RTEL1 is upregulated in gastric cancer and promotes tumor growth

Sep 21, 2026

Uploaded by Theodora

Gastric cancer (GC) is a widespread malignancy with rising incidence and mortality, often detected at advanced stages and accompanied by poor outcomes. Its heterogeneous progression reflects complex genetic and environmental interactions, making discovery of new genes and pathways essential. This study shows RTEL1 expression is markedly elevated in GC tissues and correlates with unfavorable prognosis. RTEL1 promotes GC cell proliferation in vitro and in vivo, enhances cell-cycle progression, and suggests CDC23 and TRIP13 as downstream mediators of tumor-promoting effects.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages10

Reading Time25 min

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Abstract

Introduction

Materials and methods

Public databases

GC clinical samples

Journal of Cancer Research and Clinical Oncology (2025) 151:23 [https://doi.org/10.1007/s00432-024-06062-0](https://doi.org/10.1007/s00432-024-06062-0) RESEARCH RTEL1 is upregulated in gastric cancer and promotes tumor growth Chunyu Yang1,2 · Suzeng Wang1,2 · Ge Gao1,2 · Peiwen Xu1,2 · Mengyuan Qian1,2 · Yuan Yin1,2 · Surui Yao1,2 · Zhaohui Huang1,2 · Zehua Bian1,2 Received: 15 October 2024 / Accepted: 6 December 2024 / Published online: 26 December 2024 © The Author(s) 2024 Abstract Gastric cancer (GC) is one of the most common cancers worldwide, with increasing incidence and mortality rates. It is typically diagnosed at advanced stages, leading to a poor prognosis. GC is a highly heterogeneous disease and its progression is associated with complex interplay between genetic and environmental factors. Identifying novel genes and pathways involved in GC development is crucial for improving the therapeutic outcome. Regulator of Telomerase Length 1 (RTEL1) has been found to maintain telomere stability through its helicase activity, facilitating telomere reconstruction and repair. However, the precise role of RTEL1 in human cancers, particularly in GC, is not yet fully understood. In this study, we observed significantly increased RTEL1 expression in GC tissues, which was associated with a poor prognosis. Functionally, RTEL1 promotes GC cell proliferation both in vitro and in vivo. Additionally, RTEL1 appears to regulate multiple signaling pathways, with a particular promoting effect on the cell cycle progression. Notably, CDC23 and TRIP13 are potential downstream target genes of RTEL1, which may mediate its tumor-promoting effects in GC. These findings suggest that RTEL1 plays a critical role in GC tumorigenesis and could be a promising target for the therapy and prognosis of GC. Keywords Gastric cancer · RTEL1 · Cell cycle · Tumor proliferation · CDC23 · TRIP13 Introduction Gastric cancer (GC) is a common malignant tumor in the digestive system, and it remains to be one of the leading causes of cancer-related deaths worldwide (Bray et al. 2024) . GC has a complex etiology and undergoes multiple developmental stages (Sung et al. 2021) . Due to the subtle early symptoms and the lack of specific early diagnostic markers, the majority of GC patients are diagnosed at advanced stages, leading to delayed optimal treatment, anda poor prognosis. In addition, the mechanisms mediating GC occurrence and progression are complicated and have 􀀍 Zhaohui Huang [zhaohuihuang@jiangnan.edu.cn](zhaohuihuang@jiangnan.edu.cn) 􀀍 Zehua Bian [zehua_bian@126.com](zehua_bian@126.com) 1 Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, 200 Hui He Road, Wuxi, Jiangsu 214062, China 2 Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, China not been fully understood (Zavros and Merchant 2022) . Therefore, conducting in-depth research on the mechanisms of GC could facilitate early diagnosis and effective treatment for this disease. Regulator of Telomerase Length 1 (RTEL1) is a key DNA helicase responsible for maintaining telomere stability and genomic integrity (Vannier et al. 2013, 2014) . RTEL1 can interact with DNA, RNA, and proteins, playing a role in various cellular pathways (Hourvitz et al. 2024) . Several studies have indicated that mutations in RTEL1 can lead to genomic instability and cellular malignant transformation, thereby increasing the susceptibility to various tumors, such as glioma (Saunders et al. 2022; Wrensch et al. 2009), glioblastoma (Liu et al. 2010), and lung cancer (McKay et al. 2017) . In addition, overexpression of RTEL1 can promote the occurrence and progression of tumors, such as hepatocellular carcinoma (Wu et al. 2012) and gliomas (Wang et al. 2024) . We recently revealed that RTEL1 is aberrantly upregulated in CRC and promotes cancer progression (Wu et al. 2023) . These studies suggest that RTEL1 may play an important role in the

FAQs

What is the main finding about RTEL1 in gastric cancer?

RTEL1 is significantly upregulated in gastric cancer tissues and is associated with poor prognosis. The study links higher RTEL1 levels to worse clinical outcomes.

How does RTEL1 influence gastric cancer cell behavior?

Functionally, RTEL1 promotes gastric cancer cell proliferation both in vitro and in vivo. It also shows a promoting effect on cell-cycle progression.

Which downstream genes are proposed to mediate RTEL1’s tumor-promoting effects?

CDC23 and TRIP13 are proposed as potential downstream target genes of RTEL1. They may mediate RTEL1-driven tumor-promoting effects in gastric cancer.

Sep 21, 2026

Uploaded by Theodora