Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 Cells
Sestrin2 is a highly conserved stress-inducible protein, acting as a crucial part in regulating homeostasis in response to various stress conditions in the cell. However, the role of Sestrin2 in regulating cell apoptosis related to endoplasmic reticulum (ER) has not been fully investigated. Our stud...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Hindawi Limited
2022-01-01
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| Series: | International Journal of Endocrinology |
| Online Access: | http://dx.doi.org/10.1155/2022/2009753 |
| _version_ | 1798005470853595136 |
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| author | Huiling Hu Zhijun Luo Xiuli Liu Lisi Huang Xiaoxia Lu Rui Ding Chaohui Duan Yuqing He |
| author_facet | Huiling Hu Zhijun Luo Xiuli Liu Lisi Huang Xiaoxia Lu Rui Ding Chaohui Duan Yuqing He |
| author_sort | Huiling Hu |
| collection | DOAJ |
| description | Sestrin2 is a highly conserved stress-inducible protein, acting as a crucial part in regulating homeostasis in response to various stress conditions in the cell. However, the role of Sestrin2 in regulating cell apoptosis related to endoplasmic reticulum (ER) has not been fully investigated. Our study presented here aims to reveal the effect of Sestrin2 in tunicamycin (TM)-induced cell apoptosis related to ER stress and its underlying molecular mechanisms. The results demonstrated that Sestrin2 expression was significantly upregulated correlated with ER stress responses in TM treated HepG2 cells. Sestrin2 overexpression obviously alleviated ER stress with the determination of ER stress-related proteins expression. In addition, Sestrin2 overexpression inhibited cell apoptosis with the examination of apoptosis-related proteins and TUNEL assay. However, Sestrin2 knockdown further promoted the ER stress-mediated cell apoptosis. The further mechanistic study revealed that Sestrin2 overexpression inhibited TM-induced mTOR pathway activation. Taken together, our current study indicated that Sestrin2 overexpression ameliorates ER stress-induced apoptosis via inhibiting mTOR pathway in HepG2 cells. |
| first_indexed | 2024-04-11T12:39:38Z |
| format | Article |
| id | doaj.art-452af2d2af14430ab5fb2fe46c604b70 |
| institution | Directory Open Access Journal |
| issn | 1687-8345 |
| language | English |
| last_indexed | 2024-04-11T12:39:38Z |
| publishDate | 2022-01-01 |
| publisher | Hindawi Limited |
| record_format | Article |
| series | International Journal of Endocrinology |
| spelling | doaj.art-452af2d2af14430ab5fb2fe46c604b702022-12-22T04:23:32ZengHindawi LimitedInternational Journal of Endocrinology1687-83452022-01-01202210.1155/2022/2009753Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 CellsHuiling Hu0Zhijun Luo1Xiuli Liu2Lisi Huang3Xiaoxia Lu4Rui Ding5Chaohui Duan6Yuqing He7Department of Clinical LaboratoryDepartment of EmergencyDepartment of Clinical LaboratoryDepartment of Clinical LaboratoryDepartment of Clinical LaboratoryDepartment of Clinical LaboratoryDepartment of Clinical LaboratoryTranslational Medicine Research CenterSestrin2 is a highly conserved stress-inducible protein, acting as a crucial part in regulating homeostasis in response to various stress conditions in the cell. However, the role of Sestrin2 in regulating cell apoptosis related to endoplasmic reticulum (ER) has not been fully investigated. Our study presented here aims to reveal the effect of Sestrin2 in tunicamycin (TM)-induced cell apoptosis related to ER stress and its underlying molecular mechanisms. The results demonstrated that Sestrin2 expression was significantly upregulated correlated with ER stress responses in TM treated HepG2 cells. Sestrin2 overexpression obviously alleviated ER stress with the determination of ER stress-related proteins expression. In addition, Sestrin2 overexpression inhibited cell apoptosis with the examination of apoptosis-related proteins and TUNEL assay. However, Sestrin2 knockdown further promoted the ER stress-mediated cell apoptosis. The further mechanistic study revealed that Sestrin2 overexpression inhibited TM-induced mTOR pathway activation. Taken together, our current study indicated that Sestrin2 overexpression ameliorates ER stress-induced apoptosis via inhibiting mTOR pathway in HepG2 cells.http://dx.doi.org/10.1155/2022/2009753 |
| spellingShingle | Huiling Hu Zhijun Luo Xiuli Liu Lisi Huang Xiaoxia Lu Rui Ding Chaohui Duan Yuqing He Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 Cells International Journal of Endocrinology |
| title | Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 Cells |
| title_full | Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 Cells |
| title_fullStr | Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 Cells |
| title_full_unstemmed | Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 Cells |
| title_short | Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 Cells |
| title_sort | sestrin2 overexpression ameliorates endoplasmic reticulum stress induced apoptosis via inhibiting mtor pathway in hepg2 cells |
| url | http://dx.doi.org/10.1155/2022/2009753 |
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