Evaluation of the clinical significance of long non-coding RNA MALAT1 genetic variants in human lung adenocarcinoma

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  • Shu Hui Lin
  • Lu, Jeng-Wei
  • Wang Ting Hsieh
  • Ying Erh Chou
  • Tzu Cheng Su
  • Tun Jen Tsai
  • Yun Jung Tsai
  • Po Jen Yang
  • Shun Fa Yang

Lung adenocarcinoma (LUAD) is the most frequent histological subtype of lung cancer, which is the most common malignant tumor and the main cause of cancer-related mortality globally. Recent reports revealed that long non-coding RNA (lncRNA) of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a crucial role in tumorigenesis and metastasis development in lung cancer. However, the contribution of MALAT1 genetic variants to the development of LUAD is unclear, especially in epidermal growth factor receptor (EGFR) mutation status. In this study, 272 LADC patients with different EGFR status were recruited to dissect the allelic discrimination of the MALAT1 polymorphisms at rs3200401, rs619586, and rs1194338. The findings of the study showed that MALAT1 polymorphisms rs3200401, rs619586, and rs1194338 were not associated to LUAD susceptibility; however, rs3200401 polymorphisms was significantly correlated to EGFR wild-type status and tumor stages in LUAD patients in dominant model (p=0.016). Further analyses using the datasets from The Cancer Genome Atlas (TCGA) revealed that lower MALAT1 mRNA levels were associated with the advanced stage, and lymph node metastasis in LADC patients. In conclusion, our results showed that MALAT1 rs3200401 polymorphisms dramatically raised the probability of LUAD development.

OriginalsprogEngelsk
Artikelnummer100532
TidsskriftAging
Vol/bind16
Udgave nummer6
Sider (fra-til)5740-5750
Antal sider11
ISSN1945-4589
DOI
StatusUdgivet - 2024

Bibliografisk note

Publisher Copyright:
© 2024 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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