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LncRNA-SNHG16 Silencing Inhibits Prostate Carcinoma Cell Growth, Downregulate GLUT1 Expression and Reduce Glucose
Mingfeng Shao1, Ziqiang Yu1, Jianan Zou1
1Department of Urology, The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei City, Anhui Province 230031, People's Republic of China.
Background:
lncRNA-SNHG16 was identified as an oncogene in many cancers, but its involvement in prostate carcinoma is unknown.
Material And Method:
Expression of lncRNA-SNHG16 and glucose transporter 1 (GLUT-1) in 52 prostate carcinoma tissues and 36 normal prostate tissues was analyzed by RT-qPCR. Transfections were performed to analyze gene interactions. Cell proliferation was analyzed by cell proliferation assay.
Results:
Overexpression of lncRNA-SNHG16 effectively distinguished prostate carcinoma patients from normal ones. Expression levels of lncRNA-SNHG16 and GLUT-1 mRNA were significantly and positively correlated across prostate carcinoma tissues. In vitro cancer cell experiments revealed that lncRNA-SNHG16 siRNA silencing downregulated the expressions of GLUT-1 and reduced glucose uptake. lncRNA-SNHG16 siRNA silencing also significantly inhibited prostate carcinoma cell proliferation. However, lncRNA-SNHG16 siRNA silencing did not affect the normal prostate.
Conclusion:
In conclusion, lncRNA-SNHG16 might be a possible treatment target for prostate cancer.
Insights
Long non-coding RNA SNHG16 is overexpressed in prostate carcinoma, correlating with glucose transporter 1 (GLUT-1) and inhibiting cancer cell proliferation. SNHG16 may be a therapeutic target for prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Long non-coding RNA SNHG16 (lncRNA-SNHG16) is implicated as an oncogene in various cancers.
- Its specific role in prostate carcinoma pathogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the expression and function of lncRNA-SNHG16 in prostate carcinoma.
- To determine the relationship between lncRNA-SNHG16, glucose transporter 1 (GLUT-1), and prostate cancer cell proliferation.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) was used to analyze lncRNA-SNHG16 and GLUT-1 expression in prostate carcinoma and normal tissues.
- In vitro transfections and cell proliferation assays were conducted to assess gene interactions and cellular behavior.
- RNA interference (siRNA) was employed to silence lncRNA-SNHG16 expression.
Main Results:
- lncRNA-SNHG16 overexpression significantly differentiated prostate carcinoma from normal tissues.
- Positive correlation observed between lncRNA-SNHG16 and GLUT-1 mRNA levels in prostate carcinoma.
- Silencing lncRNA-SNHG16 reduced GLUT-1 expression, glucose uptake, and inhibited prostate cancer cell proliferation without affecting normal prostate cells.
Conclusions:
- lncRNA-SNHG16 plays a crucial role in promoting prostate carcinoma progression.
- lncRNA-SNHG16 emerges as a potential therapeutic target for prostate cancer treatment.
Related Concept Videos
lncRNA - Long Non-coding RNAs
MicroRNAs
MicroRNAs
Abnormal Proliferation
