Eicosapentaenoic acid reduces indoleamine 2,3-dioxygenase 1 expression in tumor cells

Wang, Chih-Chiang; Yang, Chih‐Jen; Wu, Li-Hsien; Lin, Han-Chen; Wen, Zhi‐Hong; Lee, Che‐Hsin

doi:10.7150/ijms.27326

Cited by 11 publications

(16 citation statements)

References 29 publications

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“…Dr. Sheu and his colleagues, the experts in the field, found that hinokitiol inhibits tumor cell migration via blocking the phosphorylation of mitogen-activated protein kinase and p65 nuclear factor kappa B (NF-κB) [15]. Our findings verified that the expression of phosphorylated Akt/Erk is decreased in hinokitiol-treated B16F10 and 4T1 tumor cells, which is consistent with the results published by other groups [15][16][17][18][19]. We also used resveratrol and constitutively active Akt transfection to make a thorough inquiry on the association of heparanase and these two pathways.…”

Section: Discussionsupporting

confidence: 91%

“…Murine melanoma cells (B16F10) [16] and murine mammary carcinoma (4T1) cells [17] were maintained in 10cm culture dish with Dulbecco's Modified Eagle Medium (DMEM) containing 1% Penicillin-Streptomycin (100 units/mL penicillin and 100 μg/mL streptomycin), and 10% fetal bovine serum (FBS). Both B16F10 and 4T1 cells were incubated at 37°C, 5% CO2.…”

Section: Cell Culturementioning

confidence: 99%

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Hinokitiol reduces tumor metastasis by inhibiting heparanase via extracellular signal-regulated kinase and protein kinase B pathway

Hsu

et al. 2020

Int. J. Med. Sci.

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Heparanase cleaves the extracellular matrix by degrading heparan sulfate that ultimately leads to cell invasion and metastasis; a condition that causes high mortality among cancer patients. Many of the anticancer drugs available today are natural products of plant origin, such as hinokitiol. In the previous report, it was revealed that hinokitiol plays an essential role in anti-inflammatory and anti-oxidation processes and promote apoptosis or autophagy resulting to the inhibition of tumor growth and differentiation. Therefore, this study explored the effects of hinokitiol on the cancer-promoting pathway in mouse melanoma (B16F10) and breast (4T1) cancer cells, with emphasis on heparanase expression. We detected whether hinokitiol can elicit anti-metastatic effects on cancer cells via wound healing and Transwell assays. Besides, mice experiment was conducted to observe the impact of hinokitiol in vivo. Our results show that hinokitiol can inhibit the expression of heparanase by reducing the phosphorylation of protein kinase B (Akt) and extracellular regulated protein kinase (ERK). Furthermore, in vitro cell migration assay showed that heparanase downregulation by hinokitiol led to a decrease in metastatic activity which is consistent with the findings in the in vivo experiment.

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Section: Discussionsupporting

confidence: 91%

Section: Cell Culturementioning

confidence: 99%

Hinokitiol reduces tumor metastasis by inhibiting heparanase via extracellular signal-regulated kinase and protein kinase B pathway

Hsu

et al. 2020

Int. J. Med. Sci.

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“…EPA modulated in immunity and inhibits the expression of intracellular interleukin-2, tumor necrosis factor -α, and interleukin-4 in T cells 9. Previously, we found that EPA did not influence the proliferation of T cells 8. Meanwhile, EPA reduced the function of antigen-presenting cells 10, 11.…”

Section: Introductionmentioning

confidence: 87%

“…Humans obtain these from dietary sources, because humans are not able to synthesize EPA 7. EPA has anti-inflammatory and antitumor abilities that work by regulating cellular signal pathways 8. EPA modulated in immunity and inhibits the expression of intracellular interleukin-2, tumor necrosis factor -α, and interleukin-4 in T cells 9.…”

Section: Introductionmentioning

confidence: 99%

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Eicosapentaenoic acids enhance chemosensitivity through connexin 43 upregulation in murine melanoma models

Yang¹,

Kuo²,

Wu³

et al. 2019

Int. J. Med. Sci.

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Chemotherapy is now in common use for the treatment of tumors; however, with tumor growth retardation comes the severe side effects that occur after a chemotherapy cycle. Eicosapentaenoic acids (EPA) used in combination with chemotherapy has an additive effects and provides a rationale for using EPA in tandem with chemotherapy. To improve the efficacy and safety of this combination therapy, a further understanding that EPA modulates with the tumor microenvironment is necessary. Connexin 43 (Cx43) is involved in enhancing chemosensitivity that was suppressed in a tumor microenvironment. We aim to investigate the role of EPA in chemosensitivity in murine melanoma by inducing Cx43 expression. The dose-dependent upregulation of Cx43 expression and gap junction intercellular communication were observed in B16F10 cells after EPA treatment. Furthermore, EPA significantly increased the expression levels of mitogen-activated protein kinases (MAPK) signaling pathways. The EPA-induced Cx43 expression was reduced after MAPK inhibitors. Knockdown Cx43 in B16F10 cells reduced the therapeutic effects of combination therapy (EPA plus 5-Fluorouracil). Our results demonstrate that the treatment of EPA is a tumor induced Cx43 gap junction communication and enhances the combination of EPA and chemotherapeutic effects.

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Correlation between immune‐related Tryptophan‐Kynurenine pathway and severity of severe pneumonia and inflammation‐related polyunsaturated fatty acids

Guo,

Xue,

Zhang

et al. 2023

Immunity Inflam & Disease

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BackgroundImmune dysfunction and oxidative stress caused by severe pneumonia can lead to multiple organ dysfunction and even death, causing a significant impact on health and the economy. Currently, great progress has been made in the diagnosis and treatment of this disease, but the mortality rate remains high (approximately 50%). Therefore, there is still potential for further exploration of the immune response mechanisms against severe pneumonia.ObjectiveThis study analyzed the difference in serum metabolic profiles between patients with severe pneumonia and health individuals through metabolomics, aiming to uncover the correlation between the Tryptophan‐Kynurenine pathway and the severity of severe pneumonia, as well as N‐3/N‐6 polyunsaturated fatty acids (PUFAs).MethodsIn this study, 44 patients with severe pneumonia and 37 health controls were selected. According to the changes in the disease symptoms within the 7 days of admission, the patients were divided into aggravation (n = 22) and remission (n = 22) groups. Targeted metabolomics techniques were performed to quantify serum metabolites and analyze changes between groups.ResultsMetabolomics analysis showed that serum kynurenine and kynurenine/tryptophan (K/T) were significantly increased and tryptophan was significantly decreased in patients with severe pneumonia; HETE and HEPE in lipids increased significantly, while eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), docosahexaenoic acid (DHA), α‐linolenic acid (linolenic acid, α‐LNA), arachidonic acid (ARA), Dihomo‐γ‐linolenic acid (DGLA), and 13(s)‐hydroperoxylinoleic acid (HPODE) decreased significantly. Additionally, the longitudinal comparison revealed that Linolenic acid, DPA, and Tryptophan increased significantly in the remission group, while and kynurenine and K/T decreased significantly. In the aggravation group, Kynurenine and K/T increased significantly, while ARA, 8(S)‐hydroxyeicosatetraenoic acid (HETE), 11(S)‐HETE, and Tryptophan decreased significantly. The correlation analysis matrix demonstrated that Tryptophan was positively correlated with DGLA, 12(S)‐hydroxyeicosapentaenoic acid (HEPE), ARA, EPA, α‐LNA, DHA, and DPA. Kynurenine was positively correlated with 8(S)‐HETE and negatively correlated with DHA. Additionally, K/T was negatively correlated with DGLA, ARA, EPA, α‐LNA, DHA, and DPA.ConclusionThis study revealed that during severe pneumonia, the Tryptophan‐Kynurenine pathway was activated and was positively correlated with the disease progression. On the other hand, the activation of the Tryptophan‐Kynurenine pathway was negatively correlated with N‐3/N‐6 PUFAs.

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Eicosapentaenoic acid reduces indoleamine 2,3-dioxygenase 1 expression in tumor cells

Cited by 11 publications

References 29 publications

Hinokitiol reduces tumor metastasis by inhibiting heparanase via extracellular signal-regulated kinase and protein kinase B pathway

Hinokitiol reduces tumor metastasis by inhibiting heparanase via extracellular signal-regulated kinase and protein kinase B pathway

Eicosapentaenoic acids enhance chemosensitivity through connexin 43 upregulation in murine melanoma models

Correlation between immune‐related Tryptophan‐Kynurenine pathway and severity of severe pneumonia and inflammation‐related polyunsaturated fatty acids

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