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GPX7通过增强细胞增殖和抑制细胞凋亡促进人甲状腺乳头状癌的生长。

GPX7 promotes the growth of human papillary thyroid carcinoma via enhancement of cell proliferation and inhibition of cell apoptosis.

作者信息

Liu Li-Dan, Zhang Yi-Ni, Wang Li-Fen

机构信息

Press of Journal, Dalian Medical University, Dalian 116044, China.

Department of Pathology, The Second Affiliated Hospital of Dalian Medical University, Dalian 116023, China.

出版信息

Transl Cancer Res. 2019 Nov;8(7):2570-2580. doi: 10.21037/tcr.2019.10.14.

DOI:10.21037/tcr.2019.10.14
PMID:35117014
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8798640/
Abstract

BACKGROUND

Abnormal expression of glutathione peroxidase 7 (GPX7) has been linked to the occurrence and development of a variety of tumors. However, the role of GPX7 in the progression of papillary thyroid carcinoma (PTC) has not been elucidated. This study investigated the role of GPX7 in the progression of PTC.

METHODS

The methods employed included immunohistochemistry, Western blotting, quantitative reverse transcription-polymerase chain reaction (qRT-PCR), MTT assay, Celigo cell counting, flow cytometric analysis, caspase activity assay, cell clone formation assay, and GPX7 knockdown.

RESULTS

The data showed that GPX7 protein was localized in the cytoplasm of thyroid cells. The level of GPX7 expression was higher in PTC tissues than in the nodular goiter. The positive rate for GPX7 was also higher in the PTC group than in the nodular goiter group (100.0% 35.7%). The maximum tumor diameter in the group highly expressing GXP7 was significantly greater than that in the group with low expression of GXP7 (1.56±0.56 0.56±0.13 cm, P<0.001). The GPX7 mRNA level was higher in K1 cells. Knockdown of GPX7 decreased the number of cells, cell clone formation ability, and cell proliferation rate and increased the activity of caspase 3/7 and cell apoptosis in PTC K1 cells.

CONCLUSIONS

These results indicate that high expression of GPX7 increases the proliferation and reduces the apoptosis of PTC cells, and thus, promotes the growth and progression of human PTC.

摘要

背景

谷胱甘肽过氧化物酶7(GPX7)的异常表达与多种肿瘤的发生发展有关。然而,GPX7在甲状腺乳头状癌(PTC)进展中的作用尚未阐明。本研究探讨了GPX7在PTC进展中的作用。

方法

采用的方法包括免疫组织化学、蛋白质免疫印迹法、定量逆转录聚合酶链反应(qRT-PCR)、MTT法、Celigo细胞计数、流式细胞术分析、半胱天冬酶活性测定、细胞克隆形成试验和GPX7基因敲低。

结果

数据显示,GPX7蛋白定位于甲状腺细胞的细胞质中。PTC组织中GPX7的表达水平高于结节性甲状腺肿。PTC组中GPX7的阳性率也高于结节性甲状腺肿组(100.0%对35.7%)。高表达GXP7组的最大肿瘤直径显著大于低表达GXP7组(1.56±0.56对0.56±0.13 cm,P<0.001)。K1细胞中GPX7 mRNA水平较高。敲低GPX7可减少PTC K1细胞的数量、细胞克隆形成能力和细胞增殖率,并增加半胱天冬酶3/7的活性和细胞凋亡。

结论

这些结果表明,GPX7的高表达增加了PTC细胞的增殖并减少了其凋亡,从而促进了人类PTC的生长和进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95b3/8798640/957ac65eba3d/tcr-08-07-2570-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95b3/8798640/c0b1fc3fed4d/tcr-08-07-2570-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95b3/8798640/efecb72c5340/tcr-08-07-2570-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95b3/8798640/c827102473f9/tcr-08-07-2570-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95b3/8798640/957ac65eba3d/tcr-08-07-2570-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95b3/8798640/c0b1fc3fed4d/tcr-08-07-2570-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95b3/8798640/efecb72c5340/tcr-08-07-2570-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95b3/8798640/c827102473f9/tcr-08-07-2570-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95b3/8798640/957ac65eba3d/tcr-08-07-2570-f4.jpg

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