Down-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis

Immunoglobulin γ-1 heavy chain constant region (IGHG1) is a functional isoform of immunoglobulins and plays an important role in the cytolytic activity of immune effector cells. Dysregulated IGHG1 was implicated in the occurrence and development of various tumors. Protoporphyrin IX (PpIX) is an endo...

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Autores principales:	Yang Guangjian, Li Gang, Du Xuemei, Zhou Wenting, Zou Xiaohong, Liu Yuanfu, Lv Hong, Li Zhenjiang
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2021
Materias:	ighg1 protoporphyrin ix hemin colorectal cancer mek-fech Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/c70cbe931e124d34880f49b5f651be22
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spelling	oai:doaj.org-article:c70cbe931e124d34880f49b5f651be222021-12-05T14:10:41ZDown-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis2391-541210.1515/biol-2021-0098https://doaj.org/article/c70cbe931e124d34880f49b5f651be222021-09-01T00:00:00Zhttps://doi.org/10.1515/biol-2021-0098https://doaj.org/toc/2391-5412Immunoglobulin γ-1 heavy chain constant region (IGHG1) is a functional isoform of immunoglobulins and plays an important role in the cytolytic activity of immune effector cells. Dysregulated IGHG1 was implicated in the occurrence and development of various tumors. Protoporphyrin IX (PpIX) is an endogenous fluorophore and is used in photodynamic therapy, which induces the generation of reactive oxygen species to initiate the death of tumor cells. However, the roles of IGHG1 in the colorectal cancer cell proliferation and PpIX accumulation have not been reported yet. Data from qRT-PCR and western blot analysis showed that IGHG1 was up-regulated in the colorectal cancer cells. Colorectal cancer cells were then transfected with shRNA targeting IGHG1 to down-regulate IGHG1 and conducted with Cell Counting Kit 8 (CCK8) and colony formation assays. Results demonstrated that shRNA-mediated down-regulation of IGHG1 decreased cell viability of colorectal cancer and suppressed cell proliferation. Moreover, PpIX accumulation was promoted and the hemin content was decreased by the silence of IGHG1. Interference of IGHG1 reduced the phosphorylated extracellular signal-regulated kinase (ERK) and ferrochelatase (FECH) expression, resulting in retarded cell proliferation in an MEK-FECH axis-dependent pathway.Yang GuangjianLi GangDu XuemeiZhou WentingZou XiaohongLiu YuanfuLv HongLi ZhenjiangDe Gruyterarticleighg1protoporphyrin ixhemincolorectal cancermek-fechBiology (General)QH301-705.5ENOpen Life Sciences, Vol 16, Iss 1, Pp 930-936 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	ighg1 protoporphyrin ix hemin colorectal cancer mek-fech Biology (General) QH301-705.5
spellingShingle	ighg1 protoporphyrin ix hemin colorectal cancer mek-fech Biology (General) QH301-705.5 Yang Guangjian Li Gang Du Xuemei Zhou Wenting Zou Xiaohong Liu Yuanfu Lv Hong Li Zhenjiang Down-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis
description	Immunoglobulin γ-1 heavy chain constant region (IGHG1) is a functional isoform of immunoglobulins and plays an important role in the cytolytic activity of immune effector cells. Dysregulated IGHG1 was implicated in the occurrence and development of various tumors. Protoporphyrin IX (PpIX) is an endogenous fluorophore and is used in photodynamic therapy, which induces the generation of reactive oxygen species to initiate the death of tumor cells. However, the roles of IGHG1 in the colorectal cancer cell proliferation and PpIX accumulation have not been reported yet. Data from qRT-PCR and western blot analysis showed that IGHG1 was up-regulated in the colorectal cancer cells. Colorectal cancer cells were then transfected with shRNA targeting IGHG1 to down-regulate IGHG1 and conducted with Cell Counting Kit 8 (CCK8) and colony formation assays. Results demonstrated that shRNA-mediated down-regulation of IGHG1 decreased cell viability of colorectal cancer and suppressed cell proliferation. Moreover, PpIX accumulation was promoted and the hemin content was decreased by the silence of IGHG1. Interference of IGHG1 reduced the phosphorylated extracellular signal-regulated kinase (ERK) and ferrochelatase (FECH) expression, resulting in retarded cell proliferation in an MEK-FECH axis-dependent pathway.
format	article
author	Yang Guangjian Li Gang Du Xuemei Zhou Wenting Zou Xiaohong Liu Yuanfu Lv Hong Li Zhenjiang
author_facet	Yang Guangjian Li Gang Du Xuemei Zhou Wenting Zou Xiaohong Liu Yuanfu Lv Hong Li Zhenjiang
author_sort	Yang Guangjian
title	Down-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis
title_short	Down-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis
title_full	Down-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis
title_fullStr	Down-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis
title_full_unstemmed	Down-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis
title_sort	down-regulation of ighg1 enhances protoporphyrin ix accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the mek-fech axis
publisher	De Gruyter
publishDate	2021
url	https://doaj.org/article/c70cbe931e124d34880f49b5f651be22
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Down-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis

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