Function of CSE1L/CAS in the secretion of HT-29 human colorectal cells and its expression in human colon

Tang Yi Tsao, Chin Shaw Stella Tsai, Jai Nien Tung, Shun Liang Chen, Chia Herng Yue, Ching Fong Liao, Chi Chao Wang, Ming Chung Jiang

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

The secretion of colorectal epithelium is important for maintaining the physiological function of colorectal organ. Herein, we report that cellular apoptosis susceptibility (CAS) (or CSE1L) protein regulates the secretion of HT-29 human colorectal cells. Polarity is essential for directed secretion of substances produced by epithelial cells to the external (luminal) compartment; CAS overexpression induced polarization of HT-29 cells. CAS was punctate stained in the cytoplasm of HT-29 cells, and CAS overexpression increased the translocation of CAS-stained vesicles to the cytoplasm near cell membrane and cell protrusions. CAS overexpression increased the secretion of carcinoembryonic antigen (CEA) and cathepsin D. Immunohistochemistry showed CAS was positively stained in the goblet cells of colon mucosa and cells in the crypts of Lieberkühn of human colon as well as the glands in metastatic colorectal cancer tissue. Our results suggest that CAS regulates the secretion of colorectal cells and may regulate the metastasis of colorectal cancer.

Original languageEnglish
Pages (from-to)163-170
Number of pages8
JournalMolecular and Cellular Biochemistry
Volume327
Issue number1-2
DOIs
Publication statusPublished - 2009

Keywords

  • CAS
  • Colon
  • Colorectal cancer
  • Polarity
  • Secretion

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Molecular Biology
  • Cell Biology

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    Tsao, T. Y., Tsai, C. S. S., Tung, J. N., Chen, S. L., Yue, C. H., Liao, C. F., Wang, C. C., & Jiang, M. C. (2009). Function of CSE1L/CAS in the secretion of HT-29 human colorectal cells and its expression in human colon. Molecular and Cellular Biochemistry, 327(1-2), 163-170. https://doi.org/10.1007/s11010-009-0054-0