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Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells
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Inhibition of ribosome assembly factor PNO1 by CRISPR/Cas9 technique suppresses lung adenocarcinoma and Notch

Sanjit K Roy1,2, Shivam Srivastava3, Andrew Hancock4

  • 1Louisiana State University Health-New Orleans, School of Medicine, Stanley S. Scott Cancer Center, New Orleans, Louisiana, USA.

Journal of Cellular and Molecular Medicine
|January 10, 2023
PubMed

Insights

The RNA-binding protein PNO1 is elevated in lung adenocarcinoma and linked to disease progression. Inhibiting PNO1 suppressed tumor growth, metastasis, and Notch signaling, suggesting PNO1 as a potential biomarker and therapeutic target.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Cellular growth relies on functional ribosomes, and cancer cells upregulate ribosome biogenesis to meet energy demands.
  • The RNA-binding protein PNO1 is a key factor in ribosome assembly.
  • Lung adenocarcinoma is a significant health concern, necessitating new diagnostic and therapeutic strategies.

Purpose of the Study:

  • To investigate PNO1 as a potential biomarker for lung adenocarcinoma.
  • To explore the molecular mechanisms by which PNO1 knockdown affects lung adenocarcinoma growth and epithelial-mesenchymal transition (EMT).

Main Methods:

  • Quantitative analysis of PNO1 expression in lung adenocarcinoma tissues versus normal tissues.
  • CRISPR/Cas9-mediated PNO1 knockdown to assess its impact on cell viability, colony formation, apoptosis, and EMT.
  • Analysis of PNO1 knockdown effects on the Notch signaling pathway and related gene expression.

Main Results:

  • PNO1 expression was significantly higher in lung adenocarcinoma tissues and correlated with advanced stage, nodal metastasis, smoking history, male sex, and Tp53 mutation status.
  • PNO1 knockdown inhibited cell viability, colony formation, and EMT, while inducing apoptosis.
  • PNO1 inhibition suppressed Notch signaling, including receptors, ligands, and downstream targets, as well as CCND1, p21, PTGS-2, IL-1α, IL-8, and CXCL-8 genes.

Conclusions:

  • PNO1 is upregulated in lung adenocarcinoma and associated with adverse prognostic factors.
  • PNO1 plays a crucial role in promoting lung adenocarcinoma growth, EMT, and Notch signaling.
  • PNO1 represents a promising diagnostic biomarker and a potential therapeutic target for lung adenocarcinoma.
Keywords:
CRISPR/Cas9EMTNotchPNO1biogenesislung adenocarcinoma

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