Critical genes in head and neck squamous cell carcinoma revealed by bioinformatic analysis of gene expression data

Wang, B; Wang, T; Cao, X-L; Y, Li

doi:10.4238/2015.december.21.10

Cited by 10 publications

(8 citation statements)

References 30 publications

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“…Furthermore, MCM7 was proved as a potential biomarker in cervical cancers . And MCM7 is a tumorigenesis‐related gene, overexpression of MCM7 is common in multiple cancers like esophageal soft tissue sarcomas, head and neck squamous cell carcinoma and ESCC . Similar with our result, overexpression of MCM7 was also observed in colorectal cancer .…”

Section: Discussionsupporting

confidence: 87%

MCM7 silencing promotes cutaneous melanoma cell autophagy and apoptosis by inactivating the AKT1/mTOR signaling pathway

Yang

et al. 2019

J of Cellular Biochemistry

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Cutaneous melanoma (CM) has become a major public health concern. Studies illustrate that minichromosome maintenance protein 7 (MCM7) participate in various diseases including skin disease. Our study aimed to study the effects of MCM7 silencing on CM cell autophagy and apoptosis by modulating the AKT threonine kinase 1 (AKT1)/mechanistic target of rapamycin kinase (mTOR) signaling pathway. Initially, microarray analysis was used to screen the CM‐related gene expression data as well as differentially expressed genes. Subsequently, MCM7 expression vector and lentivirus RNA used for MCM7 silencing (LV‐shRNA‐MCM7) were constructed, and these vectors, dimethyl sulfoxide (DMSO) and AKT activator SC79 were then introduced into CM cell line SK‐MEL‐2 to validate the role of MCM7 in cell autophagy, viability, apoptosis, cell cycle, migration, and invasion. To further investigate the regulatory mechanisms of MCM7 in CM progress, the expression of MCM7, AKT1, mTOR, cyclin D1, as well as autophagy and apoptosis relative factors, such as LC3B, SOD2, DJ‐1, p62, Bcl‐2, Bax, and caspase‐3 in melanoma cells was determined. MCM7 might mediate the AKT1/mTOR signaling pathway to influence the progress of melanoma. MCM7 silencing contributed to the increased expression of Bax, capase‐3, and autophagy‐related genes (LC3B, SOD2, and DJ‐1), but decreased the expression of Bcl‐2, which suggested that MCM7 silencing promoted autophagy and cell apoptosis. At the same time, MCM7 silencing also attenuated cell viability, invasion, and migration, and reduced the cyclin D1 expression and protein levels of p‐AKT1 and p‐mTOR. Taken together, MCM7 silencing inhibited CM via inactivation of the AKT1/mTOR signaling pathway.

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Section: Discussionsupporting

confidence: 87%

MCM7 silencing promotes cutaneous melanoma cell autophagy and apoptosis by inactivating the AKT1/mTOR signaling pathway

Yang

et al. 2019

J of Cellular Biochemistry

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“…In addition to the role of 14-3-3γ in channel trafficking 30 , previous studies demonstrated the involvement of 14-3-3γ in tumorigenesis. 14-3-3γ has been shown to be one of key genes involved in osteosarcoma and head and neck squamous cell carcinoma 36 37 . Overexpression of 14-3-3γ has been reported in non-small cell lung cancer, promyelocytic leukemia and glioblastoma 38 39 40 .…”

Section: Discussionmentioning

confidence: 99%

Suppression of 14-3-3γ-mediated surface expression of ANO1 inhibits cancer progression of glioblastoma cells

Lee

Bae

Lee

et al. 2016

Sci Rep

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Anoctamin-1 (ANO1) acts as a Ca2+-activated Cl− channel in various normal tissues, and its expression is increased in several different types of cancer. Therefore, understanding the regulation of ANO1 surface expression is important for determining its physiological and pathophysiological functions. However, the trafficking mechanism of ANO1 remains elusive. Here, we report that segment a (N-terminal 116 amino acids) of ANO1 is crucial for its surface expression, and we identified 14-3-3γ as a binding partner for anterograde trafficking using yeast two-hybrid screening. The surface expression of ANO1 was enhanced by 14-3-3γ, and the Thr9 residue of ANO1 was critical for its interaction with 14-3-3γ. Gene silencing of 14-3-3γ and/or ANO1 demonstrated that suppression of ANO1 surface expression inhibited migration and invasion of glioblastoma cells. These findings provide novel therapeutic implications for glioblastomas, which are associated with poor prognosis.

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“…Identification of therapy targets in tumors represents a challenge due to the presence of different cell types in the tumor microenvironment. Previous studies have attempted to look for targets in HPV+ and HPV− HNSCC without taking into consideration the complexity of the cell type composition of tumors [20]. These studies on bulk tumor may lead to both false positives and false negatives as the intercellular differences are confounded by differences in cellular composition.…”

Section: Introductionmentioning

confidence: 99%

Histoepigenetic analysis of HPV- and tobacco-associated head and neck cancer identifies both subtype-specific and common therapeutic targets despite divergent microenvironments

et al. 2019

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Although head and neck squamous cell carcinoma (HNSCC) has in the past been largely associated with tobacco use, human papillomavirus (HPV+) oropharynx cancer has in recent years emerged as the fastest growing type of HNSCC. Patients with HPV+ HNSCC have a better prognosis; however, the 5-year survival for both HPV+ and HPV− subtypes with recurrent or metastatic disease is poor. To gain insights into the tumor microenvironments of both HNSCC subtypes and identify potential therapeutic targets, we performed epigenomic deconvolution on 580 HNSCC samples from the TCGA dataset. Deconvolution revealed distinct molecular and histoepigenetic profiles of the two tumor subtypes, including their cellular composition, epigenomic profiles and gene expression for constituent cell types, and potential cancer cell-specific targets. Our analyses show that high abundance of both CD8 T-cells and B-cells explains better prognosis in HPV+ HNSCC. Deconvolution of gene expression profiles revealed higher expression of the immunotherapy target PD-1 in HPV+ immune cells compared to HPV− cells, suggesting that HPV+ tumors may preferentially benefit from PD-1 targeted therapy. Further analyses identified HPV+ and HPV− cancer cell surface proteins that can also serve as potential targets for therapy. Specifically, Wnt pathway receptor ROR2 is preferentially overexpressed in HPV+ subtypes, suggesting opportunities for development of targeted therapy based on HPV status. In summary, the comprehensive molecular and histoepigenetic analysis of tumor microenvironments by epigenomic deconvolution reveals potential novel biomarkers and targets for precision therapy of HNSCC.

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Critical genes in head and neck squamous cell carcinoma revealed by bioinformatic analysis of gene expression data

Cited by 10 publications

References 30 publications

MCM7 silencing promotes cutaneous melanoma cell autophagy and apoptosis by inactivating the AKT1/mTOR signaling pathway

MCM7 silencing promotes cutaneous melanoma cell autophagy and apoptosis by inactivating the AKT1/mTOR signaling pathway

Suppression of 14-3-3γ-mediated surface expression of ANO1 inhibits cancer progression of glioblastoma cells

Histoepigenetic analysis of HPV- and tobacco-associated head and neck cancer identifies both subtype-specific and common therapeutic targets despite divergent microenvironments

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