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Updated: Oct 8, 2025

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
Published on: September 18, 2020
Changes in the Expression of Long Non-Coding RNA SDMGC and Its Target Gene, TRIM16, in Patients with Gastric Cancer
Mina Seifi Inallou1, Reza Safaralizadeh2, Ali Rajabi1
1Department of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran.
Purpose:
Gastric cancer (GC) has been identified worldwide as one of the most common cancer types with a high mortality rate. LncRNA SDMGC has been recognized as an oncogene with regulatory effects on its target gene, TRIM16, which is believed to play a tumor-suppressing role in various cancers. Both these genes are involved in GC development, tumorigenesis, invasion, and metastasis. The current study is aimed to investigate the association of SDMGC and TRIM16 with GC susceptibility and GC patients' clinicopathological characteristics.
Methods:
A total of 100 GC tissues and their corresponding adjacent non-tumor tissues were sampled. Total RNA was then isolated to measure SDMGC and TRIM16 expression levels using quantitative reverse transcriptase (qRT)-PCR. Statistical analyses including the Mann-Whitney U test and correlation tests were carried out using R v4.5. GraphPad Prism was also used to plot the receiver operating curve (ROC).
Results:
The results demonstrated the significant overexpression of lncRNAs SDMGC and downregulation of TRIM16 in GC tissues as compared to their corresponding marginal normal tissue samples (P = 0.005 and P = 0.009, respectively). No association with clinicopathological variables was observed for either SDMGC or TRIM16. Moreover, the results demonstrated a small positive correlation between SDMGC and TRIM16. Evaluation of the diagnostic value of SDMGC and TRIM16 showed poor biomarker potency for these genes.
Conclusion:
In conclusion, the results indicated an increase in the expression of SDMGC and a decline in the expression pattern of TRIM16 among the Iranian population. The results indicated a key tumor-accelerative function of SDMGC and a pivotal tumor-suppressing role of TRIM16 in GC patients.
Insights
Gastric cancer (GC) shows increased long non-coding RNA SDMGC and decreased TRIM16 expression in Iranian patients. SDMGC acts as an oncogene, while TRIM16 functions as a tumor suppressor in GC development.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Gastric cancer (GC) is a prevalent malignancy with high mortality.
- Long non-coding RNA SDMGC is implicated as an oncogene, potentially regulating the tumor suppressor gene TRIM16.
- Both SDMGC and TRIM16 are involved in GC progression, including tumorigenesis, invasion, and metastasis.
Purpose of the Study:
- To investigate the association between SDMGC and TRIM16 expression and GC susceptibility.
- To examine the correlation of SDMGC and TRIM16 with clinicopathological characteristics of GC patients.
- To evaluate the diagnostic potential of SDMGC and TRIM16 as biomarkers for GC.
Main Methods:
- Quantitative reverse transcriptase (qRT)-PCR was used to measure SDMGC and TRIM16 expression levels.
- Expression levels were compared between 100 GC tissues and adjacent non-tumor tissues.
- Statistical analyses included Mann-Whitney U test, correlation tests, and receiver operating curve (ROC) analysis.
Main Results:
- Significant overexpression of SDMGC and downregulation of TRIM16 were observed in GC tissues compared to normal tissues (P=0.005 and P=0.009).
- No significant association was found between SDMGC or TRIM16 expression and clinicopathological variables.
- SDMGC and TRIM16 exhibited poor biomarker potency for GC diagnosis, despite a small positive correlation between their expression levels.
Conclusions:
- SDMGC expression is increased, and TRIM16 expression is decreased in GC patients from the Iranian population.
- SDMGC demonstrates a tumor-accelerative function, whereas TRIM16 exhibits a tumor-suppressing role in GC.
- Further research may elucidate the precise molecular mechanisms underlying their roles in gastric carcinogenesis.
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