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Gene expression profiling identifies ferroptosis-related genes and pathways in human colon cancers cell lines
M Balik-Meisner1, D Phadke1, D Mav1
1Sciome LLC, Durham, NC, United States.
Introduction:
Colorectal cancer (CRC) is the third most diagnosed cancer worldwide and the second leading cause of cancer-related deaths. A major challenge in CRC treatment is drug resistance, which limits the efficacy of conventional therapies. Ferroptosis, an iron-dependent form of regulated cell death driven by the accumulation of reactive oxygen species (ROS), has emerged as a promising therapeutic strategy. Erastin (ER), a small-molecule compound, induces ferroptosis through ROS accumulation.
Methods:
We performed microarray gene expression analysis on two CRC cell lines, HCT116 and HT-29, to examine the transcriptional response to ER exposure and identify differentially expressed genes and pathways involved in ER-induced ferroptosis.
Results:
Our gene expression analysis revealed distinct transcriptional profiles between the two cell lines, and 26 transcripts commonly enriched in response to ER treatment were identified in both HCT116 and HT-29 cells. Notably, several of these genes-including ASNS, PCK2, CHAC1, and DDIT4-were significantly enriched, suggesting a conserved ferroptotic response. The induction of these genes was further confirmed in an additional CRC cell line, DLD-1. Interestingly, SOD1 and NQO1 genes, involved in oxidative stress response, were significantly upregulated by ER in HCT116 cells.
Conclusion:
Our findings highlight ASNS, CHAC1, PCK2, DDIT4, and ATF3/4 as potential biomarkers for ferroptosis in CRC. Monitoring the expression of these genes may help identify patients who are responsive to ferroptosis inducers and facilitate the development of personalized treatment strategies.
Insights
Erastin induces ferroptosis in colorectal cancer (CRC) cells by altering gene expression. Key genes like ASNS and CHAC1 may serve as biomarkers for personalized CRC treatment strategies.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Colorectal cancer (CRC) is a leading cause of cancer death worldwide.
- Drug resistance poses a significant challenge in CRC treatment.
- Ferroptosis, an iron-dependent cell death pathway, offers a novel therapeutic avenue.
Purpose of the Study:
- To investigate the transcriptional response of CRC cells to Erastin (ER).
- To identify genes and pathways involved in ER-induced ferroptosis.
- To explore potential biomarkers for ferroptosis response in CRC.
Main Methods:
- Microarray gene expression analysis was performed on two CRC cell lines (HCT116 and HT-29).
- Transcriptional profiles were analyzed to identify differentially expressed genes upon ER treatment.
- Gene expression changes were validated in an additional CRC cell line (DLD-1).
Main Results:
- Distinct transcriptional profiles were observed between HCT116 and HT-29 cells.
- Twenty-six transcripts were commonly enriched in both cell lines following ER treatment.
- Genes such as ASNS, PCK2, CHAC1, and DDIT4 were significantly upregulated, indicating a conserved ferroptotic response.
Conclusions:
- ASNS, CHAC1, PCK2, DDIT4, and ATF3/4 are potential biomarkers for ferroptosis in CRC.
- Monitoring these gene expressions could aid in identifying patients responsive to ferroptosis inducers.
- These findings support the development of personalized treatment strategies for CRC.
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