scholarly journals Association of SP1 rs1353058818 and STAT3 rs1053004 gene polymorphisms with human tongue squamous cell carcinoma

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Heqing Lai ◽  
Guochao Xu ◽  
Haifeng Meng ◽  
Haiying Zhu

Abstract Objective: To study the association between SP1 rs1353058818 and STAT3 rs1053004 gene polymorphisms and risk of human tongue squamous cell carcinoma (TSCC). Methods: Sanger sequencing was used to determine the genotypes of SP1 rs1353058818 and STAT3 rs1053004 loci in 240 TSCC patients and 240 controls. Levels of hsa-miR-149-5p and hsa-miR-21-5p and expression levels of SP1 and STAT3 proteins in tumor tissues and adjacent normal tissues of TSCC patients were ascertained. Results: Carrying the SP1 rs1353058818 locus deletion allele was a high risk factor for TSCC (OR = 2.997, 95% CI: 1.389–6.466, P = 0.003). The STAT3 rs1053004 locus A allele was a protective factor for TSCC (OR = 0.604, 95% CI: 0.460-0.793, P < 0.001). There was a negative correlation between SP1 mRNA and hsa-miR-149-5p in tumor and adjacent normal tissues (r = −0.81, −0.77). The expression of SP1 protein in tumor tissues of the SP1 rs1353058818 locus DD genotype was significantly higher than in tissues of the ID type, and in tissues of type II it was the lowest. STAT3 mRNA was positively correlated with hsa-miR-21-5p in tumor and adjacent normal tissues (r = 0.75, 0.78). The expression level of STAT3 protein in tumor tissues of patients with STAT3 rs1053004 locus GG genotype was significantly higher than in patients with type GA, and it was the lowest in patients with type AA. Conclusion: Polymorphisms in the SP1 rs1353058818 and STAT3 rs1053004 loci are associated with the risk of human TSCC.

2005 ◽  
Vol 10 (4) ◽  
pp. 121-129
Author(s):  
Makiko Kyan ◽  
Yuichiro Onodera ◽  
Tadashi Iizuka ◽  
Ken-ichi Notani ◽  
Takao Kohgo ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
pp. 102-111
Author(s):  
Liang Shi ◽  
Xiaobin Song ◽  
Ketao Wang ◽  
Shaohua Liu ◽  
Yong Wang

We investigated whether regulation of VGLL4 by miR-222 affects proliferation, migration, invasion, and apoptosis in human tongue squamous cell carcinoma (TSCC) cells. Nanometer Magnetic beads were prepared to extract RNA in CAL27/human oral keratinocytes (HOK). Correlation between expression of miR-222 and VGLL4 in CAL27/human oral keratinocytes (HOK) was analyzed using RT-PCR and western blot. The cellular effects of miR-222/VGLL4 interactions were detected by cck8, transwell, and cell scratch assays, and flow cytometry after miR-222 was silenced or overexpressed in CAL27 cells. We assessed tumor growth in vivo, in a subcutaneous tumor model in mice, and assessed VGLL4 protein expression in tumors by immunohistochemistry. We found that miR-222 expression is higher in CAL27 cells than that in HOK cells. VGLL4 was highly expressed in HOK cells relative to CAL27 cells. When miR-222 was overexpressed, VGLL4 mRNA expression was reduced in CAL27 cells, and protein expression was reduced in the in vivo tumor model. Thus, miR-222 may down-regulate VGLL4 to promote proliferation, migration, and invasion of TSCC cells.


Author(s):  
Yongzhi XU ◽  
Fang FANG ◽  
Jinghui WANG ◽  
Chunli ZHAO ◽  
Jingyang ZHAO ◽  
...  

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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