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.

Oncology Letters
|September 14, 2019
PubMed

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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