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Updated: Dec 26, 2025

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
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Published on: March 27, 2020

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The long non-coding RNA PIK3CD-AS2 promotes lung adenocarcinoma progression via YBX1-mediated suppression of p53

Xiufen Zheng1,2, Junying Zhang3, Tian Fang4

  • 1Department of Thoracic Surgery, Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, 210009, China.

Oncogenesis
|March 14, 2020
PubMed

Insights

A novel long non-coding RNA, PIK3CD-AS2, promotes lung adenocarcinoma (LUAD) by stabilizing YBX1, inhibiting p53. Targeting PIK3CD-AS2 shows therapeutic potential, especially in p53 wild-type LUAD patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Mechanisms of long non-coding RNAs (lncRNAs) in lung cancer progression remain unclear.
  • Identifying novel regulatory pathways is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of the novel lncRNA PIK3CD antisense RNA 2 (PIK3CD-AS2) in lung adenocarcinoma (LUAD) progression.
  • To elucidate the underlying molecular mechanisms and evaluate therapeutic strategies targeting PIK3CD-AS2.

Main Methods:

  • Analysis of PIK3CD-AS2 expression in LUAD datasets (microarray, TCGA, GEO) and patient tissues.
  • In vitro studies on cell growth, apoptosis, and protein interactions (YBX1, p53).
  • In vivo xenograft and patient-derived tumor xenograft (PDTX) models to assess therapeutic efficacy of LNA targeting PIK3CD-AS2.

Main Results:

  • PIK3CD-AS2 is upregulated in LUAD and associated with shorter patient survival.
  • PIK3CD-AS2 enhances cell growth and inhibits apoptosis in p53 wild-type LUAD cells by stabilizing YBX1, which in turn destabilizes p53.
  • Targeting PIK3CD-AS2 with LNA demonstrated anti-tumor activity in preclinical models.

Conclusions:

  • PIK3CD-AS2 acts as a crucial regulator in LUAD progression through the PIK3CD-AS2/YBX1/p53 signaling axis.
  • PIK3CD-AS2 represents a potential therapeutic target for LUAD, particularly in patients with wild-type p53.

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