, such as breast cancer or lung cancer, with different mutational spectrums was treated with different, so-called personalized medicine. The outcomes of this strategy, however, are mixed with encouraging and disappointing findings. In this review article, we will address the importance of non-genetic factors, the metabolic and epigenetic reprogramming, during the induction of cancer stem cells in response to arsenic, a major environmental human carcinogen. The information provided may not only advance our understanding of carcinogenic mechanism to a new level but also help in designing new strategies through targeting the metabolic and epigenetic signaling pathways for cancer therapy.
Insights
Genetic mutations are not the sole drivers of cancer. Environmental factors like arsenic can induce cancer stem cells via metabolic and epigenetic changes, offering new therapeutic targets beyond genetics.
Area of Science:
- Oncology
- Environmental Health
- Molecular Biology
Background:
- The prevailing view links cancer initiation and progression to genetic mutations.
- Current cancer therapies, including precision medicine, primarily target these genetic alterations.
- This genome-centric approach yields mixed clinical outcomes, suggesting limitations.
Purpose of the Study:
- To highlight the critical role of non-genetic factors in cancer development.
- To explore the impact of metabolic and epigenetic reprogramming in cancer stem cell induction by arsenic.
- To propose novel therapeutic strategies targeting these non-genetic pathways.
Main Methods:
- Review of existing literature on cancer biology, environmental carcinogens, and epigenetics.
- Analysis of the mechanisms by which arsenic induces cancer stem cells.
- Discussion of metabolic and epigenetic signaling pathways involved in tumorigenesis.
Main Results:
- Environmental carcinogens like arsenic can initiate cancer through non-genetic mechanisms.
- Metabolic and epigenetic reprogramming are key events in cancer stem cell induction.
- Arsenic exposure leads to significant alterations in cellular metabolism and epigenetic landscape.
Conclusions:
- Non-genetic factors, particularly metabolic and epigenetic changes, are crucial in cancer initiation and progression.
- Targeting metabolic and epigenetic pathways presents a promising avenue for novel cancer therapies.
- A comprehensive understanding of both genetic and non-genetic factors is essential for effective cancer treatment.
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