Long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1): A molecular predictor of poor survival in glioblastoma multiforme in Egyptian patients

  • Manal S. Fawzy
  • Eman A. Toraih
  • Hoda Y. Abdallah


Background: Long noncoding RNAs (lncRNAs) are a recently discovered class of transcribed RNA molecules with a length of more than 200 nucleotides. Recent studies have shown that lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) could play an important role in carcinogenesis and cancer progression in several types of malignancies.
Objective: As little is known about the role and clinical significance of lncRNA MALAT1 in glioblastoma multiform (GBM) patients in Egyptian population, this study aimed to investigate the expressions of lncRNA-MALAT1 in human GBM samples and to correlate these expressions with the available clinicopathological features including patient survival data.
Subjects and methods: The relative expression of MALAT1 was determined in 37 human glioblastoma formalin-fixed paraffin embedded (FFPE) tissue samples and 10 FFPE non-neoplastic brain tissues using quantitative reverse transcription polymerase chain reaction (qRT-PCR) technology.
Results: The current results revealed that lncRNA MALAT1 expression was down-regulated in all tumor specimens compared to normal tissues. A receiver operating characteristic (ROC) curve analysis showed high diagnostic performance; area under curve (AUC) =0.925 ± 0.038 (P <0.001), 95% CI= 0.850–1.00, with 94.6% sensitivity, and 72.7% specificity. Lower MALAT1 expression was associated with poor prognosis; higher frequency of recurrence (P < 0.044), lower overall survival (P <0.005), and shorter disease-free survival (P < 0.004).
Conclusion: Taken together, we could postulate that MALAT1 might have a tumor-suppressive function in GBM in Egyptian population and this specific type of lncRNAs may be included in the lists of both potential prognostic biomarkers and the future therapeutic targets for glioblastomas.


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eISSN: 1110-8630