Novel Targeted Agents in Head and Neck Squamous Cell Carcinoma

Velho, Pedro Henrique Isaacsson; Castro, Gilberto de; Chung, Christine H.

doi:10.1016/j.hoc.2015.07.006

Cited by 2 publications

(1 citation statement)

References 97 publications

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“…We also assessed the level of DNA damage response proteins, phosphorylated p53. Phosphorylation of p53 at serine 15 can be induced by DNA damage sensing proteins, ataxia telangiectasia mutated kinase and ataxia telangiectasia and Rad3-related kinase [21]. SIRT6 siRNA treatment did not stimulate the phosphorylation of p53 (Supplementary Figure 2).…”

Section: Sirt6 Knockdown Induces Cell Growth Arrest In Endothelial Cellsmentioning

confidence: 98%

Sirtuin 6 deficiency induces endothelial cell senescence via downregulation of forkhead box M1 expression

Lee

Woo

Moon

et al. 2020

Aging

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Cellular senescence of endothelial cells causes vascular dysfunction, promotes atherosclerosis, and contributesto the development of age-related vascular diseases. Sirtuin 6 (SIRT6), a conserved NAD+-dependent protein deacetylase, has beneficial effects against aging, despite the fact that its functional mechanisms are largely uncharacterized. Here, we show that SIRT6 protects endothelial cells from senescence. SIRT6 expression is progressively decreased during both oxidative stress-induced senescence and replicative senescence. SIRT6 deficiency leads to endothelial dysfunction, growth arrest, and premature senescence. Using genetically engineered endothelial cell-specific SIRT6 knockout mice, we also show that down-regulation of SIRT6 expression in endothelial cells exacerbates vascular aging. Expression microarray analysis demonstrated that SIRT6 modulates the expression of multiple genes involved in cell cycle regulation. Specifically, SIRT6 appears to regulate the expression of forkhead box M1 (FOXM1), a critical transcription factor for cell cycle progression and senescence. Overexpression of FOXM1 ameliorates SIRT6 deficiency-induced endothelial cell senescence. In this work, we demonstrate the role of SIRT6 as an anti-aging factor in the vasculature. These data may provide the basis for future novel therapeutic approaches against age-related vascular disorders.

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Section: Sirt6 Knockdown Induces Cell Growth Arrest In Endothelial Cellsmentioning

confidence: 98%

Sirtuin 6 deficiency induces endothelial cell senescence via downregulation of forkhead box M1 expression

Lee

Woo

Moon

et al. 2020

Aging

View full text Add to dashboard Cite

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Decursin inhibits tumor progression in head and neck squamous cell carcinoma by downregulating CXCR7 expressionin vitro

et al. 2021

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CXC chemokine receptor 7 (CXCR7) is frequently overexpressed in cancer and plays a significant role in tumor growth and metastasis. Consequently, inhibition of CXCR7 is important for treatment strategies. However, little is known concerning the biological role of CXCR7 and its underlying mechanisms in head and neck squamous cell carcinoma (HNSCC). The present study investigated the role of CXCR7 in HNSCC, as well as the effects of decursin, a pyranocoumarin compound isolated from Angelica gigas Nakai, on CXCR7 and its downstream signaling. Expression levels of CXCR7 in HNSCC cells were examined using flow cytometry, reverse transcriptase PCR, western blot analysis, and immunofluorescence. The effects of CXCR7 on cell proliferation, migration, and invasion were studied using CCK-8, gap closure, and transwell assays. The results revealed that decursin significantly reduced CXCR7 expression and inhibited cell proliferation, migration, and invasion of human HNSCC cell lines. In addition, decursin induced G0/G1 cell cycle arrest in CXCR7-overexpressing cells and decreased the levels of cyclin A, cyclin E, and CDK2. Furthermore, CXCR7 promoted cancer progression via the STAT3/c-Myc pathway in HNSCC; suppression of CXCR7 with decursin prevented this effect. These results suggest that CXCR7 promotes cancer progression through the STAT3/c-Myc pathway and that the natural compound decursin targets CXCR7 and may be valuable in the treatment of HNSCC.

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Novel Targeted Agents in Head and Neck Squamous Cell Carcinoma

Cited by 2 publications

References 97 publications

Sirtuin 6 deficiency induces endothelial cell senescence via downregulation of forkhead box M1 expression

Sirtuin 6 deficiency induces endothelial cell senescence via downregulation of forkhead box M1 expression

Decursin inhibits tumor progression in head and neck squamous cell carcinoma by downregulating CXCR7 expressionin vitro

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