GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling
The expression of G2 and S phase-expressed-1 (GTSE1) was upregulated in human cancer. However, its expression and roles in lung cancer have not been identified yet. In our study, we reported that GTSE1 expression was statistically higher in lung tissues than in the adjacent noncancerous tissues whic...
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| Format: | Article |
| Language: | English |
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Wiley
2021-01-01
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| Series: | Analytical Cellular Pathology |
| Online Access: | http://dx.doi.org/10.1155/2021/5589532 |
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| author | Fan Zhang Jingfei Meng Hong Jiang Xing Feng Dongshan Wei Wen Meng |
| author_facet | Fan Zhang Jingfei Meng Hong Jiang Xing Feng Dongshan Wei Wen Meng |
| author_sort | Fan Zhang |
| collection | DOAJ |
| description | The expression of G2 and S phase-expressed-1 (GTSE1) was upregulated in human cancer. However, its expression and roles in lung cancer have not been identified yet. In our study, we reported that GTSE1 expression was statistically higher in lung tissues than in the adjacent noncancerous tissues which might be a consequence of hypomethylation of the GTSE1 promoter. The upregulated expression of GTSE1 mRNA predicted the poorer survival of the lung patients. Ectopic expression of GTSE1 in lung cancer cells significantly increased while knockdown of GTSE1 decreased cell proliferation, cell migration, and cell invasion in H460 and A549 cells. Furthermore, knockdown of GTSE1 regulated the cell cycle and promoted cell apoptosis in H460 and A549 cells. Finally, we presented that GTSE1 was able to activate AKT/mTOR signaling in H460 and A549 cells. In conclusion, these results indicated that the overexpressed GTSE1 was involved in the progress of lung cancer by promoting proliferation migration and invasion and inhibiting apoptosis of lung cancer cells via activating AKT/mTOR signaling. |
| format | Article |
| id | doaj-art-ba7ccfab83144f878dab74984c60dadd |
| institution | Kabale University |
| issn | 2210-7177 2210-7185 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Analytical Cellular Pathology |
| spelling | doaj-art-ba7ccfab83144f878dab74984c60dadd2025-02-03T01:04:20ZengWileyAnalytical Cellular Pathology2210-71772210-71852021-01-01202110.1155/2021/55895325589532GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR SignalingFan Zhang0Jingfei Meng1Hong Jiang2Xing Feng3Dongshan Wei4Wen Meng5Department of Cardiothoracic Surgery, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, 310006, ChinaThe Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaDepartment of Cardiothoracic Surgery, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, 310006, ChinaDepartment of Cardiothoracic Surgery, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, 310006, ChinaDepartment of Cardiothoracic Surgery, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, 310006, ChinaDepartment of Cardiothoracic Surgery, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, 310006, ChinaThe expression of G2 and S phase-expressed-1 (GTSE1) was upregulated in human cancer. However, its expression and roles in lung cancer have not been identified yet. In our study, we reported that GTSE1 expression was statistically higher in lung tissues than in the adjacent noncancerous tissues which might be a consequence of hypomethylation of the GTSE1 promoter. The upregulated expression of GTSE1 mRNA predicted the poorer survival of the lung patients. Ectopic expression of GTSE1 in lung cancer cells significantly increased while knockdown of GTSE1 decreased cell proliferation, cell migration, and cell invasion in H460 and A549 cells. Furthermore, knockdown of GTSE1 regulated the cell cycle and promoted cell apoptosis in H460 and A549 cells. Finally, we presented that GTSE1 was able to activate AKT/mTOR signaling in H460 and A549 cells. In conclusion, these results indicated that the overexpressed GTSE1 was involved in the progress of lung cancer by promoting proliferation migration and invasion and inhibiting apoptosis of lung cancer cells via activating AKT/mTOR signaling.http://dx.doi.org/10.1155/2021/5589532 |
| spellingShingle | Fan Zhang Jingfei Meng Hong Jiang Xing Feng Dongshan Wei Wen Meng GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling Analytical Cellular Pathology |
| title | GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling |
| title_full | GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling |
| title_fullStr | GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling |
| title_full_unstemmed | GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling |
| title_short | GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling |
| title_sort | gtse1 facilitates the malignant phenotype of lung cancer cells via activating akt mtor signaling |
| url | http://dx.doi.org/10.1155/2021/5589532 |
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