Medical ozone induces proliferation and migration inhibition through ROS accumulation and PI3K/AKT/NF-κB suppression in human liver cancer cells in vitro

Li, J.; Zeng, Tao; Tang, Shuiying; Zhong, Meifeng; Huang, Qiaobing; Li, X.; He, Xiaofeng

doi:10.1007/s12094-021-02594-w

Cited by 11 publications

(8 citation statements)

References 34 publications

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“…This radio-mimetic effect has been observed also when comparing ozone with some CT drugs, such as 5-FU [17,20], doxorubicin, or ifosfamide [16]. Ozone induces a similar cancer cell damage to that produced by these drugs by increasing ROS in tumor cells [23]. Moreover, there is a potentiated or synergistic effect when using these CT drugs and ozone together [17,19], the same as what we can observe with the above commented RT protocols.…”

Section: Discussionsupporting

confidence: 78%

“…Recent papers, such as the ones from Mokhtari [21] or Li [23], give us more detailed information about the biochemical pathways used by ROS to induce cell apoptosis in cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…Lately, Li et al [23] verified that ozone gas on hepatocarcinoma (bel7402 and SMMC7721 cancer cell lines) cell cultures restrains the proliferation and migration potential thanks to the increase of ROS and the NFKβ suppression.…”

Section: In Vitro Studiesmentioning

confidence: 99%

“…All these mechanisms improve immunity [23,24,33] and increase radiosensibility [25][26][27][28][29][30] in some tumors, but they are not the target of this paper. Only Kuroda's team [34] has published a study in an animal model (a mouse with rectal cancer tumor-bearing) showing necrosis and the inhibited proliferation effect of an intratumor injection of 1 mL of ozonated water (ozone dissolved in bi-distilled water at concentrations of 20.8, 41.6, 104, and 208 mM in four groups of mice), compared with 1 mL of bi-distilled water and no treatment.…”

Section: In Vivo Studiesmentioning

confidence: 99%

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Systemic Review: Ozone: A Potential New Chemotherapy

Baeza-Noci

Pinto-Bonilla

2021

IJMS

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In the last sixty years, publications in reputed journals have shown the preclinical positive effect of ozone gas in cancer cells. However, the translation of these results into clinical practice is far away from success. A comprehensive approach is necessary for this, and oncologists and researchers need guidance from medical specialists with in-depth knowledge of ozone in medicine. In this article, we review the evidence around this question and suggest different potential research lines to those interested in this exciting field.

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Section: Discussionsupporting

confidence: 78%

“…Recent papers, such as the ones from Mokhtari [21] or Li [23], give us more detailed information about the biochemical pathways used by ROS to induce cell apoptosis in cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Section: In Vitro Studiesmentioning

confidence: 99%

Section: In Vivo Studiesmentioning

confidence: 99%

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Systemic Review: Ozone: A Potential New Chemotherapy

Baeza-Noci

Pinto-Bonilla

2021

IJMS

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“…Akt is an important downstream signaling molecule of PI3K, and PI3K mainly participates in the regulation of cell proliferation, apoptosis, and other signal transduction by activating Akt [ 17 ]. Recent studies have found that the PI3K/Akt signaling pathway plays an important role in the proliferation and migration of hepatoma cells [ 18 ]. Inhibition of the PI3K/Akt signaling pathway and reduction of phosphorylation of PI3K and Akt can inhibit the proliferation and migration of hepatoma cells and promote the apoptosis of hepatoma cells [ 18 – 20 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of circFOXO3 on the Proliferation and Invasion of Liver Cancer Cells by Regulating PI3K/Akt Pathway

Liu

Yao

et al. 2022

Contrast Media & Molecular Imaging

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Objective. Hepatocellular carcinoma is a malignant disease occurring in the liver and is one of the main causes of death in cancer patients. Tumor cells are the main components of tumors and have a strong proliferative capacity. They are easily transferred to other parts of the body and can produce harmful substances that destroy the normal organ structure and endanger human life and health. In this study, we investigate the effect of circFOXO3 on the proliferation and invasion of hepatocellular carcinoma cells and its possible mechanism. Methods. Human hepatocellular carcinoma cells BEL-7404, Hep G2, Hep 3B2.1–7, HuH-7, Li-7, and human normal hepatocytes HHL-5 were selected, and the expression level of circFOXO3 in the cell lines was determined by qRT-PCR. The cell line with low circFOXO3 expression level (HuH-7 cells) was used for follow-up experiments. HuH-7 liver cancer cells were divided into the control group (normal cultured), circFOXO3-NC group (transfected with circFOXO3 negative control), circFOXO3 mimic group (transfected with circFOXO3 mimic), PI3K activator group (20 μmol/L PI3K activator 740Y-P), and circFOXO3 mimic + PI3K activator group (transfected with circFOXO3 mimic + treated with PI3K activator 740Y-P). The qRT-PCR method was used to determine the expression level of circFOXO3 in HuH-7 liver cancer cells in each group, WB was used to detect the expression of apoptosis, invasion, and phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway related proteins in HuH-7 liver cancer cells in each group, the CCK-8 method was used to determine the viability of HuH-7 liver cancer cells in each group, flow cytometry was used to determine the apoptotic ability of HuH-7 liver cancer cells in each group, the transwell chamber experiment was used to determine the invasion ability of HuH-7 liver cancer cells in each group, and the scratch test was used to determine the migration ability of HuH-7 liver cancer cells in each group. Results. circFOXO3 showed low expression in liver cancer cells; compared with the control group, the circFOXO3 expression and apoptosis rate of HuH-7 liver cancer cells in the circFOXO3 mimic group were significantly increased ( P < 0.05 ) and the PI3K/Akt pathway-related protein expression, cell viability, invasion, and migration abilities were significantly reduced ( P < 0.05 ); the apoptosis rate of HuH-7 liver cancer cells in the PI3K activator group was significantly reduced ( P < 0.05 ) and the PI3K/Akt pathway related protein expression, cell viability, invasion and migration abilities were significantly increased ( P < 0.05 ). Compared with the circFOXO3 mimic group, the apoptosis rate of HuH-7 liver cancer cells in the circFOXO3 mimic + PI3K activator group was significantly reduced ( P < 0.05 ) and the PI3K/Akt pathway-related protein expression, cell viability, invasion and migration abilities were significantly increased ( P < 0.05 ). Conclusion. Highly expressed circFOXO3 can inhibit the proliferation and invasion of HuH-7 liver cancer cells, which may be achieved by inhibiting the PI3K/Akt pathway.

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NF‐κB as a regulator of cancer metastasis and therapy response: A focus on epithelial–mesenchymal transition

Mirzaei

Saghari

Bassiri

et al. 2022

Journal Cellular Physiology

101

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Metastasis of tumor cells is a complex challenge and significantly diminishes the overall survival and prognosis of cancer patients. The epithelial‐to‐mesenchymal transition (EMT) is a well‐known mechanism responsible for the invasiveness of tumor cells. A number of molecular pathways can regulate the EMT mechanism in cancer cells and nuclear factor‐kappaB (NF‐κB) is one of them. The nuclear translocation of NF‐κB p65 can induce the transcription of several genes involved in EMT induction. The present review describes NF‐κB and EMT interaction in cancer cells and their association in cancer progression. Due to the oncogenic role NF‐κB signaling, its activation enhances metastasis of tumor cells via EMT induction. This has been confirmed in various cancers including brain, breast, lung and gastric cancers, among others. The ZEB1/2, transforming growth factor‐β, and Slug as inducers of EMT undergo upregulation by NF‐κB to promote metastasis of tumor cells. After EMT induction driven by NF‐κB, a significant decrease occurs in E‐cadherin levels, while N‐cadherin and vimentin levels undergo an increase. The noncoding RNAs can potentially also function as upstream mediators and modulate NF‐κB/EMT axis in cancers. Moreover, NF‐κB/EMT axis is involved in mediating drug resistance in tumor cells. Thus, suppressing NF‐κB/EMT axis can also promote the sensitivity of cancer cells to chemotherapeutic agents.

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Medical ozone induces proliferation and migration inhibition through ROS accumulation and PI3K/AKT/NF-κB suppression in human liver cancer cells in vitro

Cited by 11 publications

References 34 publications

Systemic Review: Ozone: A Potential New Chemotherapy

Systemic Review: Ozone: A Potential New Chemotherapy

Effects of circFOXO3 on the Proliferation and Invasion of Liver Cancer Cells by Regulating PI3K/Akt Pathway

NF‐κB as a regulator of cancer metastasis and therapy response: A focus on epithelial–mesenchymal transition

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