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RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA
Published on: April 10, 2018
Long non-coding RNA mortal obligate RNA transcript suppresses tumor cell proliferation in prostate carcinoma by
Zhenfeng Shi1, Feng Guo1, Deyong Jia2
1Department of Urology, The People's Hospital of Xinjiang Uyghur Autonomous Region, Urumqi, Xinjiang Uygur Autonomous Region 830002, P.R. China.
Abstract:
A previous study reported the decreased expression of long non-coding RNA mortal obligate RNA transcript (lncRNA MORT) in 16 types of cancer, while the functionality of lncRNA MORT in cancer biology remains unknown. Therefore, the present study was conducted to characterize the functionality of lncRNA MORT in prostate carcinoma, a common cancer type worldwide. lncRNA MORT expression level was downregulated in tumor tissues compared with that in the adjacent healthy tissues of patients with prostate carcinoma. Expression of lncRNA MORT in tumor tissues was influenced by tumor size, but not by tumor metastasis. Overexpression of lncRNA MORT inhibited glucose uptake and glucose transporter 1 (GLUT-1) expression in prostate carcinoma cell lines; GLUT-1 overexpression upregulated glucose uptake and attenuated the effects of lncRNA MORT overexpression on glucose uptake, but did not significantly affect the expression of lncRNA MORT. Overexpression of lncRNA MORT inhibited, while GLUT-1 overexpression promoted the proliferation of prostate carcinoma cells. In addition, GLUT-1 overexpression attenuated the effects of lncRNA MORT on cell proliferation. Therefore, lncRNA MORT may inhibit cancer cell proliferation in prostate carcinoma by preventing glucose uptake.
Insights
Long non-coding RNA MORT (lncRNA MORT) is downregulated in prostate cancer. Overexpressing lncRNA MORT inhibits cancer cell proliferation by reducing glucose uptake, suggesting a potential therapeutic role.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Long non-coding RNA mortal obligate RNA transcript (lncRNA MORT) expression is decreased in 16 cancer types.
- The specific role of lncRNA MORT in cancer progression is currently unknown.
- Prostate carcinoma is a prevalent cancer worldwide, necessitating further research into its underlying molecular mechanisms.
Purpose of the Study:
- To investigate the functional role of lncRNA MORT in prostate carcinoma.
- To elucidate the relationship between lncRNA MORT, glucose metabolism, and cell proliferation in prostate cancer.
Main Methods:
- Quantitative analysis of lncRNA MORT expression in prostate tumor tissues versus adjacent healthy tissues.
- In vitro studies using prostate carcinoma cell lines to assess the effects of lncRNA MORT and glucose transporter 1 (GLUT-1) overexpression on glucose uptake and cell proliferation.
Main Results:
- lncRNA MORT expression was significantly downregulated in prostate tumor tissues compared to healthy tissues.
- Overexpression of lncRNA MORT inhibited glucose uptake and GLUT-1 expression in prostate cancer cells.
- GLUT-1 overexpression counteracted the inhibitory effects of lncRNA MORT on glucose uptake and cell proliferation.
- lncRNA MORT overexpression suppressed prostate cancer cell proliferation, while GLUT-1 overexpression promoted it.
Conclusions:
- lncRNA MORT functions as a tumor suppressor in prostate carcinoma.
- The inhibitory effect of lncRNA MORT on prostate cancer cell proliferation is mediated, at least in part, by the regulation of glucose uptake via GLUT-1.
- lncRNA MORT represents a potential therapeutic target for prostate cancer treatment.
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