EIF1A depletion restrains human pituitary adenoma progression

EIF1A encodes a translation initiation factor in eukaryocyte and aberrant expression of EIF1A is deemed to be associated with dysfunctions in intracranial diseases. The goal of this research was to explore the impacts of EIF1A on progression of human pituitary adenoma (PA). We employed immunohistoch...

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Autores principales:	Rongxin Geng, Xiaonan Zhu, Xiang Tao, Junhui Liu, Haitao Xu
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2022
Materias:	EIF1A Pituitary adenoma Cell proliferation Cell migration MAPK Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/e478b3169a6f4665b81d33912ebe153e
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spelling	oai:doaj.org-article:e478b3169a6f4665b81d33912ebe153e2021-12-02T05:00:22ZEIF1A depletion restrains human pituitary adenoma progression1936-523310.1016/j.tranon.2021.101299https://doaj.org/article/e478b3169a6f4665b81d33912ebe153e2022-01-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S1936523321002904https://doaj.org/toc/1936-5233EIF1A encodes a translation initiation factor in eukaryocyte and aberrant expression of EIF1A is deemed to be associated with dysfunctions in intracranial diseases. The goal of this research was to explore the impacts of EIF1A on progression of human pituitary adenoma (PA). We employed immunohistochemistry to assess the expression of EIF1A in PA and para-carcinoma tissues. After constructing EIF1A-knockdown cell models via lentivirus infection, we examined cell proliferation through CCK-8 assay and Celigo cell counting assay. Flow cytometry was utilized to detect cell apoptosis and the migration ability of experimental cells was estimated using wound-healing assay and Transwell assay. The activity of the apoptosis-related factor, Caspase 3, was also examined via Caspase 3 activity assay. Lastly, in vivo xenograft mouse models were established to verify findings derived from in vitro cell models. Our results affirmed upregulation of EIF1A in PA cells and revealed that depletion of EIF1A could seriously limit cell proliferation and weaken the capacity of cell migration, and also enhance apoptosis of tumor cells. Mechanistically, degradation in cell growth mediated by EIF1A knockdown may involve in activation of MAPK signaling but inactivation of PI3K/AKT signaling pathway. This study indicates EIF1A plays a prominent role in facilitating tumor cell proliferation and migration which may further contribute to PA progression.Rongxin GengXiaonan ZhuXiang TaoJunhui LiuHaitao XuElsevierarticleEIF1APituitary adenomaCell proliferationCell migrationMAPKNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENTranslational Oncology, Vol 15, Iss 1, Pp 101299- (2022)
institution	DOAJ
collection	DOAJ
language	EN
topic	EIF1A Pituitary adenoma Cell proliferation Cell migration MAPK Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	EIF1A Pituitary adenoma Cell proliferation Cell migration MAPK Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Rongxin Geng Xiaonan Zhu Xiang Tao Junhui Liu Haitao Xu EIF1A depletion restrains human pituitary adenoma progression
description	EIF1A encodes a translation initiation factor in eukaryocyte and aberrant expression of EIF1A is deemed to be associated with dysfunctions in intracranial diseases. The goal of this research was to explore the impacts of EIF1A on progression of human pituitary adenoma (PA). We employed immunohistochemistry to assess the expression of EIF1A in PA and para-carcinoma tissues. After constructing EIF1A-knockdown cell models via lentivirus infection, we examined cell proliferation through CCK-8 assay and Celigo cell counting assay. Flow cytometry was utilized to detect cell apoptosis and the migration ability of experimental cells was estimated using wound-healing assay and Transwell assay. The activity of the apoptosis-related factor, Caspase 3, was also examined via Caspase 3 activity assay. Lastly, in vivo xenograft mouse models were established to verify findings derived from in vitro cell models. Our results affirmed upregulation of EIF1A in PA cells and revealed that depletion of EIF1A could seriously limit cell proliferation and weaken the capacity of cell migration, and also enhance apoptosis of tumor cells. Mechanistically, degradation in cell growth mediated by EIF1A knockdown may involve in activation of MAPK signaling but inactivation of PI3K/AKT signaling pathway. This study indicates EIF1A plays a prominent role in facilitating tumor cell proliferation and migration which may further contribute to PA progression.
format	article
author	Rongxin Geng Xiaonan Zhu Xiang Tao Junhui Liu Haitao Xu
author_facet	Rongxin Geng Xiaonan Zhu Xiang Tao Junhui Liu Haitao Xu
author_sort	Rongxin Geng
title	EIF1A depletion restrains human pituitary adenoma progression
title_short	EIF1A depletion restrains human pituitary adenoma progression
title_full	EIF1A depletion restrains human pituitary adenoma progression
title_fullStr	EIF1A depletion restrains human pituitary adenoma progression
title_full_unstemmed	EIF1A depletion restrains human pituitary adenoma progression
title_sort	eif1a depletion restrains human pituitary adenoma progression
publisher	Elsevier
publishDate	2022
url	https://doaj.org/article/e478b3169a6f4665b81d33912ebe153e
work_keys_str_mv	AT rongxingeng eif1adepletionrestrainshumanpituitaryadenomaprogression AT xiaonanzhu eif1adepletionrestrainshumanpituitaryadenomaprogression AT xiangtao eif1adepletionrestrainshumanpituitaryadenomaprogression AT junhuiliu eif1adepletionrestrainshumanpituitaryadenomaprogression AT haitaoxu eif1adepletionrestrainshumanpituitaryadenomaprogression
_version_	1718400862270783488

EIF1A depletion restrains human pituitary adenoma progression

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