GTSE1 promotes nasopharyngeal carcinoma proliferation and angiogenesis by upregulating STMN1

Nasopharyngeal carcinoma (NPC) is a malignant tumor with poor survival rate. G2 and S phase-expressed-1 (GTSE1) takes part in the progression of diverse tumors as an oncogene, but its role and potential mechanism in NPC remain unknown. The GTSE1 expression was analyzed by western blot in NPC tissues...

Full description

Saved in:
Bibliographic Details
Published in:Cell division 2024-05, Vol.19 (1), p.16-16, Article 16
Main Authors: Dong, Jiadi, Chen, Jingjing, Wu, Yidong, Yan, Jiangyu
Format: Article
Language:English
Subjects:
Angiogenesis
Apoptosis
Bladder cancer
Breast cancer
Cell cycle
Cell proliferation
Cell viability
Cervical cancer
Chemotherapy
Esophagus
FOXM1
Gastric cancer
GTSE1
Invasion
Kidney cancer
Liver cancer
Lung cancer
Medical diagnosis
Medical prognosis
Melanoma
Nasopharyngeal carcinoma
Protein expression
Proteins
Radiation therapy
S phase
Squamous cell carcinoma
STMN1
Throat cancer
Tumors
Wound healing
Citations: Items that this one cites
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Nasopharyngeal carcinoma (NPC) is a malignant tumor with poor survival rate. G2 and S phase-expressed-1 (GTSE1) takes part in the progression of diverse tumors as an oncogene, but its role and potential mechanism in NPC remain unknown. The GTSE1 expression was analyzed by western blot in NPC tissues and cells. Knock-down experiments were conducted to determine the function of GTSE1 in NPC by cell counting kit-8, the 5-ethynyl-2'-deoxyuridine (EdU) incorporation experiment, cell scratch wound-healing experiment, transwell assays, tube forming experiment and western blot. In addition, the in vivo role of GTSE1 was addressed in tumor-bearing mice. The expression of was increased in NPC. Silencing of GTSE1 suppressed cell viability, the percent of EdU positive cells, and the number of invasion cells and tubes, but enhanced the scratch ratio in NPC cells. Mechanically, downregulation of GTSE1 decreased the expressions of FOXM1 and STMN1, which were restored with the upregulation of FOXM1. Increased expression of STMN1 reversed the effects of the GTSE1 silencing on proliferation, migration, invasion and angiogenesis of NPC cells. Furthermore, knockdown of GTSE1 repressed the tumor volume and tumor weight of xenografted mice. GTSE1 was highly expressed in NPC, and silencing of GTSE1 ameliorated the malignant processes of NPC cells by upregulating STMN1, suggesting a possible therapeutical target for NPC.
ISSN:1747-1028
1747-1028
DOI:10.1186/s13008-024-00119-9