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SEC61G participates in endoplasmic reticulum stress by interacting with CREB3 to promote the malignant progression of lung adenocarcinoma

  • Authors:
    • Qian Zhang
    • Zhongliang Guo
  • View Affiliations / Copyright

    Affiliations: Shanghai East Clinical Medical College, Nanjing Medical University, Nanjing, Jiangsu 211166, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 233
    |
    Published online on: May 30, 2022
       https://doi.org/10.3892/ol.2022.13316
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Abstract

As the most common type of lung cancer, lung adenocarcinoma (LUAD) poses a great threat to human health worldwide and severely compromises the quality of life of the patients. The present study aimed to explore the potential pathogenesis of LUAD. Reverse transcription‑quantitative PCR and western blotting were applied to measure the expression levels of SEC61 translocon subunit γ (SEC61G) and cyclic AMP‑responsive element‑binding protein 3 (CREB3). Western blotting was also used to determine the expression of endoplasmic reticulum (ER) stress‑, apoptosis‑ and migration‑related proteins. Cell Counting Kit‑8, colony formation, TUNEL, wound healing and Transwell assays were used, respectively, to determine the viability, proliferation, apoptosis, migration and invasion of LUAD A549 cells. The association between SEC61G and CREB3 was verified by co‑immunoprecipitation assay. The results revealed that SEC61G was upregulated in A549 cells and its downregulation could activate ER stress. It was also found that silencing SEC61G inhibited the malignant development of LUAD through ER stress. In addition, SEC61G was verified to participate in ER stress in LUAD via CREB3 and silencing SEC61G exerted inhibitory effects on the malignant progression of LUAD by regulating CREB3. In summary, SEC61G participated in ER stress and its knockdown exerted inhibitory effects on A549 cells via regulating CREB3, which suggests that SEC61G may be a potential therapy for patients with LUAD.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang Q and Guo Z: SEC61G participates in endoplasmic reticulum stress by interacting with CREB3 to promote the malignant progression of lung adenocarcinoma. Oncol Lett 24: 233, 2022.
APA
Zhang, Q., & Guo, Z. (2022). SEC61G participates in endoplasmic reticulum stress by interacting with CREB3 to promote the malignant progression of lung adenocarcinoma. Oncology Letters, 24, 233. https://doi.org/10.3892/ol.2022.13316
MLA
Zhang, Q., Guo, Z."SEC61G participates in endoplasmic reticulum stress by interacting with CREB3 to promote the malignant progression of lung adenocarcinoma". Oncology Letters 24.1 (2022): 233.
Chicago
Zhang, Q., Guo, Z."SEC61G participates in endoplasmic reticulum stress by interacting with CREB3 to promote the malignant progression of lung adenocarcinoma". Oncology Letters 24, no. 1 (2022): 233. https://doi.org/10.3892/ol.2022.13316
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang Q and Guo Z: SEC61G participates in endoplasmic reticulum stress by interacting with CREB3 to promote the malignant progression of lung adenocarcinoma. Oncol Lett 24: 233, 2022.
APA
Zhang, Q., & Guo, Z. (2022). SEC61G participates in endoplasmic reticulum stress by interacting with CREB3 to promote the malignant progression of lung adenocarcinoma. Oncology Letters, 24, 233. https://doi.org/10.3892/ol.2022.13316
MLA
Zhang, Q., Guo, Z."SEC61G participates in endoplasmic reticulum stress by interacting with CREB3 to promote the malignant progression of lung adenocarcinoma". Oncology Letters 24.1 (2022): 233.
Chicago
Zhang, Q., Guo, Z."SEC61G participates in endoplasmic reticulum stress by interacting with CREB3 to promote the malignant progression of lung adenocarcinoma". Oncology Letters 24, no. 1 (2022): 233. https://doi.org/10.3892/ol.2022.13316
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