Carboxylesterase 4A Inhibits the Malignant Biological Behavior of Nasopharyngeal Carcinoma via the PI3K/AKT Pathway
Background Carboxylesterase 4A (CES4A) belongs to the member of the carboxylesterase family, yet there has been limited research into its malignant biological behavior in malignant tumors. Here, we aim to investigate the expression, cellular biological functions, and the potential underlying mechani...
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Format: | Article |
Language: | English |
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SAGE Publishing
2025-02-01
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Series: | Technology in Cancer Research & Treatment |
Online Access: | https://doi.org/10.1177/15330338251319144 |
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author | Qiaoli Chen MS Quanxiang Hao MBBS Yanping Yang MBBS Limei Li PhD Danping Li MS Ran Zhao MS Wanqi Wei MBBS Lixian Deng MBBS Jiaming Su MBBS Ziyuan Liang MBBS Shiyue Tang MS Yaomin Lu MBBS Yushan Liang PhD Zhe Zhang PhD Xiaoying Zhou PhD Xue Xiao PhD Ping Li PhD Yi Huang PhD Weilin Zhao PhD |
author_facet | Qiaoli Chen MS Quanxiang Hao MBBS Yanping Yang MBBS Limei Li PhD Danping Li MS Ran Zhao MS Wanqi Wei MBBS Lixian Deng MBBS Jiaming Su MBBS Ziyuan Liang MBBS Shiyue Tang MS Yaomin Lu MBBS Yushan Liang PhD Zhe Zhang PhD Xiaoying Zhou PhD Xue Xiao PhD Ping Li PhD Yi Huang PhD Weilin Zhao PhD |
author_sort | Qiaoli Chen MS |
collection | DOAJ |
description | Background Carboxylesterase 4A (CES4A) belongs to the member of the carboxylesterase family, yet there has been limited research into its malignant biological behavior in malignant tumors. Here, we aim to investigate the expression, cellular biological functions, and the potential underlying mechanism of CES4A in nasopharyngeal carcinoma (NPC). Method A standardized mean difference (SMD) analysis was used to analyze the dysregulation of CES4A based on the gene expression omnibus (GEO) database. qRT-PCR and immunohistochemical staining (IHC) were used to identify the mRNA and protein levels of CES4A in NPC cell lines and tissues, respectively. CCK-8, colony formation, wound healing and transwell assays were utilized to estimate cellular growth and metastasis, respectively. Western blot was conducted to evaluate the activity of PI3K/AKT signaling pathway. Result Both mRNA and protein expression of CES4A was significantly diminished both in NPC cell lines and primary tumor tissues. Ectopic expression of CES4A restrains the proliferation, colony formation, migration and invasion of NPC. Additionally, KEGG analysis based on GEO data and high-throughput transcriptome sequencing of cell lines all strongly suggested that CES4A was involved in regulating phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. It was observed that AKT and phosphorylated AKT were remarkably reduced in CES4A overexpressing NPC cells, indicating that PI3K/AKT signaling pathway is hindered by CES4A. Conclusion CES4A expression is silenced in NPC, functioning as a tumor suppressor by negatively modulating the PI3K/AKT signaling pathway. |
format | Article |
id | doaj-art-71b8653a3c7c410d92e5fee8c17757d0 |
institution | Kabale University |
issn | 1533-0338 |
language | English |
publishDate | 2025-02-01 |
publisher | SAGE Publishing |
record_format | Article |
series | Technology in Cancer Research & Treatment |
spelling | doaj-art-71b8653a3c7c410d92e5fee8c17757d02025-02-06T11:03:20ZengSAGE PublishingTechnology in Cancer Research & Treatment1533-03382025-02-012410.1177/15330338251319144Carboxylesterase 4A Inhibits the Malignant Biological Behavior of Nasopharyngeal Carcinoma via the PI3K/AKT PathwayQiaoli Chen MS0Quanxiang Hao MBBS1Yanping Yang MBBS2Limei Li PhD3Danping Li MS4Ran Zhao MS5Wanqi Wei MBBS6Lixian Deng MBBS7Jiaming Su MBBS8Ziyuan Liang MBBS9Shiyue Tang MS10Yaomin Lu MBBS11Yushan Liang PhD12Zhe Zhang PhD13Xiaoying Zhou PhD14Xue Xiao PhD15Ping Li PhD16Yi Huang PhD17Weilin Zhao PhD18 Guangxi Regional Key Laboratory of Early Prevention and Treatment of High Incidence Tumors, Nanning, China Guangxi Regional Key Laboratory of Early Prevention and Treatment of High Incidence Tumors, Nanning, China Department of Otolaryngology-Head and Neck Surgery, , Nanning, China Key Laboratory of Oral Infectious Disease Prevention and Control, Health Commission of Guangxi Zhuang Autonomous Region, Nanning, China Key Laboratory of Oral Infectious Disease Prevention and Control, Health Commission of Guangxi Zhuang Autonomous Region, Nanning, China Life Science Institute, , Nanning, China Department of Otolaryngology-Head and Neck Surgery, , Nanning, China Life Science Institute, , Nanning, China Department of Otolaryngology-Head and Neck Surgery, , Nanning, China Life Science Institute, , Nanning, China Department of Otolaryngology-Head and Neck Surgery, , Nanning, China Life Science Institute, , Nanning, China Department of Otolaryngology-Head and Neck Surgery, , Nanning, China Department of Otolaryngology-Head and Neck Surgery, , Nanning, China Life Science Institute, , Nanning, China Department of Otolaryngology-Head and Neck Surgery, , Nanning, China Key Laboratory of Oral Infectious Disease Prevention and Control, Health Commission of Guangxi Zhuang Autonomous Region, Nanning, China Department of Otolaryngology-Head and Neck Surgery, , Nanning, China Department of Otolaryngology-Head and Neck Surgery, , Nanning, ChinaBackground Carboxylesterase 4A (CES4A) belongs to the member of the carboxylesterase family, yet there has been limited research into its malignant biological behavior in malignant tumors. Here, we aim to investigate the expression, cellular biological functions, and the potential underlying mechanism of CES4A in nasopharyngeal carcinoma (NPC). Method A standardized mean difference (SMD) analysis was used to analyze the dysregulation of CES4A based on the gene expression omnibus (GEO) database. qRT-PCR and immunohistochemical staining (IHC) were used to identify the mRNA and protein levels of CES4A in NPC cell lines and tissues, respectively. CCK-8, colony formation, wound healing and transwell assays were utilized to estimate cellular growth and metastasis, respectively. Western blot was conducted to evaluate the activity of PI3K/AKT signaling pathway. Result Both mRNA and protein expression of CES4A was significantly diminished both in NPC cell lines and primary tumor tissues. Ectopic expression of CES4A restrains the proliferation, colony formation, migration and invasion of NPC. Additionally, KEGG analysis based on GEO data and high-throughput transcriptome sequencing of cell lines all strongly suggested that CES4A was involved in regulating phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. It was observed that AKT and phosphorylated AKT were remarkably reduced in CES4A overexpressing NPC cells, indicating that PI3K/AKT signaling pathway is hindered by CES4A. Conclusion CES4A expression is silenced in NPC, functioning as a tumor suppressor by negatively modulating the PI3K/AKT signaling pathway.https://doi.org/10.1177/15330338251319144 |
spellingShingle | Qiaoli Chen MS Quanxiang Hao MBBS Yanping Yang MBBS Limei Li PhD Danping Li MS Ran Zhao MS Wanqi Wei MBBS Lixian Deng MBBS Jiaming Su MBBS Ziyuan Liang MBBS Shiyue Tang MS Yaomin Lu MBBS Yushan Liang PhD Zhe Zhang PhD Xiaoying Zhou PhD Xue Xiao PhD Ping Li PhD Yi Huang PhD Weilin Zhao PhD Carboxylesterase 4A Inhibits the Malignant Biological Behavior of Nasopharyngeal Carcinoma via the PI3K/AKT Pathway Technology in Cancer Research & Treatment |
title | Carboxylesterase 4A Inhibits the Malignant Biological Behavior of Nasopharyngeal Carcinoma via the PI3K/AKT Pathway |
title_full | Carboxylesterase 4A Inhibits the Malignant Biological Behavior of Nasopharyngeal Carcinoma via the PI3K/AKT Pathway |
title_fullStr | Carboxylesterase 4A Inhibits the Malignant Biological Behavior of Nasopharyngeal Carcinoma via the PI3K/AKT Pathway |
title_full_unstemmed | Carboxylesterase 4A Inhibits the Malignant Biological Behavior of Nasopharyngeal Carcinoma via the PI3K/AKT Pathway |
title_short | Carboxylesterase 4A Inhibits the Malignant Biological Behavior of Nasopharyngeal Carcinoma via the PI3K/AKT Pathway |
title_sort | carboxylesterase 4a inhibits the malignant biological behavior of nasopharyngeal carcinoma via the pi3k akt pathway |
url | https://doi.org/10.1177/15330338251319144 |
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