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Updated: Feb 5, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
Jinfukang induces cellular apoptosis through activation of
Jun Lu1, Jian Chen1, Yani Kang1,2
1Shanghai Center for Systems Biomedicine, School of Biomedical Engineering and Bio-ID Center, Shanghai Jiao Tong University, Shanghai 200240, P.R. China.
Abstract:
The traditional Chinese medicine Jinfukang (JFK) has been shown as a valuable drug to treat non-small cell lung cancer (NSCLC). Previously, it was reported that JFK-induced epigenetic alteration is involved in anti-lung cancer activity. In the present study, the effect of JFK on lung cancer cell lines was examined with the aim to further understand the underlying mechanisms of JFK-induced anti-lung cancer activity by transcriptome profiling analysis. JFK was observed to decrease lung cancer cell viability and simultaneously induce cellular morphology alteration. Additionally, this causes cell cycle arrest and apoptosis in A549 cells. The present RNA-seq analysis identified 5,281 genes with differential expression (P<0.05). Gene ontology analysis indicated that genes involved in the cell cycle pathway are downregulated, including cyclin-dependent kinase 2, cyclin-dependent kinase 4, cyclin B1 and cyclin A2, and apoptosis-associated genes are upregulated, including Fas, death receptor 4 (DR4), tumor protein P53 binding protein 2 and BCL2 interacting protein 3 like. Particularly, the present results indicate knockdown of Fas and DR4 attenuates JFK-induced apoptosis in A549 cells. Overall, the present study suggests JFK induces cellular apoptosis through activation of Fas and DR4 in A549 cells and provides an insight for understanding the antitumor mechanisms of this Chinese traditional medicine.
Insights
Jinfukang (JFK), a traditional Chinese medicine, effectively reduces non-small cell lung cancer cell viability. JFK triggers apoptosis by activating Fas and death receptor 4 (DR4) in A549 cells, offering insights into its anti-cancer mechanisms.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Traditional Chinese medicine Jinfukang (JFK) shows promise for non-small cell lung cancer (NSCLC).
- Previous studies suggest JFK's anti-cancer effects involve epigenetic alterations.
- Understanding JFK's precise molecular mechanisms is crucial for its clinical application.
Purpose of the Study:
- To investigate the molecular mechanisms underlying Jinfukang's anti-cancer activity in lung cancer cell lines.
- To identify key genes and pathways affected by JFK treatment using transcriptome profiling.
- To elucidate JFK's role in inducing apoptosis and cell cycle arrest.
Main Methods:
- Transcriptome profiling (RNA-seq) was employed to analyze gene expression changes in A549 lung cancer cells treated with JFK.
- Gene ontology analysis was performed to identify significantly altered biological pathways.
- Gene knockdown experiments were conducted to validate the role of specific apoptosis-related genes.
Main Results:
- JFK significantly decreased lung cancer cell viability and altered cell morphology.
- JFK induced cell cycle arrest and apoptosis in A549 cells.
- RNA-seq identified 5,281 differentially expressed genes, with downregulation of cell cycle genes and upregulation of apoptosis-associated genes like Fas and death receptor 4 (DR4).
- Knockdown of Fas and DR4 partially abrogated JFK-induced apoptosis.
Conclusions:
- Jinfukang induces apoptosis in non-small cell lung cancer cells, specifically A549, through the activation of Fas and DR4.
- JFK's anti-cancer effects are mediated by the modulation of cell cycle and apoptosis pathways.
- This study provides valuable insights into the antitumor mechanisms of Jinfukang as a traditional Chinese medicine for NSCLC treatment.
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