NEIL3 and TOP2A as key drivers of esophageal cancer through WNT signaling

Esophageal cancer (EC) is a highly aggressive malignancy with limited treatment options. Nei like DNA glycosylase 3 (NEIL3) and DNA topoisomerase II alpha (TOP2A) have been identified as potential therapeutic targets, though their roles in EC remain unclear. This study investigates the effects of N...

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Main Authors: Hui Li, Panpan Wang, Huijuan Chen, Yanyan Shao, Hui Luo
Format: Article
Language:English
Published: Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina 2025-01-01
Series:Biomolecules & Biomedicine
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Online Access:https://www.bjbms.org/ojs/index.php/bjbms/article/view/11365
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author Hui Li
Panpan Wang
Huijuan Chen
Yanyan Shao
Hui Luo
author_facet Hui Li
Panpan Wang
Huijuan Chen
Yanyan Shao
Hui Luo
author_sort Hui Li
collection DOAJ
description Esophageal cancer (EC) is a highly aggressive malignancy with limited treatment options. Nei like DNA glycosylase 3 (NEIL3) and DNA topoisomerase II alpha (TOP2A) have been identified as potential therapeutic targets, though their roles in EC remain unclear. This study investigates the effects of NEIL3 overexpression and TOP2A knockdown, focusing on the WNT signaling pathway. ECA109 esophageal cancer cells were used to assess the impact of NEIL3 overexpression and TOP2A knockdown on proliferation, colony formation, migration, invasion, and apoptosis. The involvement of the WNT signaling pathway was also explored. NEIL3 overexpression significantly enhanced proliferation, colony formation, migration, and invasion while reducing apoptosis. In contrast, TOP2A knockdown suppressed these functions and promoted apoptosis, independent of NEIL3. NEIL3 overexpression could not reverse the effects of TOP2A knockdown. Both NEIL3 and TOP2A acted through the WNT signaling pathway. In vivo, NEIL3 knockdown reduced tumor size and weight via WNT pathway modulation. NEIL3 and TOP2A play key roles in EC progression through the WNT signaling pathway. Targeting these molecules may offer promising therapeutic strategies for EC.
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institution Kabale University
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language English
publishDate 2025-01-01
publisher Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina
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series Biomolecules & Biomedicine
spelling doaj-art-866e92f0d73147fc98b2d8de8c2453842025-01-30T16:41:55ZengAssociation of Basic Medical Sciences of Federation of Bosnia and HerzegovinaBiomolecules & Biomedicine2831-08962831-090X2025-01-0110.17305/bb.2025.11365NEIL3 and TOP2A as key drivers of esophageal cancer through WNT signalingHui Li0Panpan Wang1Huijuan Chen2Yanyan Shao3Hui Luo4Tumor Medical Center, The First Affiliated Hospital, Jiangxi Medical College of Nanchang University, Nanchang, China; Department of Oncology, The First Hospital of Nanchang, Nanchang, ChinaDepartment of Oncology, The First Hospital of Nanchang, Nanchang, ChinaDepartment of Oncology, The First Hospital of Nanchang, Nanchang, ChinaDepartment of Oncology, The First Hospital of Nanchang, Nanchang, ChinaTumor Medical Center, The First Affiliated Hospital, Jiangxi Medical College of Nanchang University, Nanchang, China Esophageal cancer (EC) is a highly aggressive malignancy with limited treatment options. Nei like DNA glycosylase 3 (NEIL3) and DNA topoisomerase II alpha (TOP2A) have been identified as potential therapeutic targets, though their roles in EC remain unclear. This study investigates the effects of NEIL3 overexpression and TOP2A knockdown, focusing on the WNT signaling pathway. ECA109 esophageal cancer cells were used to assess the impact of NEIL3 overexpression and TOP2A knockdown on proliferation, colony formation, migration, invasion, and apoptosis. The involvement of the WNT signaling pathway was also explored. NEIL3 overexpression significantly enhanced proliferation, colony formation, migration, and invasion while reducing apoptosis. In contrast, TOP2A knockdown suppressed these functions and promoted apoptosis, independent of NEIL3. NEIL3 overexpression could not reverse the effects of TOP2A knockdown. Both NEIL3 and TOP2A acted through the WNT signaling pathway. In vivo, NEIL3 knockdown reduced tumor size and weight via WNT pathway modulation. NEIL3 and TOP2A play key roles in EC progression through the WNT signaling pathway. Targeting these molecules may offer promising therapeutic strategies for EC. https://www.bjbms.org/ojs/index.php/bjbms/article/view/11365Esophageal cancerECnei like DNA glycosylase 3NEIL3DNA topoisomerase II alphaTOP2A
spellingShingle Hui Li
Panpan Wang
Huijuan Chen
Yanyan Shao
Hui Luo
NEIL3 and TOP2A as key drivers of esophageal cancer through WNT signaling
Biomolecules & Biomedicine
Esophageal cancer
EC
nei like DNA glycosylase 3
NEIL3
DNA topoisomerase II alpha
TOP2A
title NEIL3 and TOP2A as key drivers of esophageal cancer through WNT signaling
title_full NEIL3 and TOP2A as key drivers of esophageal cancer through WNT signaling
title_fullStr NEIL3 and TOP2A as key drivers of esophageal cancer through WNT signaling
title_full_unstemmed NEIL3 and TOP2A as key drivers of esophageal cancer through WNT signaling
title_short NEIL3 and TOP2A as key drivers of esophageal cancer through WNT signaling
title_sort neil3 and top2a as key drivers of esophageal cancer through wnt signaling
topic Esophageal cancer
EC
nei like DNA glycosylase 3
NEIL3
DNA topoisomerase II alpha
TOP2A
url https://www.bjbms.org/ojs/index.php/bjbms/article/view/11365
work_keys_str_mv AT huili neil3andtop2aaskeydriversofesophagealcancerthroughwntsignaling
AT panpanwang neil3andtop2aaskeydriversofesophagealcancerthroughwntsignaling
AT huijuanchen neil3andtop2aaskeydriversofesophagealcancerthroughwntsignaling
AT yanyanshao neil3andtop2aaskeydriversofesophagealcancerthroughwntsignaling
AT huiluo neil3andtop2aaskeydriversofesophagealcancerthroughwntsignaling