Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancer

BACKGROUND: Zinc finger RNA binding protein (ZFR) is involved in the regulation of growth and cancer development. However, little is known about ZFR function in pancreatic cancer. METHODS: Herein, to investigate whether ZFR is involved in tumor growth, Oncomine microarray data was firstly used to ev...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Zhao,Xiaolan, Chen,Man, Tan,Jishan
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2016
Materias:	Pancreatic cancer RNA interference Targeted therapy Zinc finger RNA binding protein
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602016000100026
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:scielo:S0716-97602016000100026
record_format	dspace
spelling	oai:scielo:S0716-976020160001000262016-12-01Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancerZhao,XiaolanChen,ManTan,Jishan Pancreatic cancer RNA interference Targeted therapy Zinc finger RNA binding protein BACKGROUND: Zinc finger RNA binding protein (ZFR) is involved in the regulation of growth and cancer development. However, little is known about ZFR function in pancreatic cancer. METHODS: Herein, to investigate whether ZFR is involved in tumor growth, Oncomine microarray data was firstly used to evaluate ZFR gene expression in human pancreatic tumors. Then short hairpin RNA (shRNA) targeting ZFR was designed and delivered into PANC-1 pancreatic cancer cells to knock down ZFR expression. Cell viability, cell proliferation and cell cycle analysis after ZFR knockdown were determined by MTT, colony forming and FACS, respectively. In addition, cell migration and invasion were assessed using the Transwell system. RESULTS: The expression of ZFR was significantly higher in pancreatic tumors than normal pancreas tissues by Oncomine database analysis. Knockdown of ZFR by shRNA-expressing lentivirus significantly decreased the viability and invasion ability of pancreatic cancer cells. Moreover, FACS analysis showed that knockdown of ZFR in PANC-1 cells caused a significant cell cycle arrest at G0/G1 phase. Furthermore, knockdown of ZFR decreased the levels of CDK2, CDK4, CyclinA and CyclinD1 and enhanced the expression of p27, which has evidenced by qRT-PCR and Western blot analysis. CONCLUSIONS: Knockdown of ZFR might provide a novel alternative to targeted therapy of pancreatic cancer and deserves further investigation.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.49 20162016-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602016000100026en10.1186/s40659-016-0086-3
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	Pancreatic cancer RNA interference Targeted therapy Zinc finger RNA binding protein
spellingShingle	Pancreatic cancer RNA interference Targeted therapy Zinc finger RNA binding protein Zhao,Xiaolan Chen,Man Tan,Jishan Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancer
description	BACKGROUND: Zinc finger RNA binding protein (ZFR) is involved in the regulation of growth and cancer development. However, little is known about ZFR function in pancreatic cancer. METHODS: Herein, to investigate whether ZFR is involved in tumor growth, Oncomine microarray data was firstly used to evaluate ZFR gene expression in human pancreatic tumors. Then short hairpin RNA (shRNA) targeting ZFR was designed and delivered into PANC-1 pancreatic cancer cells to knock down ZFR expression. Cell viability, cell proliferation and cell cycle analysis after ZFR knockdown were determined by MTT, colony forming and FACS, respectively. In addition, cell migration and invasion were assessed using the Transwell system. RESULTS: The expression of ZFR was significantly higher in pancreatic tumors than normal pancreas tissues by Oncomine database analysis. Knockdown of ZFR by shRNA-expressing lentivirus significantly decreased the viability and invasion ability of pancreatic cancer cells. Moreover, FACS analysis showed that knockdown of ZFR in PANC-1 cells caused a significant cell cycle arrest at G0/G1 phase. Furthermore, knockdown of ZFR decreased the levels of CDK2, CDK4, CyclinA and CyclinD1 and enhanced the expression of p27, which has evidenced by qRT-PCR and Western blot analysis. CONCLUSIONS: Knockdown of ZFR might provide a novel alternative to targeted therapy of pancreatic cancer and deserves further investigation.
author	Zhao,Xiaolan Chen,Man Tan,Jishan
author_facet	Zhao,Xiaolan Chen,Man Tan,Jishan
author_sort	Zhao,Xiaolan
title	Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancer
title_short	Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancer
title_full	Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancer
title_fullStr	Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancer
title_full_unstemmed	Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancer
title_sort	knockdown of zfr suppresses cell proliferation and invasion of human pancreatic cancer
publisher	Sociedad de Biología de Chile
publishDate	2016
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602016000100026
work_keys_str_mv	AT zhaoxiaolan knockdownofzfrsuppressescellproliferationandinvasionofhumanpancreaticcancer AT chenman knockdownofzfrsuppressescellproliferationandinvasionofhumanpancreaticcancer AT tanjishan knockdownofzfrsuppressescellproliferationandinvasionofhumanpancreaticcancer
_version_	1718441553059381248

Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancer

Ejemplares similares