Downregulations of AKT/mTOR Signaling Pathway for Salmonella-Mediated Suppression of Matrix Metalloproteinases-9 Expression in Mouse Tumor Models

Tsao, Yu-Tzu; Kuo, Chun-Yu; Cheng, Su-Fen; Lee, Che‐Hsin

doi:10.3390/ijms19061630

Cited by 28 publications

(35 citation statements)

References 31 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%

“…B16F10 or 4T1 cells (1 × 10 6 cells per well) were seeded in 6-well culture plates incubated for 24 h at 37°C, 5% CO2. Then, the cells were either transfected with 5 μg pCDNA 3.1 control plasmid or constitutively active AKT plasmid (Provided by Dr. Chiau-Yuang Tsai of the Department of Molecular Immunology, Osaka University, Japan) using Lipofectamine 2000 [18,19] and then incubated for another 24 h at 37°C, 5% CO2. Afterwards, the cells were washed and treated with hinokitiol (Sigma Aldrich, St. Louis, MO, USA) for 16 h and prepared for Western blotting.…”

Section: Gene Transfectionmentioning

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: Gene Transfectionmentioning

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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“…Modified Eagle Medium (DMEM) with 1.5 g/L sodium bicarbonate, 25 mM glucose, and 10% fetal bovine serum (FBS), as previously described 14. EPA, SB203580, SP600125, 5-Fluorouracil (5-FU), and Lucifer yellow were purchased from Sigma-Aldrich (Sigma Aldrich, St. Louis, MO, USA).…”

Section: Methodsmentioning

confidence: 99%

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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“…MMP‐9 plays a very important role in tumour growth and migration, and suppression of MM‐9 is expected to affect tumour metastasis (Tsao et al . ).…”

Section: Other Host Pathways In Salmonella–tumour Interactionmentioning

confidence: 97%

Nontyphoidal Salmonella : a potential anticancer agent

et al. 2019

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Summary Use of bacteria in cancer therapy, despite being considered as a potent strategy, has not really picked up the way other methods of cancer therapies have evolved. However, in recent years, the interest on use of bacteria to kill cancer cells has renewed considerably. The standard and widely followed strategies of cancer treatment often fail either due to the complexity of tumour biology or because of the accompanying side effects. In contrast, these limitations can be easily overcome in a bacteria‐mediated approach. Salmonella is a bacterium, which is known for its ability to colonize solid or semisolid tumours more efficiently than any other bacteria. Among more than 2500 serovars of Salmonella, S. Typhimurium has been widely studied for its antagonistic effects on cancer cells. Here in, we review the current status of the preclinical and the clinical studies with a focus on the mechanisms that attribute the anticancer properties to nontyphoidal Salmonella.

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Downregulations of AKT/mTOR Signaling Pathway for Salmonella-Mediated Suppression of Matrix Metalloproteinases-9 Expression in Mouse Tumor Models

Cited by 28 publications

References 31 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

Nontyphoidal Salmonella : a potential anticancer agent

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