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Author Spotlight: A Computational Pipeline for Analyzing Chimeric Noncoding RNA-Target RNA Interactions in High-Throughput Sequencing Data
Published on: December 1, 2023
Long noncoding RNA DINO (damage induced noncoding) represses the development of gastric cancer by modulating p21 and
Qinqiang Liu1, Yan Xiao2, Peng Cai1
1Department of General Surgery, Xuzhou Hospital of Traditional Chinese medicine, Xuzhou, Jiangsu, China.
Abstract:
lncRNAs are responsible for a variety of diseases, including gastric cancer (GC). Many recent studies have reported that lncRNAs can serve as crucial regulators of various genes. Nevertheless, the biological function of lncRNA damage induced noncoding (DINO) remained poorly investigated in GC. Therefore, in our present study, the detailed role of DINO was investigated. It was manifested that DINO was significantly downregulated in GC tissues. Then, DINO was modulated by infecting LV-DINO or by LV-shRNA in BGC-823 and MGC-803 cells. Moreover, it was displayed that GC cell proliferation was suppressed by DINO overexpression, whereas silencing DINO increased cell proliferation significantly. For another, it was indicated that DINO dramatically induced apoptotic ratios of BGC-823 and MGC-803 cells, whereas the decrease of DINO depressed GC cell apoptosis. Apart from these, GC cell cycle progression was greatly blocked by LV-DINO. Furthermore, Western blot results displayed that upregulation of DINO elevated p21 expression and Bax expression. Oppositely, inhibition of DINO greatly suppressed p21 and Bax protein expression level. Taken these, DINO might exert a tumor inhibitory role in the progression of GC through modulating p21 and Bax.
Insights
Long non-coding RNA damage induced noncoding (DINO) is downregulated in gastric cancer (GC). Restoring DINO suppresses GC cell proliferation and promotes apoptosis, suggesting its tumor-inhibitory role.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are implicated in various diseases, including gastric cancer (GC).
- The specific role of lncRNA damage induced noncoding (DINO) in GC progression has been underexplored.
- lncRNAs function as critical regulators of gene expression.
Purpose of the Study:
- To investigate the biological function and mechanism of lncRNA DINO in gastric cancer.
- To determine the expression levels of DINO in GC tissues and cell lines.
- To elucidate the effect of DINO modulation on GC cell behavior.
Main Methods:
- Quantitative analysis of DINO expression in GC tissues.
- Overexpression and knockdown of DINO in GC cell lines (BGC-823, MGC-803) using lentiviral vectors.
- Assessment of cell proliferation, apoptosis, and cell cycle progression.
- Western blot analysis to detect protein expression levels of p21 and Bax.
Main Results:
- DINO expression was significantly downregulated in GC tissues compared to normal tissues.
- Overexpression of DINO suppressed GC cell proliferation and induced apoptosis.
- Silencing DINO enhanced GC cell proliferation and inhibited apoptosis.
- DINO overexpression led to cell cycle arrest and increased expression of p21 and Bax.
- DINO inhibition decreased p21 and Bax protein levels.
Conclusions:
- DINO acts as a tumor suppressor in gastric cancer.
- DINO exerts its inhibitory effects by promoting apoptosis and cell cycle arrest.
- The tumor-suppressive function of DINO may be mediated through the modulation of p21 and Bax expression in GC.
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