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Updated: Jan 28, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
PADI4‑mediated epithelial‑mesenchymal transition in lung cancer cells
Meiyan Liu1, Yang Qu2, Xue Teng3
1Department of Internal Medicine, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150040, P.R. China.
Abstract:
Lung cancer is a complex disease involving multiple genetic and phenotypic alterations. As a histone modification enzyme, protein‑arginine deiminase type‑4 (PADI4) and its downstream signaling have been studied in the progression of a variety of types of human cancer, but data on PADI4‑mediated posttranslational modification in lung cancer are lacking. The aim of present study was to evaluate the expression of PADI4 and its associated molecular signaling in lung cancer metastasis. The results of the present study indicated that PADI4 was overexpressed in lung cancer cells, while knockdown of PADI4 could lead to attenuation of the lung cancer cell invasion and migration phenotype, which was further verified by determining the epithelial‑mesenchymal transition (EMT) marker proteins. Additionally, it was demonstrated that stable knockdown of PADI4 in A549 lung cancer cells resulted in a striking reduction of the EMT‑associated Snail1/mothers against decapentaplegic homolog 3/4 transcriptional complex, which was consistent with alterations in migratory and invasive phenotypes of A549 lung cancer cells. Therefore, PADI4‑mediated EMT transition is proposed to represent a novel mechanism underlying the epigenetic and phenotypic alterations in lung cancer cells, and the PADI4 associated signaling pathway may be a therapeutic target for treating lung cancer in a clinical setting.
Insights
Protein-arginine deiminase type-4 (PADI4) is overexpressed in lung cancer, driving cell invasion and migration. Targeting PADI4 may offer a new therapeutic strategy for lung cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Lung cancer involves complex genetic and phenotypic changes.
- Protein-arginine deiminase type-4 (PADI4) is implicated in various cancers, but its role in lung cancer metastasis is unclear.
Purpose of the Study:
- To investigate the expression of PADI4 and its associated signaling pathways in lung cancer metastasis.
- To determine the effect of PADI4 on lung cancer cell invasion, migration, and epithelial-mesenchymal transition (EMT).
Main Methods:
- Quantitative analysis of PADI4 expression in lung cancer cells.
- Knockdown of PADI4 in A549 lung cancer cells.
- Assessment of epithelial-mesenchymal transition (EMT) marker proteins.
- Analysis of the Snail1/mothers against decapentaplegic homolog 3/4 (SMAD3/4) transcriptional complex.
Main Results:
- PADI4 was found to be overexpressed in lung cancer cells.
- Knockdown of PADI4 significantly reduced lung cancer cell invasion and migration.
- PADI4 knockdown led to decreased expression of EMT markers and the Snail1/SMAD3/4 complex.
Conclusions:
- PADI4 promotes lung cancer cell metastasis through mediating EMT.
- PADI4-associated signaling represents a potential therapeutic target for lung cancer treatment.
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