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lncRNA THAP7-AS1, transcriptionally activated by SP1 and post-transcriptionally stabilized by METTL3-mediated m6A

Hai-Ting Liu1,2, Yong-Xin Zou1, Wen-Jie Zhu1

  • 1Key Laboratory for Experimental Teratology of the Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, P.R. China.

Cell Death and Differentiation
|October 5, 2021
PubMed

Insights

This study reveals THAP7-AS1, a long noncoding RNA, promotes gastric cancer (GC) progression by enhancing CUL4B nuclear entry. Targeting THAP7-AS1 offers a potential therapeutic strategy for GC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Long noncoding RNAs (lncRNAs) are implicated in cancer, but their roles in gastric cancer (GC) are not fully understood.
  • Identifying novel molecular regulators is crucial for developing effective GC therapies.

Purpose of the Study:

  • To elucidate the function and mechanism of THAP7-AS1 in gastric cancer.
  • To investigate THAP7-AS1 as a potential therapeutic target for GC.

Main Methods:

  • lncRNA microarray analysis to identify differentially expressed lncRNAs in GC.
  • Investigation of transcriptional regulation by SP1 and m6A modification by METTL3.
  • Functional assays to assess the impact of THAP7-AS1 on GC cell progression and metastasis.
  • Mechanism studies involving protein-RNA interactions, nuclear import, and downstream signaling pathways.

Main Results:

  • THAP7-AS1 was significantly upregulated in GC tissues and correlated with poor prognosis and lymph node metastasis.
  • SP1 transcriptionally activated THAP7-AS1, while METTL3-mediated m6A modification enhanced its expression.
  • THAP7-AS1 promoted GC cell progression by facilitating CUL4B nuclear entry, leading to repression of miR-22-3p and miR-320a, and activation of the PI3K/AKT pathway.
  • Inhibition of THAP7-AS1 suppressed GC growth, invasion, and metastasis.

Conclusions:

  • THAP7-AS1 acts as an oncogene in gastric cancer through a novel mechanism involving CUL4B nuclear translocation.
  • THAP7-AS1 is a promising molecular target for GC therapy.

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