Microarray Analysis of Gene Expression Involved in Butyrate-Resistant Colorectal Carcinoma HCT116 Cells

Khonthun, Chakkraphong; Saikachain, Nongluk; Popluechai, Siam; Kespechara, Kongkiat; Hiranyakas, Art; Srikummool, Metawee; Surangkul, Damratsamon

doi:10.31557/APJCP.2020.21.6.1739

Microarray Analysis of Gene Expression Involved in Butyrate-Resistant Colorectal Carcinoma HCT116 Cells

Document Type : Research Articles

Authors

¹ Department of Biochemistry, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand.

² School of Science, Mae Fah Luang University, Chaiang Rai, Thailand.

³ Gut microbiome research group, Mae Fah Luang University, Chaiang Rai, Thailand.

⁴ Bangkok Hospital Pattaya, Chonburi, Thailand.

⁵ Bangkok Hospital Phuket, Phuket, Thailand.

10.31557/APJCP.2020.21.6.1739

Abstract

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.

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