Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell lines

Abstract Background: Phosphoribosylaminoimidazole carboxylase, phosphoribosylaminoimidazole succinocarboxamide synthetase (PAICS), an enzyme required for de novo purine biosynthesis, is associated with and involved in tumorigenesis. This study aimed to evaluate the role of PAICS in human breast can...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Meng,Minjun, Chen,Yanling, Jia,Jianbo, Li,Lianghui, Yang,Sumei
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2018
Materias:	Breast cancer PAICS Proliferation Cell cycle Cell apoptosis
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100220
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:scielo:S0716-97602018000100220
record_format	dspace
spelling	oai:scielo:S0716-976020180001002202018-09-05Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell linesMeng,MinjunChen,YanlingJia,JianboLi,LianghuiYang,Sumei Breast cancer PAICS Proliferation Cell cycle Cell apoptosis Abstract Background: Phosphoribosylaminoimidazole carboxylase, phosphoribosylaminoimidazole succinocarboxamide synthetase (PAICS), an enzyme required for de novo purine biosynthesis, is associated with and involved in tumorigenesis. This study aimed to evaluate the role of PAICS in human breast cancer, which remains the most frequently diagnosed cancer and the leading cause of cancer-related death among women in less developed countries. Results: Lentivirus-based short hairpin RNA targeting PAICS specifically depleted its endogenous expression in ZR-75-30 and MDA-MB-231 breast cancer cells. Depletion of PAICS led to a significant decrease in cell viability and proliferation. To ascertain the mechanisms through which PAICS modulates cell proliferation, flow cytometry was performed, and it was confirmed that G1-S transition was blocked in ZR-75-30 cells through PAICS knockdown. This might have occurred partly through the suppression of Cyclin E and the upregulation of Cyclin D1, P21, and CDK4. Moreover, PAICS knockdown obviously promoted cell apoptosis in ZR-75-30 cells through the activation of PARP and caspase 3 and downregulation of Bcl-2 and Bcl-xl expression in ZR-75-30 cells. Conclusions: These findings demonstrate that PAICS plays an essential role in breast cancer proliferation in vitro, which provides a new opportunity for discovering and identifying novel effective treatment strategies.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.51 20182018-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100220en10.1186/s40659-018-0172-9
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	Breast cancer PAICS Proliferation Cell cycle Cell apoptosis
spellingShingle	Breast cancer PAICS Proliferation Cell cycle Cell apoptosis Meng,Minjun Chen,Yanling Jia,Jianbo Li,Lianghui Yang,Sumei Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell lines
description	Abstract Background: Phosphoribosylaminoimidazole carboxylase, phosphoribosylaminoimidazole succinocarboxamide synthetase (PAICS), an enzyme required for de novo purine biosynthesis, is associated with and involved in tumorigenesis. This study aimed to evaluate the role of PAICS in human breast cancer, which remains the most frequently diagnosed cancer and the leading cause of cancer-related death among women in less developed countries. Results: Lentivirus-based short hairpin RNA targeting PAICS specifically depleted its endogenous expression in ZR-75-30 and MDA-MB-231 breast cancer cells. Depletion of PAICS led to a significant decrease in cell viability and proliferation. To ascertain the mechanisms through which PAICS modulates cell proliferation, flow cytometry was performed, and it was confirmed that G1-S transition was blocked in ZR-75-30 cells through PAICS knockdown. This might have occurred partly through the suppression of Cyclin E and the upregulation of Cyclin D1, P21, and CDK4. Moreover, PAICS knockdown obviously promoted cell apoptosis in ZR-75-30 cells through the activation of PARP and caspase 3 and downregulation of Bcl-2 and Bcl-xl expression in ZR-75-30 cells. Conclusions: These findings demonstrate that PAICS plays an essential role in breast cancer proliferation in vitro, which provides a new opportunity for discovering and identifying novel effective treatment strategies.
author	Meng,Minjun Chen,Yanling Jia,Jianbo Li,Lianghui Yang,Sumei
author_facet	Meng,Minjun Chen,Yanling Jia,Jianbo Li,Lianghui Yang,Sumei
author_sort	Meng,Minjun
title	Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell lines
title_short	Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell lines
title_full	Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell lines
title_fullStr	Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell lines
title_full_unstemmed	Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell lines
title_sort	knockdown of paics inhibits malignant proliferation of human breast cancer cell lines
publisher	Sociedad de Biología de Chile
publishDate	2018
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100220
work_keys_str_mv	AT mengminjun knockdownofpaicsinhibitsmalignantproliferationofhumanbreastcancercelllines AT chenyanling knockdownofpaicsinhibitsmalignantproliferationofhumanbreastcancercelllines AT jiajianbo knockdownofpaicsinhibitsmalignantproliferationofhumanbreastcancercelllines AT lilianghui knockdownofpaicsinhibitsmalignantproliferationofhumanbreastcancercelllines AT yangsumei knockdownofpaicsinhibitsmalignantproliferationofhumanbreastcancercelllines
_version_	1718441572849156096

Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell lines

Ejemplares similares