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CDCA4 interacts with IGF2BP1 to regulate lung adenocarcinoma proliferation via the PI3K/AKT pathway
BACKGROUND: Lung adenocarcinomas (LUAD) remain the leading cause of death in many countries. In this study, we investigated the role of division cycle‐associated 4 (CDCA4) in the carcinogenesis of LUADs. METHODS: Real‐time fluorescent quantitative polymerase chain reaction and western blot were perf...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons Australia, Ltd
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10008677/ https://www.ncbi.nlm.nih.gov/pubmed/36737405 http://dx.doi.org/10.1111/1759-7714.14800 |
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author | Feng, Sitong Cao, Haixia Sui, Ying Shen, Ziyang Wu, Jianzhong Ma, Rong Feng, Jifeng |
author_facet | Feng, Sitong Cao, Haixia Sui, Ying Shen, Ziyang Wu, Jianzhong Ma, Rong Feng, Jifeng |
author_sort | Feng, Sitong |
collection | PubMed |
description | BACKGROUND: Lung adenocarcinomas (LUAD) remain the leading cause of death in many countries. In this study, we investigated the role of division cycle‐associated 4 (CDCA4) in the carcinogenesis of LUADs. METHODS: Real‐time fluorescent quantitative polymerase chain reaction and western blot were performed to detect the messenger RNA and protein levels of CDCA4 in cells. Cell counting kit 8, real‐time cell analysis, clone formation, EdU assays, and cell‐cycle assays were used to preliminarily investigate the proliferation and cell‐cycle–related functions of CDCA4 in lung adenocarcinoma. Immunoprecipitation assays were used to identify possible targets of CDCA4. A xenograft model was used to examine how CDCA4 knockdown affects LUAD cells growth in vivo. RESULTS: We found that the expression of CDCA4 was upregulated in LUAD cell lines. When CDCA4 was knocked out, the ability of LUAD cells to proliferate was dramatically reduced, and the cell cycle was stalled in the S phase. Meanwhile, boosting the CDCA4 expression had the opposite effect. The critical protein levels of phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signaling pathway were subsequently examined. The findings demonstrated that elevated CDCA4 lowered the phosphate and tensin homolog expression and increased the p‐PI3K and p‐AKT levels. Moreover, we demonstrated that CDCA4 favorably regulated IGF2BP1, a downstream target. The downregulation of the IGF2BP1 expression could reverse the proliferation promotion effect induced by the CDCA4 overexpression. CONCLUSIONS: CDCA4 can operate as an oncogenic factor to control the growth of lung adenocarcinoma via the PI3K/AKT pathway. |
format | Online Article Text |
id | pubmed-10008677 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley & Sons Australia, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-100086772023-03-14 CDCA4 interacts with IGF2BP1 to regulate lung adenocarcinoma proliferation via the PI3K/AKT pathway Feng, Sitong Cao, Haixia Sui, Ying Shen, Ziyang Wu, Jianzhong Ma, Rong Feng, Jifeng Thorac Cancer Original Articles BACKGROUND: Lung adenocarcinomas (LUAD) remain the leading cause of death in many countries. In this study, we investigated the role of division cycle‐associated 4 (CDCA4) in the carcinogenesis of LUADs. METHODS: Real‐time fluorescent quantitative polymerase chain reaction and western blot were performed to detect the messenger RNA and protein levels of CDCA4 in cells. Cell counting kit 8, real‐time cell analysis, clone formation, EdU assays, and cell‐cycle assays were used to preliminarily investigate the proliferation and cell‐cycle–related functions of CDCA4 in lung adenocarcinoma. Immunoprecipitation assays were used to identify possible targets of CDCA4. A xenograft model was used to examine how CDCA4 knockdown affects LUAD cells growth in vivo. RESULTS: We found that the expression of CDCA4 was upregulated in LUAD cell lines. When CDCA4 was knocked out, the ability of LUAD cells to proliferate was dramatically reduced, and the cell cycle was stalled in the S phase. Meanwhile, boosting the CDCA4 expression had the opposite effect. The critical protein levels of phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signaling pathway were subsequently examined. The findings demonstrated that elevated CDCA4 lowered the phosphate and tensin homolog expression and increased the p‐PI3K and p‐AKT levels. Moreover, we demonstrated that CDCA4 favorably regulated IGF2BP1, a downstream target. The downregulation of the IGF2BP1 expression could reverse the proliferation promotion effect induced by the CDCA4 overexpression. CONCLUSIONS: CDCA4 can operate as an oncogenic factor to control the growth of lung adenocarcinoma via the PI3K/AKT pathway. John Wiley & Sons Australia, Ltd 2023-02-03 /pmc/articles/PMC10008677/ /pubmed/36737405 http://dx.doi.org/10.1111/1759-7714.14800 Text en © 2023 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Original Articles Feng, Sitong Cao, Haixia Sui, Ying Shen, Ziyang Wu, Jianzhong Ma, Rong Feng, Jifeng CDCA4 interacts with IGF2BP1 to regulate lung adenocarcinoma proliferation via the PI3K/AKT pathway |
title |
CDCA4 interacts with IGF2BP1 to regulate lung adenocarcinoma proliferation via the PI3K/AKT pathway |
title_full |
CDCA4 interacts with IGF2BP1 to regulate lung adenocarcinoma proliferation via the PI3K/AKT pathway |
title_fullStr |
CDCA4 interacts with IGF2BP1 to regulate lung adenocarcinoma proliferation via the PI3K/AKT pathway |
title_full_unstemmed |
CDCA4 interacts with IGF2BP1 to regulate lung adenocarcinoma proliferation via the PI3K/AKT pathway |
title_short |
CDCA4 interacts with IGF2BP1 to regulate lung adenocarcinoma proliferation via the PI3K/AKT pathway |
title_sort | cdca4 interacts with igf2bp1 to regulate lung adenocarcinoma proliferation via the pi3k/akt pathway |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10008677/ https://www.ncbi.nlm.nih.gov/pubmed/36737405 http://dx.doi.org/10.1111/1759-7714.14800 |
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