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lncRNA SNHG4 enhanced gastric cancer progression by modulating miR-409-3p/CREB1 axis

ZHOUYANG CHENG1,#, YUCHEN HUA2,#, YANG CAO3, JUN QIN1,*
1 Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, China
2 Department of Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, China
3 Department of Operation, Affiliated Hospital of Nantong University, Nantong, 226001, China
* Corresponding Author: JUN QIN. Email: email
(This article belongs to the Special Issue: Signaling Pathway Crosstalk in Malignant Tumors: Molecular Targets and Combinatorial Therapeutics)

Oncology Research https://doi.org/10.32604/or.2024.042281

Received 25 May 2023; Accepted 24 August 2023; Published online 08 April 2024

Abstract

Gastric cancer (GC) is a globally common cancer characterized by high incidence and mortality worldwide. Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy. Long non-coding RNAs (lncRNAs) and their downstream regulators are regarded to be implicated in the progression of multiple types of malignancies. Studies have shown that the lncRNA small nucleolar RNA host gene 4 (SNHG4) serves as a tumor promoter in various malignancies, while its function in GC has yet to be characterized. Herein, we discovered that SNHG4 was overexpressed in GC tissues and cell lines, and was linked with poor survival rate of GC patients. According to cellular function experiments, we concluded that SNHG4 promoted GC cell proliferation, migration, and invasion while inhibited cell apoptosis and cell cycle arrest in vitro. The in vivo experiment indicated that SNHG4 facilitated GC tumor growth in xenograft mouse models. Furthermore, SNHG4 was demonstrated to bind to miR-409-3p. Moreover, cAMP responsive element binding protein 1 (CREB1) was directly targeted by miR-409-3p. Rescue assays demonstrated that miR-409-3p deficiency reversed the suppressive impact of SNHG4 knockdown on GC cell malignancy. Additionally, miR-409-3p was also revealed to inhibit GC cell proliferation, migration, and invasion by targeting CREB1. In conclusion, we verified that the SNHG4 promoted GC growth and metastasis by binding to miR-409-3p to upregulate CREB1, which may deepen the understanding of the underlying mechanism in GC development.

Keywords

Gastric cancer; Small nucleolar RNA host gene 4 (SNHG4); MicroRNA (miR)-409-3p; cAMP responsive element binding protein 1 (CREB1)
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