Sulforaphane suppresses oral cancer cell migration by regulating cathepsin S expression

Chen, Chang-Tai; Hsieh, Ming‐Ju; Hsieh, Yi‐Hsien; Hsin, Min‐Chieh; Chuang, Yi-Ting; Yang, Shun‐Fa; Yang, Jyh Bin

doi:10.18632/oncotarget.24786

Cited by 16 publications

(9 citation statements)

References 49 publications

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“…Thus, these studies emphasized the role of ADAM9 in various cancers and highlighted the association of ADAM9 with a poor RCC prognosis. However, the current study showed that sulforaphane or hispolon could similarly activate autophagy and suppress the invasion and metastasis of oral cancer cells or cervical cancer cells by downregulating CTSS through the upregulation of the MEK/ERK signaling pathway [42,43]. Consistent with the above studies, we were able to demonstrate that fisetin inhibited the metastatic ability of human RCC cells through the activation of the MEK/ERK pathways involved in CTSS/ADAM9 expression.…”

Section: Discussionsupporting

confidence: 87%

Fisetin Suppresses the Proliferation and Metastasis of Renal Cell Carcinoma through Upregulation of MEK/ERK-Targeting CTSS and ADAM9

Hsieh

Tsai

Yang

et al. 2019

Cells

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Fisetin, a natural flavonoid, is known to have anticarcinogenic effects against several cancers, but its role in mediating renal cell carcinoma (RCC) progression has not been delineated. Cell viability, cytotoxicity, and cell cycle distribution were measured using the 3‐(4,5‐cimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide assay and propidium iodide staining with flow cytometry. The in vitro migration and invasion assay was used to examine in vivo cell migration and invasion. Human protease antibody array analysis was conducted with cell migration/invasion-related proteins. Western blotting and quantitative reverse transcription polymerase chain reaction were used for assessing protein expression related to the cell cycle, cell invasion, and mitogen-activated protein kinase (MAPK) signaling pathway. We found that fisetin significantly inhibited cell viability through cell cycle arrest in the G2/M phase, in addition to downregulating cyclin D1 and upregulating p21/p27. Fisetin inhibited the migration and invasion of human RCC cells through the downregulation of CTSS and a disintegrin and metalloproteinase 9 (ADAM9). Fisetin also upregulated ERK phosphorylation in 786-O and Caki-1 cells. Furthermore, treatment with a MEK inhibitor (UO126) reduced the inhibitory effects of fisetin on the metastasis of RCC cells through the ERK/CTSS/ADAM9 pathway. Fisetin inhibits proliferation and metastasis of RCC cells by downregulating CTSS and ADAM9 through the MEK/ERK signaling pathway. These findings indicate that fisetin is a promising antitumor agent against RCC.

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Section: Discussionsupporting

confidence: 87%

Fisetin Suppresses the Proliferation and Metastasis of Renal Cell Carcinoma through Upregulation of MEK/ERK-Targeting CTSS and ADAM9

Hsieh

Tsai

Yang

et al. 2019

Cells

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“…ERK activation prevents cancer cell apoptosis [41]. Furthermore, the activation of the ERK/MAPK pathways is also involved in the regulation of LC3 and cathepsin S proteins and is potentially associated with cell autophagy and metastasis in oral cancer cells [42]. Therefore, MAPK proteins are implicated in numerous processes in cancer progression and are therefore worthy of further investigation.…”

Section: Discussionmentioning

confidence: 99%

Antimetastatic Effects of Sesamin on Human Head and Neck Squamous Cell Carcinoma through Regulation of Matrix Metalloproteinase-2

Chen

Lin

et al. 2020

Molecules

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Background: Sesamin is a lignin present in sesame oil from the bark of Zanthoxylum spp. Sesamin reportedly has anticarcinogenic potential and exerts anti-inflammatory effects on several tumors. Hypothesis/Purpose: However, the effect of sesamin on metastatic progression in human head and neck squamous carcinoma (HNSCC) remains unknown in vitro and in vivo; hence, we investigated the effect of sesamin on HNSCC cells in vitro. Methods and Results: Sesamin-treated human oral cancer cell lines FaDu, HSC-3, and Ca9-22 were subjected to a wound-healing assay. Furthermore, Western blotting was performed to assess the effect of sesamin on the expression levels of matrix metalloproteinase (MMP)-2 and proteins of the MAPK signaling pathway, including p-ERK1/2, P-p38, and p-JNK1/2. In addition, we investigated the association between MMP-2 expression and the MAPK pathway in sesamin-treated oral cancer cells. Sesamin inhibited cell migration and invasion in FaDu, Ca9-22, and HSC-3 cells and suppressed MMP-2 at noncytotoxic concentrations (0 to 40 μM). Furthermore, sesamin significantly reduced p38 MAPK and JNK phosphorylation in a dose-dependent manner in FaDu and HSC-3 cells. Conclusions: These results indicate that sesamin suppresses the migration and invasion of HNSCC cells by regulating MMP-2 and is thus a potential antimetastatic agent for treating HNSCC.

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“…This last activity would be mediated by upregulation of two genes, heme oxygenase 1 ( HMOX1 ) and heat shock protein family A (Hsp70) member 1A ( HSPA1A ), as well as the MICA/B ligand of a natural killer cell activator protein, NKG2D [ 108 ]. In addition, SFN interferes with cell migration, downregulates cathepsin S expression through the ERK signaling pathway, and upregulates microtubule-associated protein 1A/1B-light chain 3 (LC3) [ 109 ].…”

Section: Other Antioxidants With Potential Epigenetic Effect On Squamous Cell Carcinoma Of the Head And Neckmentioning

confidence: 99%

Usefulness of Melatonin and Other Compounds as Antioxidants and Epidrugs in the Treatment of Head and Neck Cancer

Guerra¹,

Devesa²

2021

Antioxidants

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Along with genetic mutations, aberrant epigenetic alterations are the initiators of head and neck cancer carcinogenesis. Currently, several drugs are being developed to correct these epigenetic alterations, known as epidrugs. Some compounds with an antioxidant effect have been shown to be effective in preventing these malignant lesions and in minimizing the complications derived from cytotoxic treatment. Furthermore, in vitro and in vivo studies show a promising role in the treatment of head and neck squamous cell carcinoma (HNSCC). This is the case of supplements with DNA methylation inhibitory function (DNMTi), such as epigallocatechin gallate, sulforaphane, and folic acid; histone deacetylase inhibitors (HDACi), such as sodium butyrate and melatonin or histone acetyltransferase inhibitors (HATi), such as curcumin. The objective of this review is to describe the role of some antioxidants and their epigenetic mechanism of action, with special emphasis on melatonin and butyric acid given their organic production, in the prevention and treatment of HNSCC.

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Sulforaphane suppresses oral cancer cell migration by regulating cathepsin S expression

Cited by 16 publications

References 49 publications

Fisetin Suppresses the Proliferation and Metastasis of Renal Cell Carcinoma through Upregulation of MEK/ERK-Targeting CTSS and ADAM9

Fisetin Suppresses the Proliferation and Metastasis of Renal Cell Carcinoma through Upregulation of MEK/ERK-Targeting CTSS and ADAM9

Antimetastatic Effects of Sesamin on Human Head and Neck Squamous Cell Carcinoma through Regulation of Matrix Metalloproteinase-2

Usefulness of Melatonin and Other Compounds as Antioxidants and Epidrugs in the Treatment of Head and Neck Cancer

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