Related Experiment Video
Updated: Dec 17, 2025
Colorectal Cancer Cell Surface Protein Profiling Using an Antibody Microarray and Fluorescence Multiplexing
Published on: September 25, 2011
Microarray Analysis of Gene Expression Involved in Butyrate-Resistant Colorectal Carcinoma HCT116 Cells
Chakkraphong Khonthun1, Nongluk Saikachain1, Siam Popluechai2,3
1Department of Biochemistry, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand.
Background:
Resistance to chemotherapeutic agents is usually found in cancer stem cells (CSCs) and cancer stem-like cells that are often regarded as the target for cancer monitoring. However, the different patterns of their transcriptomic profiling is still unclear.
Objective:
This study aims to illustrate the transcriptomic profile of CSCs and butyrate-resistant colorectal carcinoma cells (BR-CRCs), by comparing them with parental colorectal cancer (CRC) cells in order to identify distinguishing transcription patterns of the CSCs and BR-CRCs.
Methods:
Parental CRC cells HCT116 (HCT116-PT) were cultured and induced to establish the butyrate resistant cell model (HCT116-BR). Commercial enriching of the HCT116-CSCs were grown in a tumorsphere suspension culture, which was followed firstly by the assessment of butyrate tolerance using MTT and PrestoBlue. Then their gene expression profiling was analyzed by microarray.
Results:
The results showed that both butyrate-resistant HCT116 cells (HCT116-BR) and HCT116-CSCs were more tolerant a butyrate effects than HCT116-PT cells. Differentially expressed gene profiles exhibited that IFI27, FOXQ1, PRF1, and SLC2A3 genes were increasingly expressed in CSCs, and were dramatically overexpressed in HCT116-BR cells when compared with HCT116-PT cells. Moreover, PKIB and LOC399959 were downregulated both in HCT116-CSCs and HCT116-BR cells.
Conclusion:
Our findings shed light on the transcriptomic profiles of chemoresistant CRC cells. This data should be useful for further study to provide guidelines for clinical prognosis to determine the guidelines for CRC treatment, especially in patients with chemoresistance and designing novel anti-neoplastic agents.
Insights
This study reveals distinct gene expression patterns in chemoresistant colorectal cancer cells, identifying key genes like IFI27 and FOXQ1 that are overexpressed in cancer stem cells and butyrate-resistant cells. These findings offer insights into chemoresistance mechanisms and potential therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Chemotherapeutic resistance in colorectal cancer (CRC) is often linked to cancer stem cells (CSCs).
- Transcriptomic differences between CSCs and chemoresistant cells remain largely uncharacterized.
- Understanding these profiles is crucial for effective cancer monitoring and treatment.
Purpose of the Study:
- To elucidate the transcriptomic profiles of CSCs and butyrate-resistant CRC cells (BR-CRCs).
- To compare these profiles with parental CRC cells (HCT116-PT).
- To identify unique transcriptional patterns distinguishing CSCs and BR-CRCs.
Main Methods:
- Established a butyrate-resistant CRC cell model (HCT116-BR) from parental HCT116 cells.
- Enriched and cultured cancer stem cells (HCT116-CSCs) using tumorsphere suspension culture.
- Assessed butyrate tolerance and analyzed gene expression profiling via microarray.
Main Results:
- Both HCT116-BR and HCT116-CSCs exhibited increased tolerance to butyrate compared to HCT116-PT cells.
- Genes IFI27, FOXQ1, PRF1, and SLC2A3 were upregulated in CSCs and significantly overexpressed in HCT116-BR cells.
- Genes PKIB and LOC399959 were downregulated in both HCT116-CSCs and HCT116-BR cells.
Conclusions:
- The study illuminates transcriptomic profiles of chemoresistant CRC cells.
- Identified specific gene expression patterns associated with chemoresistance.
- Findings support further research for clinical prognosis, CRC treatment guidelines, and novel anti-neoplastic agent design, particularly for chemoresistant cases.
