# Evaluation of t-DARPP Expression Alteration in Association with DDR1 Expression in Non-Small Cell Lung Cancer

**Authors:** Zahra Damavandi, Pardis Riahi, Tayebeh Majidizadeh, Massoud Houshmand

PMC · DOI: 10.61186/ibj.3878 · 2023-06-24

## TL;DR

This study explores how DDR1 and t-DARPP expression changes in non-small cell lung cancer and suggests a potential new target for treatment.

## Contribution

The study reveals a novel link between DDR1 and t-DARPP expression in NSCLC, suggesting DDR1 as a potential therapeutic target.

## Key findings

- Collagen type I increases DDR1 expression in NSCLC cells.
- DDR1 upregulation significantly increases t-DARPP expression.
- DDR1 suppression significantly decreases t-DARPP expression.

## Abstract

DDR1 signaling plays a critical role in various cellular functions. Increased DDR1 expression has been shown in different human cancers. t-DARPP is a truncated isoform of DARPP-32, and its upregulation promotes cell survival and migration. Most lung cancer patients have NSCLC, and their survival rate is low. Therefore, it is necessary to study new and effective targeted therapies. Increased t-DARPP expression in NSCLC patients is associated with patient survival and can act as a prognostic marker correlated with increasing stages of NSCLC. The current study aimed to evaluate alteration in DDR1 expression and its effects on t-DARPP expression in NSCLC.

Two human lung adenocarcinoma cell lines, A549 and Calu-3, were treated with collagen type I and transfected with DDR1 siRNA. The relative expression of DDR1 and t-DARPP was evaluated using qRT-PCR.

The results indicated that collagen type I could stimulate DDR1 expression in NSCLC cells. Also, DDR1 upregulation resulted in a significant increase in t-DARPP expression. In contrast, suppression of DDR1 expression significantly decreased t-DARPP expression.

Our findings propose that modification in the expression of DDR1, caused by collagen type I and siRNA, might influence the expression of t-DARPP in NSCLC that is linked to NSCLC progression. Moreover, this alteration could potentially serve as an innovative target for therapeutic intervention.

## Linked entities

- **Genes:** DDR1 (discoidin domain receptor tyrosine kinase 1) [NCBI Gene 780], PPP1R1B (protein phosphatase 1 regulatory inhibitor subunit 1B) [NCBI Gene 84152]
- **Diseases:** non-small cell lung cancer (MONDO:0005233), NSCLC (MONDO:0005233)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** PPP1R1B (protein phosphatase 1 regulatory inhibitor subunit 1B) [NCBI Gene 84152] {aka DARPP-32, DARPP32}, DDR1 (discoidin domain receptor tyrosine kinase 1) [NCBI Gene 780] {aka CAK, CD167, DDR, EDDR1, HGK2, MCK10}
- **Diseases:** lung cancer (MESH:D008175), Non-Small Cell Lung Cancer (MESH:D002289), cancers (MESH:D009369), lung adenocarcinoma (MESH:D000077192)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** A549 — Homo sapiens (Human), Lung adenocarcinoma, Cancer cell line (CVCL_0023), Calu-3 — Homo sapiens (Human), Lung adenocarcinoma, Cancer cell line (CVCL_0609)

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC10994641/full.md

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Source: https://tomesphere.com/paper/PMC10994641