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STAMBPL1 promotes the progression of lung adenocarcinoma by inhibiting DHRS2 expression

BACKGROUND: Lung cancer is responsible for the majority of cancer deaths in the world. We found a significant increase of STAMBPL1 expression in lung adenocarcinoma (LUAD) tissues and cells. However, its mechanism has not been clarified. METHODS: LUAD tissues and adjacent normal tissues were collect...

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Autores principales: Yang, Xiang, Ling, Liqun, Li, Changhong, Hu, Tianqi, Zhou, Chenkang, Chen, Jian, Wang, Yumin, Hu, Lijuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Neoplasia Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10331841/
https://www.ncbi.nlm.nih.gov/pubmed/37393834
http://dx.doi.org/10.1016/j.tranon.2023.101728
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author Yang, Xiang
Ling, Liqun
Li, Changhong
Hu, Tianqi
Zhou, Chenkang
Chen, Jian
Wang, Yumin
Hu, Lijuan
author_facet Yang, Xiang
Ling, Liqun
Li, Changhong
Hu, Tianqi
Zhou, Chenkang
Chen, Jian
Wang, Yumin
Hu, Lijuan
author_sort Yang, Xiang
collection PubMed
description BACKGROUND: Lung cancer is responsible for the majority of cancer deaths in the world. We found a significant increase of STAMBPL1 expression in lung adenocarcinoma (LUAD) tissues and cells. However, its mechanism has not been clarified. METHODS: LUAD tissues and adjacent normal tissues were collected from 62 patients treated in the First Affiliated Hospital of Wenzhou Medical University from August 2018 to August 2021. In vivo, the clinical data and STAMBPL1 expression of 62 patients with LUAD were analyzed by qPCR. In vitro, cell experiments were carried out after STAMBPL1 knockdown in A549 and H1299 cells to determine cell growth, migration rate, evasiveness, colony-forming ability, and apoptosis. Gene sequencing was used to explore the expression of various genes in A549 and H1299 cells to verify that DHRS2 was up-regulated after STAMBPL1 knockdown; cell experiments further detected the role of the DHRS2 gene after DHRS2 overexpression in A549 and H1299 cells. A rescue experiment was conducted to certify that STAMBPL1 promotes NSCLC progression by regulating DHRS2 expression. RESULTS: After STAMBPL1 knockdown by siRNA. Migration, invasion, colony formation, and proliferation of siRNA groups were suppressed than those of NC groups in A549 and H1299 cells, while the cell apoptosis rate of siRNA groups increased significantly. By using gene-sequence analysis, we found that the expression level of the DHRS2 gene was up-regulated in STAMBPL1 siRNA groups, compared with STAMBPL1 NC (negative control) groups in A549 and H1299, which was verified by qPCR and WB. Further experiments showed that the DHRS2 OE group was suppressed in cell proliferation, migration, and invasion in the A549 and H1299 cell lines compared to the DHRS2 NC group, while DHRS2 OE group was significantly enhanced in the cell apoptosis in the A549 and H1299 cell lines. According to the rescue experiment, cell proliferation, migration, and invasion of the STAMBPL1 SI+DHRS2 SI group were enhanced compared with the STAMBPL1 SI+DHRS2 NC group in A549 and H1299 cells, while the STAMBPL1 SI+DHRS2 OE group were further decreased. CONCLUSIONS: The expression of STAMBPL1 mRNA is significantly up-regulated in LUAD, promoting the progression of LUAD by down-regulating the expression of DHRS2 and acting as a potential biomarker of LUAD.
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spelling pubmed-103318412023-07-11 STAMBPL1 promotes the progression of lung adenocarcinoma by inhibiting DHRS2 expression Yang, Xiang Ling, Liqun Li, Changhong Hu, Tianqi Zhou, Chenkang Chen, Jian Wang, Yumin Hu, Lijuan Transl Oncol Original Research BACKGROUND: Lung cancer is responsible for the majority of cancer deaths in the world. We found a significant increase of STAMBPL1 expression in lung adenocarcinoma (LUAD) tissues and cells. However, its mechanism has not been clarified. METHODS: LUAD tissues and adjacent normal tissues were collected from 62 patients treated in the First Affiliated Hospital of Wenzhou Medical University from August 2018 to August 2021. In vivo, the clinical data and STAMBPL1 expression of 62 patients with LUAD were analyzed by qPCR. In vitro, cell experiments were carried out after STAMBPL1 knockdown in A549 and H1299 cells to determine cell growth, migration rate, evasiveness, colony-forming ability, and apoptosis. Gene sequencing was used to explore the expression of various genes in A549 and H1299 cells to verify that DHRS2 was up-regulated after STAMBPL1 knockdown; cell experiments further detected the role of the DHRS2 gene after DHRS2 overexpression in A549 and H1299 cells. A rescue experiment was conducted to certify that STAMBPL1 promotes NSCLC progression by regulating DHRS2 expression. RESULTS: After STAMBPL1 knockdown by siRNA. Migration, invasion, colony formation, and proliferation of siRNA groups were suppressed than those of NC groups in A549 and H1299 cells, while the cell apoptosis rate of siRNA groups increased significantly. By using gene-sequence analysis, we found that the expression level of the DHRS2 gene was up-regulated in STAMBPL1 siRNA groups, compared with STAMBPL1 NC (negative control) groups in A549 and H1299, which was verified by qPCR and WB. Further experiments showed that the DHRS2 OE group was suppressed in cell proliferation, migration, and invasion in the A549 and H1299 cell lines compared to the DHRS2 NC group, while DHRS2 OE group was significantly enhanced in the cell apoptosis in the A549 and H1299 cell lines. According to the rescue experiment, cell proliferation, migration, and invasion of the STAMBPL1 SI+DHRS2 SI group were enhanced compared with the STAMBPL1 SI+DHRS2 NC group in A549 and H1299 cells, while the STAMBPL1 SI+DHRS2 OE group were further decreased. CONCLUSIONS: The expression of STAMBPL1 mRNA is significantly up-regulated in LUAD, promoting the progression of LUAD by down-regulating the expression of DHRS2 and acting as a potential biomarker of LUAD. Neoplasia Press 2023-06-30 /pmc/articles/PMC10331841/ /pubmed/37393834 http://dx.doi.org/10.1016/j.tranon.2023.101728 Text en © 2023 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Research
Yang, Xiang
Ling, Liqun
Li, Changhong
Hu, Tianqi
Zhou, Chenkang
Chen, Jian
Wang, Yumin
Hu, Lijuan
STAMBPL1 promotes the progression of lung adenocarcinoma by inhibiting DHRS2 expression
title STAMBPL1 promotes the progression of lung adenocarcinoma by inhibiting DHRS2 expression
title_full STAMBPL1 promotes the progression of lung adenocarcinoma by inhibiting DHRS2 expression
title_fullStr STAMBPL1 promotes the progression of lung adenocarcinoma by inhibiting DHRS2 expression
title_full_unstemmed STAMBPL1 promotes the progression of lung adenocarcinoma by inhibiting DHRS2 expression
title_short STAMBPL1 promotes the progression of lung adenocarcinoma by inhibiting DHRS2 expression
title_sort stambpl1 promotes the progression of lung adenocarcinoma by inhibiting dhrs2 expression
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10331841/
https://www.ncbi.nlm.nih.gov/pubmed/37393834
http://dx.doi.org/10.1016/j.tranon.2023.101728
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