THE ROLE OF LONG NON-CODING RNA-MALAT1 EXPRESSION IN BLADDER CANCER CELL LINES


Demir B., Karpuzoğlu F. H.

TBD Uluslararası Laboratuvar Tıbbı Zirvesi, Erzurum, Türkiye, 28 - 31 Ekim 2025, ss.1, (Özet Bildiri)

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: Erzurum
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.1
  • İstanbul Üniversitesi Adresli: Evet

Özet

THE ROLE OF LONG NON-CODING RNA-MALAT1 EXPRESSION IN BLADDER CANCER CELL LINES

 

Bekircan Demir.1,  Hande Karpuzoğlu.1

1Department of Biochemistry, Faculty of Medicine, İstanbul University, İstanbul, Turkey

 

Objectives:

Bladder cancer (BC) is the 10th most common cancer worldwide. LncRNAs are believed to contribute to carcinogenesis. MALAT1 is recognized as a significant prognostic biomarker. However, the roles of MALAT1 in BC remain largely unknown. In the study, we aim to explore the potential role of  MALAT1 in the BC

 

Material and Methods:

Expression levels of MALAT1 were detected in BC cell lines with non-muscle invasive bladder cancer cell  (RT112), muscle invasive bladder cancer  (T24), and healthy epithelial cell SV-HUC-1. Total RNA was isolated, and then complementary DNA (cDNA) was synthesized. Expression levels were measured by real-time Reverse Transcriptase Polymerase Chain Reaction (qRT-PCR). The 2- ∆∆Ct method was employed to analyse fold changes by normalising to GAPDH expression. GraphPad Prism was used. Student’s t-test was performed to compare the differences among groups, p<0.05 was regarded as statistically significant.

 

Results:

Our findings show that MALAT1 is significantly increased in RT112 and T24 compared with SV-HUC-1  (p<0.05). 

Conclusions:  

High MALAT1 expression has been demonstrated to correlate with increased malignancy potential in patient-based studies. Consistent with these findings, our cell culture experiments also supported that MALAT1 expression was elevated compared to normal conditions.

Based on these results, we are continuing our investigations to elucidate the mechanistic relationship between MALAT1 and the microRNAs involved in this pathway.