Knockdown of GRHL3 Inhibits Activities and Induces Cell Cycle Arrest and Apoptosis of Human Colorectal Cancer Cells
The Grainyhead-like 3（GRHL3） is involved in epidermal barrier formation, neural tube closure and wound repair. Previous studies have suggested that GRHL3 has been linked to many different types of cancers. However, to date, its effects on human colorectal cancer（CRC） has not been clarified yet. Our...
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| Published in | Current medical science Vol. 37; no. 6; pp. 880 - 885 |
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| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
Wuhan
Huazhong University of Science and Technology
01.12.2017
Department of Oncology,Zhongnan Hospital of Wuhan University,Wuhan 430071,China%School of Clinical Medicine,Fenyang Medical College,Shanxi Medical University,Fenyang 032200,China%Department of General Surgery,Tongshan Renmin Hospital,Tongshan 437400,China |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1672-0733 2096-5230 1993-1352 1993-1352 2523-899X |
| DOI | 10.1007/s11596-017-1821-x |
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| Summary: | The Grainyhead-like 3（GRHL3） is involved in epidermal barrier formation, neural tube closure and wound repair. Previous studies have suggested that GRHL3 has been linked to many different types of cancers. However, to date, its effects on human colorectal cancer（CRC） has not been clarified yet. Our microarray analysis has indicated predominant GRHL3 expression in CRC. The purpose of this study was to investigate the expression and significance of GRHL3 in CRC tumorigenesis using CRC tissues and paired paracancerous tissues, as well as using distinct CRC cell lines（HT29 and DLD1）. We observed increased GRHL3 expression at both m RNA and protein levels in CRC tissues and CRC cell lines using quantitative real-time polymerase chain reaction（q RT-PCR） and Western blotting. Moreover, silencing GRHL3 with si RNA could suppress CRC cell proliferation, viability and migration in vitro. We also found that knockdown of GRHL3 could promote cell cycle arrest at G0/G1 phase in HT29 cells and DLD1 cells, and induce cell apoptosis in HT29 cells. Together, our study revealed the down-regulation of GRHL3 in vitro could inhibit CRC cell activity and trigger cell cycle arrest at G0/G1 phase and apoptosis. |
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| Bibliography: | The Grainyhead-like 3（GRHL3） is involved in epidermal barrier formation, neural tube closure and wound repair. Previous studies have suggested that GRHL3 has been linked to many different types of cancers. However, to date, its effects on human colorectal cancer（CRC） has not been clarified yet. Our microarray analysis has indicated predominant GRHL3 expression in CRC. The purpose of this study was to investigate the expression and significance of GRHL3 in CRC tumorigenesis using CRC tissues and paired paracancerous tissues, as well as using distinct CRC cell lines（HT29 and DLD1）. We observed increased GRHL3 expression at both m RNA and protein levels in CRC tissues and CRC cell lines using quantitative real-time polymerase chain reaction（q RT-PCR） and Western blotting. Moreover, silencing GRHL3 with si RNA could suppress CRC cell proliferation, viability and migration in vitro. We also found that knockdown of GRHL3 could promote cell cycle arrest at G0/G1 phase in HT29 cells and DLD1 cells, and induce cell apoptosis in HT29 cells. Together, our study revealed the down-regulation of GRHL3 in vitro could inhibit CRC cell activity and trigger cell cycle arrest at G0/G1 phase and apoptosis. Grainyhead-like 3 colorectal cancer proliferation migration cell cycle apoptosis 42-1679/R Xiao-kang WANG , Fen-fang ZHOU , Hao-ran TAO Xin WANG , Chi ZHANG, Fei SU, Shi-pei WANG , Li-hua XU , Xue-kai PAN 1, Mao-hui FENG , Wei XIE （1Department of Oncology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China 2School of Clinical Medicine, Fenyang Medical College, Shanxi Medical University, Fenyang 032200, China 3Department of General Surgery, Tongshan Renmin Hospital, Tongshan 437400, China） ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| ISSN: | 1672-0733 2096-5230 1993-1352 1993-1352 2523-899X |
| DOI: | 10.1007/s11596-017-1821-x |