scholarly journals KRT84 is a potential tumor suppressor and good prognosis signature of oral squamous cell carcinoma

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Yi Liu ◽  
Ronghua Li ◽  
Gang Ren
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Suppressor ◽  
Oral Squamous Cell Carcinoma ◽  
Western Blot ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Expression Level ◽  
Protein Levels ◽  
Multiple Factors ◽  
Presentation Pathway

Abstract Aims: Oral squamous cell carcinoma (OSCC) is a common oral cancer; however, current therapeutic approaches still show limited efficacy. Our research aims to explore effective biomarkers related to OSCC. Main methods: Gene expression profiles of paired OSCC tumor and paracancerous samples from The Cancer Genome Atlas (TCGA) were analyzed. mRNA and protein levels of KRT84 in OSCC cell line HSC-3 were measured by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. KRT84 protein levels in OSCC tumor samples of different stages were determined by immunohistochemistry. Overall survival (OS) of OSCC samples was evaluated and association of multiple factors with OS was assessed. Key findings: Compared with paracancerous samples, 4642 DEGs were identified in OSCC tumor samples. Among them, KRT84 expression level in OSCC tumor tissues was obviously decreased, which was validated in HSC-3 cells. KRT84 expression level showed decreasing tendency with the increase of tumor grade and stage. Patients with low KRT84 expression level had inferior OS independently of multiple factors. Besides, antigen processing and presentation pathway were significantly activated in OSCC samples with high KRT84 expression. Elevated KRT84 mRNA as well as protein levels were confirmed by RT-qPCR and Western blot in OSCC and normal cell lines, and immunohistochemistry in OSCC tumor and paracancerous tissues. Significance: Our study suggests KRT84 as a tumor suppressor and good prognostic indicator for OSCC, which might be significant for OSCC diagnosis and treatment.

scholarly journals Regulation of Oral Squamous Cell Carcinoma Proliferation Through Crosstalk Between SMAD7 and CYLD

2016 ◽  
Vol 38 (3) ◽  
pp. 1209-1217 ◽  
Author(s):  
Wei-Li Ge ◽  
Jun-Feng Xu ◽  
Jun Hu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Western Blot ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Invasion ◽  
Protein Levels ◽  
Protein Ubiquitination ◽  
Cell Conversion ◽  
Cell Invasiveness

Background/Aims: SMAD7 is a key inhibitor of transforming growth factor β (TGFβ) receptor signaling, which regulates the alteration of cancer cell invasiveness through epithelial-mesenchymal cell conversion. Dysfunction of protein ubiquitination plays a critical role in carcinogenesis, whereas the involvement a deubiquitinating enzyme, cylindromatosis gene (CYLD), in the tumor invasion of oral squamous cell carcinoma (OSCC) is unknown. Methods: Here, we studied the role of CYLD in regulation of OSCC cell invasion, using clinic specimens and cell lines. We modified SMAD7 levels in OSCC cells, and examined its effects on CYLD mRNA and protein levels by RT-qPCR and by Western blot, respectively. We also modified CYLD levels in OSCC cells, and examined its effects on SMAD7 mRNA and protein levels by RT-qPCR and by Western blot, respectively. Then, we examined the cell invasiveness in CYLD and/or SMAD7-modified OSCC cells in a transwell cell invasion assay. Results: We found that the levels of CYLD and SMAD7 were significantly decreased in OSCC specimens, compared to the paired normal tissue. Metastatic OSCC appeared to contained lower levels of CYLD and SMAD7. Moreover, CYLD and SMAD7 levels strongly correlated in OSCC specimens. Low CYLD levels were associated with poor patients' survival. Moreover, SMAD did not regulate CYLD, but CYLD regulated the levels of SMAD7 in OSCC cells. Furthermore, CYLD overexpression inhibited SMAD7-mediated cell invasion, while CYLD depletion increased SMAD7-mediated cell invasion in OSCC cells. Conclusion: Suppression of CYLD in OSCC cells may promote SMAD7-mediated cancer invasion. Thus, CYLD appears to be an intriguing therapeutic target to prevent OSCC metastases.

Expression, Proliferation and Apoptosis of miR‑92b in Oral Squamous Cell Carcinoma

2020 ◽  
Author(s):  
Yongzhi XU ◽  
Fang FANG ◽  
Jinghui WANG ◽  
Chunli ZHAO ◽  
Jingyang ZHAO ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Expression Level ◽  
Normal Tissues ◽  
Tumor Tissues ◽  
Proliferation And Apoptosis ◽  
Proliferation Ability ◽  
Rat Tissue

Background: Expression of miR‑92b in oral squamous cell carcinoma (OSCC) rat tissue and its effect on the OSCC CAL‑27 cells were investigated. Methods: The study was performed in Qingdao Stomatological Hospital, Qingdao, China on December 2018. Thirty Wistar rats were used to construct models of oral squamous cell carcinoma. CAL‑27 cells trascfected by Lipofectamine 2000 were divided into miR‑92b inhibitor, miR‑NC and blank groups. RT‑qPCR was used for the detection of the expression level of miR‑92b, and MTT and flow cytometry were carried out for the detection of the effect of miR‑92b on the proliferation and apoptosis of CAL‑27 cells, respectively. Results: The expression level of miR‑92b was significantly higher in tumor tissues than that in normal tissues (P<0.001). The miR‑92b inhibitor group had significantly lower proliferation ability but higher apoptosis rate of CAL‑27 cells than the miR‑NC and blank groups. After miR‑92b was downregulated by trans-fecting cells, the expression level of miR‑92b was significantly lower in the miR‑92b inhibitor group than that in the miR‑NC and blank groups. Conclusion: miR‑92b inhibitor can inhibit the proliferation of CAL‑27 cells and promote apoptosis, which provides certain references for clinical treatment. It is expected to be a potential target for treating OSCC.

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