TMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway

Abstract Transmembrane protein (TMEM) is a family of protein that spans cytoplasmic membranes and allows cell–cell and cell–environment communication. Dysregulation of TMEMs has been observed in multiple cancers. However, little is known about TMEM116 in cancer development. In this study, we demonst...

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Autores principales:	Suhong Zhang, Haiting Dai, Wenya Li, Runming Wang, Hanyu Wu, Ming Shen, Ye Hu, Lixin Xie, Yiming Xing
Formato:	article
Lenguaje:	EN
Publicado:	Nature Publishing Group 2021
Materias:	Cytology QH573-671
Acceso en línea:	https://doaj.org/article/932f2a4982f340baad1ead0b9e90513c
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spelling	oai:doaj.org-article:932f2a4982f340baad1ead0b9e90513c2021-11-21T12:03:34ZTMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway10.1038/s41419-021-04369-12041-4889https://doaj.org/article/932f2a4982f340baad1ead0b9e90513c2021-11-01T00:00:00Zhttps://doi.org/10.1038/s41419-021-04369-1https://doaj.org/toc/2041-4889Abstract Transmembrane protein (TMEM) is a family of protein that spans cytoplasmic membranes and allows cell–cell and cell–environment communication. Dysregulation of TMEMs has been observed in multiple cancers. However, little is known about TMEM116 in cancer development. In this study, we demonstrate that TMEM116 is highly expressed in non-small-cell lung cancer (NSCLC) tissues and cell lines. Inactivation of TMEM116 reduced cell proliferation, migration and invasiveness of human cancer cells and suppressed A549 induced tumor metastasis in mouse lungs. In addition, TMEM116 deficiency inhibited PDK1-AKT-FOXO3A signaling pathway, resulting in accumulation of TAp63, while activation of PDK1 largely reversed the TMEM116 deficiency induced defects in cancer cell motility, migration and invasive. Together, these results demonstrate that TMEM116 is a critical integrator of oncogenic signaling in cancer metastasis.Suhong ZhangHaiting DaiWenya LiRunming WangHanyu WuMing ShenYe HuLixin XieYiming XingNature Publishing GrouparticleCytologyQH573-671ENCell Death and Disease, Vol 12, Iss 12, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Cytology QH573-671
spellingShingle	Cytology QH573-671 Suhong Zhang Haiting Dai Wenya Li Runming Wang Hanyu Wu Ming Shen Ye Hu Lixin Xie Yiming Xing TMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway
description	Abstract Transmembrane protein (TMEM) is a family of protein that spans cytoplasmic membranes and allows cell–cell and cell–environment communication. Dysregulation of TMEMs has been observed in multiple cancers. However, little is known about TMEM116 in cancer development. In this study, we demonstrate that TMEM116 is highly expressed in non-small-cell lung cancer (NSCLC) tissues and cell lines. Inactivation of TMEM116 reduced cell proliferation, migration and invasiveness of human cancer cells and suppressed A549 induced tumor metastasis in mouse lungs. In addition, TMEM116 deficiency inhibited PDK1-AKT-FOXO3A signaling pathway, resulting in accumulation of TAp63, while activation of PDK1 largely reversed the TMEM116 deficiency induced defects in cancer cell motility, migration and invasive. Together, these results demonstrate that TMEM116 is a critical integrator of oncogenic signaling in cancer metastasis.
format	article
author	Suhong Zhang Haiting Dai Wenya Li Runming Wang Hanyu Wu Ming Shen Ye Hu Lixin Xie Yiming Xing
author_facet	Suhong Zhang Haiting Dai Wenya Li Runming Wang Hanyu Wu Ming Shen Ye Hu Lixin Xie Yiming Xing
author_sort	Suhong Zhang
title	TMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway
title_short	TMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway
title_full	TMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway
title_fullStr	TMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway
title_full_unstemmed	TMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway
title_sort	tmem116 is required for lung cancer cell motility and metastasis through pdk1 signaling pathway
publisher	Nature Publishing Group
publishDate	2021
url	https://doaj.org/article/932f2a4982f340baad1ead0b9e90513c
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TMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway

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