LncRNA RP11-138J23.1 Contributes to Gastric Cancer Progression by Interacting With RNA-Binding Protein HuR.

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• Gastric cancer (GC) remains a leading cause of cancer-related deaths globally.
• Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
• The specific functions of many lncRNAs in GC are yet to be fully elucidated.

Purpose of the Study:

• To investigate the expression and function of lncRNA RP11-138J23.1 in gastric cancer.
• To explore the underlying molecular mechanisms of RP11-138J23.1 in GC progression.
• To assess the potential of RP11-138J23.1 as a therapeutic target for GC.

Main Methods:

• Bioinformatics analysis and in situ hybridization (ISH) to determine RP11-138J23.1 expression.
• In vitro knockdown and overexpression studies to assess functional roles in cell proliferation and metastasis.
• In vivo loss-of-function assays to validate findings.
• Mechanistic studies involving HuR protein binding and VAV3 mRNA stability analysis.

Main Results:

• RP11-138J23.1 was found to be significantly upregulated in GC tissues.
• Knockdown of RP11-138J23.1 inhibited GC cell proliferation and metastasis.
• Overexpression of RP11-138J23.1 promoted tumor cell growth and metastasis in vitro.
• RP11-138J23.1 was confirmed to play a role in vivo.
• Mechanistically, RP11-138J23.1 enhances GC progression by stabilizing VAV3 mRNA via HuR protein interaction.

Conclusions:

• RP11-138J23.1 plays a crucial oncogenic role in gastric cancer.
• RP11-138J23.1 promotes GC cell proliferation and metastasis.
• RP11-138J23.1 represents a promising therapeutic target for gastric cancer treatment.