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lncRNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression via miR-655-3p

Yuxin Zhao1, Zhaoxia Wang2, Meili Gao1

  • 1Department of Ophthalmology, Weihai Central Hospital, No. 3, Mishandongluxi, Wendeng District, Weihai, 264400, Shandong, China.

Open Medicine (Warsaw, Poland)
|July 5, 2021
PubMed

Insights

Long noncoding RNA MALAT1 acts as an oncogene in retinoblastoma (RB). It promotes RB progression by inhibiting miR-655-3p, leading to increased ATAD2 expression and tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is implicated as an oncogene in various cancers.
  • Retinoblastoma (RB) is a significant ocular malignancy where the role of MALAT1 requires further elucidation.

Purpose of the Study:

  • To investigate the functional role and underlying molecular mechanism of MALAT1 in retinoblastoma.
  • To explore the regulatory relationship between MALAT1, miR-655-3p, and ATAD2 in RB.

Main Methods:

  • Quantitative real-time PCR to assess MALAT1, miR-655-3p, and ATAD2 expression levels in RB tissues and cells.
  • In vitro assays including cell proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) assays following MALAT1 knockdown.
  • In vivo xenograft tumor growth assays in a mouse model.
  • Bioinformatic analysis and luciferase reporter assays to confirm the interaction between MALAT1, miR-655-3p, and ATAD2.

Main Results:

  • MALAT1 was significantly upregulated in RB tissues and cells compared to normal controls.
  • MALAT1 acted as a competing endogenous RNA (ceRNA), sponging miR-655-3p and consequently increasing the expression of its target, ATAD2.
  • MALAT1 depletion suppressed RB cell proliferation, metastasis, and EMT, induced apoptosis in vitro, and inhibited tumor growth in vivo.
  • miR-655-3p levels were decreased, while ATAD2 levels were increased in RB tissues and cells.

Conclusions:

  • MALAT1 functions as an oncogene in retinoblastoma by regulating the miR-655-3p/ATAD2 axis.
  • Targeting the MALAT1/miR-655-3p/ATAD2 pathway presents a potential therapeutic strategy for retinoblastoma.
Keywords:
ATAD2MALAT1miR-655-3pretinoblastomatumor progression

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