Sodium Butyrate Induces Apoptosis of Human Colon Cancer Cells by Modulating ERK and Sphingosine Kinase 2

XIAO Min; LIU Yun Gang; ZOU Meng Chen; ZOU Fei

doi:10.3967/bes2014.040

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Volume 27 Issue 3

Mar. 2014

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Article Navigation > Biomedical and Environmental Sciences > 2014 > 27(3): 197-203

XIAO Min, LIU Yun Gang, ZOU Meng Chen, ZOU Fei. Sodium Butyrate Induces Apoptosis of Human Colon Cancer Cells by Modulating ERK and Sphingosine Kinase 2[J]. Biomedical and Environmental Sciences, 2014, 27(3): 197-203. doi: 10.3967/bes2014.040

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XIAO Min, LIU Yun Gang, ZOU Meng Chen, ZOU Fei. Sodium Butyrate Induces Apoptosis of Human Colon Cancer Cells by Modulating ERK and Sphingosine Kinase 2[J]. Biomedical and Environmental Sciences, 2014, 27(3): 197-203. doi: 10.3967/bes2014.040

Sodium Butyrate Induces Apoptosis of Human Colon Cancer Cells by Modulating ERK and Sphingosine Kinase 2

doi: 10.3967/bes2014.040

Department of 0ccupational Health and 0ccupational Medicine, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou 510515, Guangdong, China
Department of Toxicology, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou 510515, Guangdong, China
Department of Endocrinology, Nanfang Hospital, Guangzhou 510515, Guangdong, China

Funds: National Natural Science Foundation of China(81272180)%National Basic Research Program of China(2012CB518200)

Abstract

Objective To investigate the role of extracellular signal-regulated kinase (ERK) in apoptosis of human colon cancer (HCT116) cells.
Methods After the HCT116 cells were pretreated with specific ERK inhibitor (U0126) or specific siRNA and exposed to 10 mmol/L sodium butyrate (NaBT) for 24 h, their apoptosis was detected by flow cytometry, levels of SphK2 and ERK protein were measured by Western blot, and translocation of SphK2 was assayed by immunofluorescence microscopy.
Results The U0126 and siRNAs specific for SphK2 blocked the export of SphK2 from nuclei to cytoplasm and increased the apoptosis of HCT116 cells following NaBT exposure. Over-expression of PKD decreased NaBT-induced apoptosis of HCT116 cells, which was reversed by U0126. Furthermore, transfection of HCT116 cells with constitutively activated PKD plasmids recovered the U0126-blocked export of SphK2.
Conclusion ERK regulates the export of SphK2 and apoptosis of HCT116 cells by modulating PKD. Modulation of these molecules may help increase the sensitivity of colon cancer cells to the physiologic anti-colon cancer agent, NaBT.
- Sodium butyrate,
- Apoptosis,
- ERK,
- Sphingosine kinase 2,
- Colon caner
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通讯作者: 陈斌, bchen63@163.com

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沈阳化工大学材料科学与工程学院沈阳 110142

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Sodium Butyrate Induces Apoptosis of Human Colon Cancer Cells by Modulating ERK and Sphingosine Kinase 2

doi: 10.3967/bes2014.040

Department of 0ccupational Health and 0ccupational Medicine, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou 510515, Guangdong, China

Department of Toxicology, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou 510515, Guangdong, China

Department of Endocrinology, Nanfang Hospital, Guangzhou 510515, Guangdong, China

Funds: National Natural Science Foundation of China(81272180)%National Basic Research Program of China(2012CB518200)

Key words:

Abstract: Objective To investigate the role of extracellular signal-regulated kinase (ERK) in apoptosis of human colon cancer (HCT116) cells.
Methods After the HCT116 cells were pretreated with specific ERK inhibitor (U0126) or specific siRNA and exposed to 10 mmol/L sodium butyrate (NaBT) for 24 h, their apoptosis was detected by flow cytometry, levels of SphK2 and ERK protein were measured by Western blot, and translocation of SphK2 was assayed by immunofluorescence microscopy.
Results The U0126 and siRNAs specific for SphK2 blocked the export of SphK2 from nuclei to cytoplasm and increased the apoptosis of HCT116 cells following NaBT exposure. Over-expression of PKD decreased NaBT-induced apoptosis of HCT116 cells, which was reversed by U0126. Furthermore, transfection of HCT116 cells with constitutively activated PKD plasmids recovered the U0126-blocked export of SphK2.
Conclusion ERK regulates the export of SphK2 and apoptosis of HCT116 cells by modulating PKD. Modulation of these molecules may help increase the sensitivity of colon cancer cells to the physiologic anti-colon cancer agent, NaBT.

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