Quercetin in elimination of tumor initiating stem‐like and mesenchymal transformation property in head and neck cancer

Chang, Wen‐Wei; Hu, Fang‐Wei; Yu, Cheng–Chia; Wang, Hsiu–Huan; Feng, Hsiang-Pu; Lan, Chih; Tsai, Lo–Lin; Chang, Yu‐Chao

doi:10.1002/hed.22982

Cited by 46 publications

(29 citation statements)

References 36 publications

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“…The ability of cancer cells to migrate and invade is increased by the reduction of the expression of E-cadherin, a cell-cell adhesion molecule, whereas the expression of N-cadherin is decreased, which is inversely proportional to that of E-cadherin [42]. Quercetin regulates the expression of EMT markers, such as E-cadherin, vimentin, and β-catenin, in head and neck cancer-derived sphere cells and breast cancer cells [43,44]. In addition, quercetin prevented the EGF-induced expression of N-cadherin and vimentin and increased the expression of E-cadherin in prostate cells [45].…”

Section: Discussionmentioning

confidence: 99%

Quercetin Inhibits Cell Survival and Metastatic Ability via the EMT-Mediated Pathway in Oral Squamous Cell Carcinoma

et al. 2020

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This study aimed to investigate whether quercetin exerts anticancer effects on oral squamous cell carcinoma (OSCC) cell lines and to elucidate its mechanism of action. These anticancer effects in OSCC cells were assessed using an MTT assay, flow cytometry (to assess the cell cycle), wound-healing assay, invasion assay, Western blot analysis, gelatin zymography, and immunofluorescence. To investigate whether quercetin also inhibits transforming growth factor β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) in human keratinocyte cells, HaCaT cells were treated with TGF-β1. Overall, our results strongly suggest that quercetin suppressed the viability of OSCC cells by inducing cell cycle arrest at the G2/M phase. However, quercetin did not affect cell viability of human keratinocytes such as HaCaT (immortal keratinocyte) and nHOK (primary normal human oral keratinocyte) cells. Additionally, quercetin suppresses cell migration through EMT and matrix metalloproteinase (MMP) in OSCC cells and decreases TGF-β1-induced EMT in HaCaT cells. In conclusion, this study is the first, to our knowledge, to demonstrate that quercetin can inhibit the survival and metastatic ability of OSCC cells via the EMT-mediated pathway, specifically Slug. Quercetin may thus provide a novel pharmacological approach for the treatment of OSCCs.Molecules 2020, 25, 757 2 of 15 Statistical AnalysesStatistical analyses were performed by a one-way analysis of variance (ANOVA) followed by a Bonferroni post-test, whereby three or more experimental groups were compared. p-values of < 0.05 were considered statistically significant. All data are the means ± standard error of the mean (SEM).

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Section: Discussionmentioning

confidence: 99%

Quercetin Inhibits Cell Survival and Metastatic Ability via the EMT-Mediated Pathway in Oral Squamous Cell Carcinoma

et al. 2020

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“…[Hsu et al, 2013] In head and neck cancer-derived sphere cells, quercetin (a major polyphenol and flavonoid, commonly detected in many fruits and vegetables) minimizes migration ability partially by decreasing the production of Twist, N-cadherin, and vimentin. [Chang et al, 2013] Thymoquinone (major active ingredient of the plant Nigella sativa ) increases Twist1 promoter methylation resulting in Twist1 downregulation and inhibition of migration, invasion, and upregulation of E-cadherin. [Khan et al, 2015] Imipramine blue promotes degradation of the EMT inducer Twist1 by enhancing F-box and leucine-rich repeat protein 14 (FBXL14)-mediated polyubiquitination mediated destruction of Twist1.…”

Section: Targeting Orchestrators Of Emtmentioning

confidence: 99%

“…[Sadler et al, 2013] Quercetin, a natural polyphenol found in vegetables, reduced migration ability of head partially due to the decreased production of N-cadherin, vimentin and the EMT-TF, Twist1. [Chang et al, 2013]…”

Section: Targeting Effectors Of Emtmentioning

confidence: 99%

Therapeutic Targeting of Epithelial Plasticity Programs: Focus on the Epithelial-Mesenchymal Transition

Malek

Wang

Taparra

et al. 2017

Cells Tissues Organs

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Mounting data points to epithelial plasticity programs such as the epithelial-mesenchymal transition (EMT) as clinically relevant therapeutic targets for the treatment of malignant tumors. In addition to the widely realized role of EMT in increasing cancer cell invasiveness during cancer metastasis, the EMT has also been implicated in allowing cancer cells to avoid tumor suppressor pathways during early tumorigenesis. In addition, data linking EMT to innate and acquired treatment resistance further points towards the desire to develop pharmacological therapies to target epithelial plasticity in cancer. In this review we organized our discussion on pathways and agents that can be used to target the EMT in cancer into 3 groups: (1) extracellular inducers of EMT, (2) the transcription factors that orchestrate the EMT transcriptome, and (3) the downstream effectors of EMT. We highlight only briefly specific canonical pathways known to be involved in EMT, such as the signal transduction pathways TGFβ, EFGR, and Axl-Gas6. We emphasize in more detail pathways that we believe are emerging novel pathways and therapeutic targets such as epigenetic therapies, glycosylation pathways, and immunotherapy. The heterogeneity of tumors and the dynamic nature of epithelial plasticity in cancer cells make it likely that targeting only 1 EMT-related process will be unsuccessful or only transiently successful. We suggest that with greater understanding of epithelial plasticity regulation, such as with the EMT, a more systematic targeting of multiple EMT regulatory networks will be the best path forward to improve cancer outcomes.

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“…The increasing interest in the cancer stem cell (CSC) model is dramatically altering the current directions in cancer treatments and drug developments . We identified a subpopulation of oral cancer‐derived CSCs from OSCC cells by sphere formation assay . Oral cancer‐CSCs have been known to have the capacity to promote tumor progression and metastasis, and also contribute to chemoresistance .…”

Section: Introductionmentioning

confidence: 99%

“…3 We identified a subpopulation of oral cancer-derived CSCs from OSCC cells by sphere formation assay. 4 Oral cancer-CSCs have been known to have the capacity to promote tumor progression and metastasis, and also contribute to chemoresistance. [5][6][7][8][9][10][11] Side population technology by Hoechst dye exclusion property is among the successful methodologies for CSC isolation.…”

Section: Introductionmentioning

confidence: 99%

Quercetin in elimination of tumor initiating stem‐like and mesenchymal transformation property in head and neck cancer

Abstract: Quercetin suppressing HNC-TICs characteristics may therefore be valuable therapeutics clinically in combination with standard treatment modalities.

Cited by 46 publications

References 36 publications

Quercetin Inhibits Cell Survival and Metastatic Ability via the EMT-Mediated Pathway in Oral Squamous Cell Carcinoma

Quercetin Inhibits Cell Survival and Metastatic Ability via the EMT-Mediated Pathway in Oral Squamous Cell Carcinoma

Therapeutic Targeting of Epithelial Plasticity Programs: Focus on the Epithelial-Mesenchymal Transition

Targeting CD133 in the enhancement of chemosensitivity in oral squamous cell carcinoma–derived side population cancer stem cells

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