Published online Oct 15, 2024. doi: 10.4251/wjgo.v16.i10.4194
Revised: June 9, 2024
Accepted: June 28, 2024
Published online: October 15, 2024
Processing time: 261 Days and 21.8 Hours
The clinical effects and detailed roles of long non-coding RNA (LncRNA) steroid receptor RNA activator 1 (SRA1) in esophageal squamous cell carcinoma (ESCC) remain ambiguous. In the present study, the complementary sites between lncRNA SRA1, miRNA-363-5p, and phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) predicted via bioinformatics analysis stimulated us to hypothesize that miRNA-363-5p/LHPP axis might be required for SRA1-mediated ESCC progression.
To investigate the molecular events of SRA1 in the malignant behavior in ESCC.
Thirty-eight ESCC tissues and paired adjacent normal tissues were acquired. SRA1 expression was detected in ESCC tissues and cell lines using quantitative reverse transcription-polymerase chain reaction. Cell counting Kit-8 assay, transwell invasion assay, glycolysis assay, and xenograft tumor model were performed to address the malignant biological behaviors of ESCC cells after the introduction of SRA1. The t-test and the χ2 test were used for com
SRA1 downregulation was identified in ESCC. ESCC patients exhibiting a low SRA1 expression faced shorter overall survival than those with a high SRA1 expression. The introduction of SRA1 inhibited cell proliferation, glucose uptake, and lactate production in ESCC. In vivo, the growth of ESCC was hindered by SRA1 overexpression. Then, SRA1 overexpresses the LHPP by inhibiting miRNA-363-5p. Lastly, the introduction of small interfering RNA si-LHPP or miRNA-363-5p mimic could abrogate the inhibition roles triggered by SRA1.
SRA1 inhibits the oncogenicity of ESCC via miRNA-363-5p/LHPP axis. The SRA1/miRNA-363-5p/LHPP pathway may be a therapeutic target for ESCC.
Core Tip: In this study, we identified abnormal expression of steroid receptor RNA activator 1 (SRA1) in esophageal squamous cell carcinoma (ESCC). SRA1 was significantly downregulated in ESCC tissues and cell lines, and its low expression was strongly associated with advanced tumor stage, metastasis, larger tumor size, and poor survival. Functional and rescue assays demonstrated that SRA1 could impede ESCC cell proliferation and glycolysis via miRNA-363-5p and phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP). Mechanistically, SRA1 elevated LHPP expression by sponging miRNA-363-5p, thereby inhibiting ESCC cell proliferation and glycolysis.