Sodium propionate exerts anticancer effect in mice bearing breast cancer cell xenograft by regulating JAK2/STAT3/ROS/p38 MAPK signaling

Park, Hyunsoo; Han, Joo‐Hui; Park, Jeong Won; Lee, Do‐Hyung; Jang, Keun‐Woo; Lee, Miji; Heo, Kyung‐Sun; Myung, Chang‐Seon

doi:10.1038/s41401-020-00522-2

Cited by 33 publications

(30 citation statements)

References 46 publications

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“…The MAPK pathway can be activated by growth factors, transcription factors, ligands of G protein-coupled receptors, and more (27). Abnormal activation of the P38 MAPK pathway can promote the expression of various cancer cell-related proteins and promote the resistance of cancer cells to chemotherapeutic drugs (28). This work was intended to probe whether MAPK and PI3K/Akt pathways were involved in the process of EpCAM Mglycosylation on the occurrence of EMT in breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

The Regulatory Mechanism of EpCAM N-Glycosylation-Mediated MAPK and PI3K/Akt Pathways on Epithelial-Mesenchymal Transition in Breast Cancer Cells

Wen¹,

Lin²,

Li³

et al. 2022

Cell Mol Biol (Noisy-le-grand)

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It was to investigate the regulation of motigen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) pathways mediated by epithelial cell adhesion molecules (EpCAM) N-glycosylation on epithelial-mesenchymal transition (EMT) in breast cancer cells. Breast cancer cells MCF-7 and MDA-MB-231 were taken in the control group; the blank vector plasmid transfection (blank plasmid group) and EpCAM N-glycosylation mutant plasmid transfection (Mutant-EpCAM group) were analyzed. The EpCAM in breast cancer cells was localized by immunofluorescence technique, the proliferation activity of cells in each group was detected by methyl thiazolyl tetrazolium (MTT) assay, and the clonality of cells was detected by plate cloning. and apoptosis-related proteins (Caspase-3, Bcl-2, and Bax), EMT-related molecular markers (E-cadherin, Ncadherin, and Vimentin), as well as MAPK and PI3K/Akt pathway-related proteins (p38, PI3K, and Akt) in cells were detected by western blotting (WB). EpCAM N-glycosylation mutations did not alter the expression localization of EpCAM in breast cancer cells. Compared with the control group and the blank plasmid group, the cell proliferation activity and the number of colonies formed were decreased in the Mutant-EpCAM group (P<0.05). The protein expressions of Caspase-3, Bax, and E-cadherin were up-regulated significantly, and the expressions of Bcl-2, N-cadherin, Vimentin, p-p38, p-PI3K, and p-Akt were greatly down-regulated (P<0.05). EpCAM N-glycosylation could regulate the EMT in breast cancer cells through MAPK and PI3K/Akt pathways.

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Section: Discussionmentioning

confidence: 99%

The Regulatory Mechanism of EpCAM N-Glycosylation-Mediated MAPK and PI3K/Akt Pathways on Epithelial-Mesenchymal Transition in Breast Cancer Cells

Wen¹,

Lin²,

Li³

et al. 2022

Cell Mol Biol (Noisy-le-grand)

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“…5G). ROS regulate the autophagy pathway in cancer cells (33)(34)(35). Notably, excessively high levels of ROS can induce cell death through oxidative damage (36).…”

Section: Ea Does Not Affect Apoptosis and Necrosis Apoptosis And Necr...mentioning

confidence: 99%

Eupalinolide A induces autophagy via the ROS/ERK signaling pathway in hepatocellular carcinoma cells in vitro and in vivo

et al. 2022

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Hepatocellular carcinoma is the most common primary malignancy of the liver. The current systemic drugs used to treat hepatocellular carcinoma result in low overall survival time. It has therefore been suggested that new small-molecule drugs should be developed for treating hepatocellular carcinoma. Eupatorium lindleyanum DC. (EL) has been used to treat numerous diseases, particularly respiratory diseases; however, to the best of our knowledge, studies have not yet fully elucidated the effect of EL on hepatocellular carcinoma. In the present study, the effect of eupalinolide A (EA), one of the extracts of EL, was evaluated on tumor growth in a xenograft model of human hepatocellular carcinoma cells, and on the proliferation and migration of hepatocellular carcinoma cell lines. Cell cycle progression and the type of cell death were then evaluated using the Cell Counting Kit 8 assay, flow cytometry, electron microscopy and western blotting. EA significantly inhibited cell proliferation and migration by arresting the cell cycle at the G 1 phase and inducing autophagy in hepatocellular carcinoma cells. EA-induced autophagy was mediated by reactive oxygen species (ROS) and ERK signaling activation. Specific inhibitors of ROS, autophagy and ERK inhibited EA-induced cell death and migration. In conclusion, the present study revealed that EA may inhibit the proliferation and migration of hepatocellular carcinoma cells, highlighting its potential as a promising antitumor compound for treating hepatocellular carcinoma.

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“…Pasteurellales [118] Alcohol consumption and high temperature beverages [119] Fruit and vegetable [120] Polyphenols [76,100] Breast Bacteroides plebeius [54,55] Acid-producing diets [121,122] B-glucuronidase [63] Valproic acid [123,124] Seaweed [54,55] Sodium propionate [45] Sodium butyrate [102][103][104][105][106] Mediterranean diet [112,123,124] Sorbate [47] Benzoate [47] Ovarian Clostridia [125] Valproic acid [90] Vitamin D [35] Prostate Possibly Enterobacteriaceae and Proteobacteria [73] High-fat (keto) diet [72] SCFA [72,126] Sodium phenylbutyrate [107,108,110] Sodium butyrate [102][103][104][105][106]…”

Section: Cancer Type Possible Microbes Involved Dietary Risk Factors mentioning

confidence: 99%

“…The sodium salt of propionic acid, sodium propionate, is often used as a food preservative in bakery products and has been shown to exert an antitumour effect through the mitogen-associated protein kinase (MAPK) signalling pathway in breast cancer xenograft models. [ 45 ] This example illustrates the complexity between food preservatives, microbes, and cancer, as most are observed to be negatively associated. Nitrates have also been well-described to be associated with colorectal cancer [ 46 ], while sorbate and benzoate correlate with the occurrence of breast cancer [ 47 ].…”

Section: Impact Of Select Dietary Factors On Cancer Biologymentioning

confidence: 99%

The Multifaceted Roles of Diet, Microbes, and Metabolites in Cancer

Armstrong

Bording-Jorgensen

Wine

2021

Cancers

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Many studies performed to date have implicated select microbes and dietary factors in a variety of cancers, yet the complexity of both these diseases and the relationship between these factors has limited the ability to translate findings into therapies and preventative guidelines. Here we begin by discussing recently published studies relating to dietary factors, such as vitamins and chemical compounds used as ingredients, and their contribution to cancer development. We further review recent studies, which display evidence of the microbial-diet interaction in the context of cancer. The field continues to advance our understanding of the development of select cancers and how dietary factors are related to the development, prevention, and treatment of these cancers. Finally, we highlight the science available in the discussion of common misconceptions with regards to cancer and diet. We conclude this review with thoughts on where we believe future research should focus in order to provide the greatest impact towards human health and preventative medicine.

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Sodium propionate exerts anticancer effect in mice bearing breast cancer cell xenograft by regulating JAK2/STAT3/ROS/p38 MAPK signaling

Cited by 33 publications

References 46 publications

The Regulatory Mechanism of EpCAM N-Glycosylation-Mediated MAPK and PI3K/Akt Pathways on Epithelial-Mesenchymal Transition in Breast Cancer Cells

The Regulatory Mechanism of EpCAM N-Glycosylation-Mediated MAPK and PI3K/Akt Pathways on Epithelial-Mesenchymal Transition in Breast Cancer Cells

Eupalinolide A induces autophagy via the ROS/ERK signaling pathway in hepatocellular carcinoma cells in vitro and in vivo

The Multifaceted Roles of Diet, Microbes, and Metabolites in Cancer

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