ISSN: 1837-9664Journal of Cancer
Global reach, higher impact
J Cancer 2018; 9(17):3177-3186. doi:10.7150/jca.24756 This issue Cite
Research Paper
Alternative Splicing of SMAD4 and Its Function in HaCaT Cells in Response to UVB Irradiation
1. Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400044, China
2. Department of Cardiothoracic Surgery, Southwest Hospital, Third Military Medical University Chongqing, China
3. Department of Anesthesiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China
Citation:
Ullah I, Liao Y, Wan R, Tang L, Feng J. Alternative Splicing of SMAD4 and Its Function in HaCaT Cells in Response to UVB Irradiation. J Cancer 2018; 9(17):3177-3186. doi:10.7150/jca.24756. https://www.jcancer.org/v09p3177.htm
Other stylesAbstract
Alternative splicing is one of the most common mechanisms of human gene regulation and plays a crucial role in increasing the diversity of functional proteins. Many diseases are linked to alternative splicing, especially cancer. SMAD4 is a member of the SMAD family and plays a critical role in mediating of TGF-β signal transduction and gene regulatory events. Smad4 is a tumour suppressor and acts as a shuttling protein between nucleus and cytoplasm. The splicing variants of Smad4 have been found in many cancers. The present study performed nested PCR to detect alternative splicing of Smad4 in HaCaT cells lines in response to UVB irradiation. The UVB induced a novel Smad4B isoform that led to decrease the Smad4 expression. The hnRNPA1 splicing factor is responsible for Smad4 alternative splicing in response to UVB. The UVB increased the expression of SF2 and hnRNPA1 Splicing factors. The hnRNPA1 overexpression induced Smad4B by regulating Smad4 alternative splicing. The Smad4B isoform supported the function of Smad4 full length in UVB resistance with certain limitation. The western blot analyses showed that the overexpressed Smad4 full length significantly increased N-cadherin expression while Smad4B overexpression decreased the expression the N-cadherin (P<0.05). Furthermore, overexpression of the isoform in HaCaT cells decreased cell invasion as compared to Smad4 full-length overexpression. These results will be helpful to understand the importance of Smad4 alternative splicing in skin tumorigenesis.
Keywords: Alternative splicing, Cancer, hnRNPA1, Proteins, Smad4, UVB
Citation styles
APA
Ullah, I., Liao, Y., Wan, R., Tang, L., Feng, J. (2018). Alternative Splicing of SMAD4 and Its Function in HaCaT Cells in Response to UVB Irradiation. Journal of Cancer, 9(17), 3177-3186. https://doi.org/10.7150/jca.24756.
ACS
Ullah, I.; Liao, Y.; Wan, R.; Tang, L.; Feng, J. Alternative Splicing of SMAD4 and Its Function in HaCaT Cells in Response to UVB Irradiation. J. Cancer 2018, 9 (17), 3177-3186. DOI: 10.7150/jca.24756.
NLM
Ullah I, Liao Y, Wan R, Tang L, Feng J. Alternative Splicing of SMAD4 and Its Function in HaCaT Cells in Response to UVB Irradiation. J Cancer 2018; 9(17):3177-3186. doi:10.7150/jca.24756. https://www.jcancer.org/v09p3177.htm
CSE
Ullah I, Liao Y, Wan R, Tang L, Feng J. 2018. Alternative Splicing of SMAD4 and Its Function in HaCaT Cells in Response to UVB Irradiation. J Cancer. 9(17):3177-3186.
This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.