Dietary Intervention by Phytochemicals and Their Role in Modulating Coding and Non-Coding Genes in Cancer

Budişan, Liviuţa; Gulei, Diana; Zănoagă, Oana; Irimie, Alexandra Iulia; Chira, Sergiu; Braicu, Cornelia; Gherman, Claudia; Berindan‐Neagoe, Ioana

doi:10.3390/ijms18061178

Cited by 80 publications

(61 citation statements)

References 200 publications

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“…In this regard, our study is based on the synergistic effect of the in-house-synthesized allicin, as an adjuvant treatment in combination with 5-FU, which is a cytotoxic compound widely used in cancer treatment. Natural compounds interact with different molecular mechanisms and depending on the disease or therapeutic molecules, some bioactive compounds can reduce DNA damage and oxidative stress, can inhibit proliferation, and can reduce genetic and proteomic alterations, and can thus be used as antitumor agents [19,[32][33][34][35].…”

Section: Discussionmentioning

confidence: 99%

The Synergistic Antitumor Effect of 5-Fluorouracil Combined with Allicin against Lung and Colorectal Carcinoma Cells

et al. 2020

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5-fluorouracil (5-FU) is an anticancer drug used to inhibit the proliferation of many different tumor cells. Since severe events are associated with this compound, its combination with different anticancer drugs or adjuvants would allow the use of a significantly lower dose of 5-FU. In this study, we highlighted that the combination of allicin with 5-FU inhibited the cell migration and proliferation of colorectal and lung cancer cells. 5-FU inhibited cell growth with a similar inhibitory concentration for both normal and tumor cells (~200µM), while allicin showed different inhibitory concentrations. With an IC50 of 8.625 µM, lung cancer cells were the most sensitive to allicin. Compared to 5-FU and allicin single-agent treatments, the co-treatment showed a reduced viability rate, with p < 0.05. The morphological changes were visible on all three cell lines, indicating that the treatment inhibited the proliferation of both normal and tumor cells. We highlighted different cell death mechanisms—apoptosis for lung cancer and a non-apoptotic cell death for colorectal cancer. The synergistic antitumor effect of 5-FU combined with allicin was visible against lung and colorectal carcinoma cells. Better results were obtained when a lower concentration of 5-FU was combined with allicin than the single-agent treatment at IC50.

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Section: Discussionmentioning

confidence: 99%

The Synergistic Antitumor Effect of 5-Fluorouracil Combined with Allicin against Lung and Colorectal Carcinoma Cells

et al. 2020

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“…Data were expressed as means ± SD. *p < .05, **p < .01, ***p < .001, ****p < .0001 versus control group Most studies focused on the antioxidative effects of EGCG in various types of disease (Budisan et al, 2017). Many antitumor agents based on the antioxidant activities of EGCG targeting oncogenes were used (Cerezo-Guisado et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

EGCG regulates CTR1 expression through its pro‐oxidative property in non‐small‐cell lung cancer cells

Chen

Jiang

Zeb

et al. 2020

Journal Cellular Physiology

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Copper transporter 1 (CTR1) plays an important role in increasing cisplatin intake. Our previous studies showed that CTR1 expression was upregulated by (−)‐epigallocatechin‐3‐gallate (EGCG), a green tea polyphenol, therefore enhanced cisplatin sensitivity in ovary cancer and non‐small‐cell lung cancer (NSCLC) cells. In the current study in the non‐small‐cell lung cancer cells, we uncovered a potential mechanism of EGCG‐induced CTR1 through its pro‐oxidative property. We found that EGCG increased reactive oxygen species (ROS) generation, while in the presence of ROS scavenger N‐acetyl‐cysteine (NAC), ROS production was eliminated. Changes of CTR1 expression were consistent with the ROS level. Simultaneously, EGCG downregulated ERK1/2 while upregulated lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) through ROS to induce CTR1 expression. Besides, in a nude mouse xenografts model, EGCG treatment raised ROS level, expression of CTR1 and NEAT1 in tumor tissue. Also, ERK1/2 and p‐ERK1/2 were suppressed as well. Taken together, these results suggested a novel mechanism that EGCG mediated ROS to regulate CTR1 expression through the ERK1/2/NEAT1 signaling pathway, which provided more possibilities for EGCG as a natural agent in adjuvant therapy of lung cancer.

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“…Phytochemicals are non-established nutrients with significant health promotion and protective effects [214]. When it comes to specifying the recommended phytochemical intake, several points need to be recognized: (i) the health benefits associated with phytochemicals cannot be attributed to a specific phytochemical compound, (ii) different biological activities make it hard to select a specific key biological role for phytochemicals and generalize this to the whole population, and (iii) there is no assigned disease or impaired function linked to one or any of the members of the phytochemical group [215].…”

Section: Estimated Consumption Level Of Phytochemicalsmentioning

confidence: 99%

Phytochemicals and Gastrointestinal Cancer: Cellular Mechanisms and Effects to Change Cancer Progression

2020

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Gastrointestinal (GI) cancer is a prevailing global health disease with a high incidence rate which varies by region. It is a huge economic burden on health care providers. GI cancer affects different organs in the body such as the gastric organs, colon, esophagus, intestine, and pancreas. Internal and external factors like smoking, obesity, urbanization, genetic mutations, and prevalence of Helicobacter pylori and Hepatitis B and Hepatitis C viral infections could increase the risk of GI cancer. Phytochemicals are non-nutritive bioactive secondary compounds abundantly found in fruits, grains, and vegetables. Consumption of phytochemicals may protect against chronic diseases like cardiovascular disease, neurodegenerative disease, and cancer. Multiple studies have assessed the chemoprotective effect of selected phytochemicals in GI cancer, offering support to their potential towards reducing the pathogenesis of the disease. The aim of this review was to summarize the current knowledge addressing the anti-cancerous effects of selected dietary phytochemicals on GI cancer and their molecular activities on selected mechanisms, i.e., nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), detoxification enzymes, adenosine monophosphate activated protein kinase (AMPK), wingless-related integration site/β-catenin (wingless-related integration site (Wnt) β-catenin, cell apoptosis, phosphoinositide 3-kinases (PI3K)/ protein kinase B AKT/ mammalian target of rapamycin (mTOR), and mitogen-activated protein kinase (MAPK). In this review phytochemicals were classified into four main categories: (i) carotenoids, including lutein, lycopene, and β-carotene; (ii) proanthocyanidins, including quercetin and ellagic acid; (iii) organosulfur compounds, including allicin, allyl propyl disulphide, asparagusic acid, and sulforaphane; and (iv) other phytochemicals including pectin, curcumins, p-coumaric acid and ferulic acid. Overall, phytochemicals improve cancer prognosis through the downregulation of β-catenin phosphorylation, therefore enhancing apoptosis, and upregulation of the AMPK pathway, which supports cellular homeostasis. Nevertheless, more studies are needed to provide a better understanding of the mechanism of cancer treatment using phytochemicals and possible side effects associated with this approach.

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Dietary Intervention by Phytochemicals and Their Role in Modulating Coding and Non-Coding Genes in Cancer

Cited by 80 publications

References 200 publications

The Synergistic Antitumor Effect of 5-Fluorouracil Combined with Allicin against Lung and Colorectal Carcinoma Cells

The Synergistic Antitumor Effect of 5-Fluorouracil Combined with Allicin against Lung and Colorectal Carcinoma Cells

EGCG regulates CTR1 expression through its pro‐oxidative property in non‐small‐cell lung cancer cells

Phytochemicals and Gastrointestinal Cancer: Cellular Mechanisms and Effects to Change Cancer Progression

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