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...
Saved in:
Main Authors: | , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina
2025-01-01
|
Series: | Biomolecules & Biomedicine |
Subjects: | |
Online Access: | https://www.bjbms.org/ojs/index.php/bjbms/article/view/11365 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
_version_ | 1832577752671191040 |
---|---|
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.
|
format | Article |
id | doaj-art-866e92f0d73147fc98b2d8de8c245384 |
institution | Kabale University |
issn | 2831-0896 2831-090X |
language | English |
publishDate | 2025-01-01 |
publisher | Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina |
record_format | Article |
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 |