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Updated: Sep 10, 2025
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
LncRNA SNHG5 modulates cell proliferation and migration through the miR-92a-3p/BTG2 axis in gastric cancer by the
Qi-Qi Mao1, Mei-Lin Zhang2, Liang Zhong3
1Department of Gastroenterology, Huashan Hospital, Fudan University, Shanghai 201907, China.
Background:
Gastric cancer (GC) is a widespread malignancy and associated with high rates of morbidity and mortality worldwide.
Aim:
To examine the functional role of long non-coding RNAs small nucleolar RNA host gene 5 (SNHG5) and its regulation of miR-92a-3p and B-cell translocation gene 2 (BTG2) in GC progression.
Methods:
Quantitative reverse transcription PCR and western blot analysis determined the expression of SNHG5, miR-92a-3p, and BTG2 in GC and adjacent non-neoplastic mucosa. Dual-luciferase assays demonstrated interactions of SNHG5 with miR-92a-3p and BTG2. AGS cells were transfected with SNHG5 overexpression and miR-92a-3p knockdown models. Various assays, including CCK-8, colony formation, scratch wound healing, and Transwell assays, were used to determine cell proliferation and migration. An experimental model of a xenograft mouse was used to determine in vivo tumor growth. At the same time histological changes were evaluated by hematoxylin and eosin staining, with western blot analysis used to evaluate signaling pathway protein expression.
Results:
BTG2 and SNHG5 were downregulated in GC tissues, and miR-92a-3p was upregulated. Overexpression of SNHG5 or knockdown of miR-92a-3p reduced GC cell proliferation and migration, and increased BTG2 expression while decreasing PI3K/AKT signaling activity. The dual-luciferase assays demonstrated direct binding of miR-92a-3p to SNHG5 and BTG2. Tumor volume and weight were significantly reduced in mice transplanted with AGS cells treated with miR-92a-3p inhibitor or SNHG5 overexpression compared with control AGS cells. Hematoxylin and eosin staining revealed that treated tumors exhibited degenerative characteristics, including irregular morphology and nucleolysis.
Conclusion:
LncRNA SNHG5 inhibited GC cell growth and migration by modulating the PI3K/AKT pathway via the miR-92a-3p/BTG2 axis.
Insights
Long non-coding RNA SNHG5 inhibits gastric cancer progression by regulating miR-92a-3p and BTG2. This study reveals SNHG5 as a potential therapeutic target for gastric cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Gastric cancer (GC) is a significant global health concern with high mortality rates.
- Understanding the molecular mechanisms underlying GC progression is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the functional role of long non-coding RNA SNHG5 (small nucleolar RNA host gene 5) in gastric cancer.
- To elucidate the regulatory relationship between SNHG5, miR-92a-3p, and BTG2 in GC progression.
Main Methods:
- Quantitative reverse transcription PCR and western blot to assess SNHG5, miR-92a-3p, and BTG2 expression in GC tissues.
- Dual-luciferase assays to confirm interactions between SNHG5, miR-92a-3p, and BTG2.
- In vitro (cell lines) and in vivo (xenograft mouse models) experiments to evaluate the impact of SNHG5 and miR-92a-3p on GC cell proliferation, migration, and tumor growth.
Main Results:
- SNHG5 and BTG2 were downregulated, while miR-92a-3p was upregulated in GC tissues.
- SNHG5 overexpression or miR-92a-3p knockdown suppressed GC cell proliferation and migration, increased BTG2 expression, and inhibited the PI3K/AKT pathway.
- In vivo studies showed reduced tumor growth with SNHG5 overexpression or miR-92a-3p inhibition.
Conclusions:
- LncRNA SNHG5 acts as a tumor suppressor in gastric cancer.
- SNHG5 inhibits GC cell growth and migration by modulating the PI3K/AKT pathway through the miR-92a-3p/BTG2 axis.
- SNHG5 represents a potential therapeutic target for gastric cancer.
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