Fatty acid synthesis and cancer: Aberrant expression of the ACACA and ACACB genes increases the risk for cancer

Bhattacharjee, Kasturi; Nath, Moumita; Choudhury, Yashmin

doi:10.1016/j.mgene.2020.100798

Cited by 19 publications

(8 citation statements)

References 129 publications

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“…ACC is a rate limiting enzyme in fatty acid (FA) synthesis. FA, on the other hand, is a building block for more complex lipids, as the vital source of structural membrane components, fuel source for growing and dividing cells, and second messengers in signal transduction (Bhattacharjee et al, 2020;Mozolewska et al, 2020). Cancer cells reportedly more rely on de novo FA synthesis pathway, while normal cells getting FA mostly from dietary sources (M. Chen and Huang, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…Several enzymes are required biotin as co-enzymes for their activities. Most of them are carboxylases such as acetyl-CoA carboxylase (ACC) that involved in fatty acid synthesis (Bhattacharjee et al, 2020;Mozolewska et al, 2020), pyruvate carboxylase (PC) involved in gluconeogenesis pathway (Kiesel et al, 2021;Ngamkham et al, 2020) and methylcrotonyl-CoA carboxylase (MCC) involved in branched-chain amino acids catabolism (Chen et al, 2021;He et al, 2020). All these enzymes…”

Section: Introductionmentioning

confidence: 99%

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The Effect of Avidin on Viability and Proliferation of Colorectal Cancer Cells HT-29

Dewi

Ramadhan

Abdullah

et al. 2022

Asian Pac J Cancer Prev

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Objective:The aim of this study was to analyze the effect of avidin treatment on cell viability, proliferation and cyclin D1 expression in colorectal cancer cells HT-29. Methods: Colorectal cancer cell line HT-29 incubated with 50, 100, 150, and 200 μg/mL of avidin concentration during 24, 48, and 72 hours, then the cell viability and proliferation were analyzed. Each avidin concentration was conducted together with HT-29 cell line without avidin treatment as a control group. The cell viability was measured by MTS assay and the proliferation was measured by BrdU (5-bromo-2′-deoxyuridine) cell proliferation assay. According to cell viability and proliferation result, we determined the 100 μg/ mL avidin concentration for analyzing mRNA and protein of cyclin D1. Results: We demonstrated that the viability and proliferation of HT-29 cells were significantly decreased in all concentration of avidin treatment compared to control. The cell proliferation showed larger reduction in avidin treatment rather than cell viability. This proves avidin could inhibit proliferation of colorectal cancer cell HT-29 quite well. The expression of cyclin D1, both mRNA and protein, was also significantly decreased after the avidin treatment group compared to control group, it supports the suppression of proliferation result. Conclusion: We concluded that avidin treatment could decrease cell viability and proliferation, accompanied by suppression of cyclin D1 expression in colorectal cells HT-29.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Effect of Avidin on Viability and Proliferation of Colorectal Cancer Cells HT-29

Dewi

Ramadhan

Abdullah

et al. 2022

Asian Pac J Cancer Prev

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“…Recent studies have found that transcripts involved in lipogenesis and cholesterol synthesis pathways are upregulated in tumors, which are essential for development and progression of a wide variety of tumors [32,33]. Elevated expression or aberrant activity of the major lipogenic enzymes such as fatty acid synthase (FASN) and acetyl-CoA carboxylase (ACC) critically contribute to lipogenic phenotype of tumor cells [1,34,35]. Besides the de novo lipogenesis, cancer cells also rely on exogenous fatty acids (FAs) uptake and consumption for survival and metastasis.…”

Section: Accepted Articlementioning

confidence: 99%

PPARα at the crossroad of metabolic–immune regulation in cancer

et al. 2021

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Rewiring metabolism to sustain cell growth, division and survival is the most prominent feature of cancer cells. In particular, dysregulated lipid metabolism in cancer has received accumulating interest, since lipid molecules serve as cell membrane structure components, secondary signaling messengers, and energy sources. Given the critical role of immune cells in host defense against cancer, recent studies have revealed that immune cells compete for nutrients with cancer cells in the tumor microenvironment and accordingly develop adaptive metabolic strategies for survival at the expense of compromised immune functions. Among these strategies, lipid metabolism reprogramming toward fatty acid oxidation is closely related to the immunosuppressive phenotype of tumor infiltrated immune cells, including macrophages, dendritic cells, etc. Therefore, it is important to understand the lipid-mediated crosstalk between cancer cells and immune cells in the tumor microenvironment.Peroxisome proliferator-activated receptors (PPARs) consist of a nuclear receptor family for lipid sensing, and one of the family members PPARα is responsible for fatty acid oxidation, energy homeostasis and regulation of immune cell functions. In this review, we discuss the emerging role of PPARα-associated metabolic-immune regulation in tumor infiltrated immune cells, and key metabolic events and pathways involved, and as well as their influences on anti-tumor immunity.

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“…In addition, reports suggest that certain of the above-mentioned lipid metabolism enzymes play a significant role in BC progression. For instance, acetyl-CoA carboxylase alpha (ACACA) overexpression associates with increased cancer risk [74] and can be detected in early-stage BC [75], while fatty acid synthase (FASN) promoted BC metastasis [76,77] and was proposed as a potential therapeutic target for BC treatment [78].…”

Section: Bc Metabolic Markersmentioning

confidence: 99%

Multi-Omic Approaches to Breast Cancer Metabolic Phenotyping: Applications in Diagnosis, Prognosis, and the Development of Novel Treatments

Gómez-Cebrián

Domingo-Ortí

Poveda

et al. 2021

Cancers

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Breast cancer (BC) is characterized by high disease heterogeneity and represents the most frequently diagnosed cancer among women worldwide. Complex and subtype-specific gene expression alterations participate in disease development and progression, with BC cells known to rewire their cellular metabolism to survive, proliferate, and invade. Hence, as an emerging cancer hallmark, metabolic reprogramming holds great promise for cancer diagnosis, prognosis, and treatment. Multi-omics approaches (the combined analysis of various types of omics data) offer opportunities to advance our understanding of the molecular changes underlying metabolic rewiring in complex diseases such as BC. Recent studies focusing on the combined analysis of genomics, epigenomics, transcriptomics, proteomics, and/or metabolomics in different BC subtypes have provided novel insights into the specificities of metabolic rewiring and the vulnerabilities that may guide therapeutic development and improve patient outcomes. This review summarizes the findings of multi-omics studies focused on the characterization of the specific metabolic phenotypes of BC and discusses how they may improve clinical BC diagnosis, subtyping, and treatment.

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Fatty acid synthesis and cancer: Aberrant expression of the ACACA and ACACB genes increases the risk for cancer

Cited by 19 publications

References 129 publications

The Effect of Avidin on Viability and Proliferation of Colorectal Cancer Cells HT-29

The Effect of Avidin on Viability and Proliferation of Colorectal Cancer Cells HT-29

PPARα at the crossroad of metabolic–immune regulation in cancer

Multi-Omic Approaches to Breast Cancer Metabolic Phenotyping: Applications in Diagnosis, Prognosis, and the Development of Novel Treatments

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