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