Death-Associated Protein Kinase 1 Inhibits Progression of Thyroid Cancer by Regulating Stem Cell Markers

The activation of metastatic reprogramming is vital for cancer metastasis, but little is known about its mechanism. This study investigated the potential role of death-associated protein kinase 1 (DAPK1) in thyroid cancer progression. We generated knockdown (KD) DAPK1 using siRNA or shRNA in 8505C a...

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Autores principales:	Mi-Hyeon You, Woo Kyung Lee, Meihua Jin, Dong Eun Song, Sheue-yann Cheng, Tae Yong Kim, Won Bae Kim, Min Ji Jeon, Won Gu Kim
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	<i>DAPK1</i> thyroid cancer neoplastic stem cells tumor suppressor Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/7d14c5ee76f3475d887debc1f60cb4d3
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spelling	oai:doaj.org-article:7d14c5ee76f3475d887debc1f60cb4d32021-11-25T17:10:14ZDeath-Associated Protein Kinase 1 Inhibits Progression of Thyroid Cancer by Regulating Stem Cell Markers10.3390/cells101129942073-4409https://doaj.org/article/7d14c5ee76f3475d887debc1f60cb4d32021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/2994https://doaj.org/toc/2073-4409The activation of metastatic reprogramming is vital for cancer metastasis, but little is known about its mechanism. This study investigated the potential role of death-associated protein kinase 1 (DAPK1) in thyroid cancer progression. We generated knockdown (KD) DAPK1 using siRNA or shRNA in 8505C and KTC-1 cell lines, which we transiently or stably overexpressed in MDA-T32 and BCPAP cell lines. DAPK1 KD in 8505C and KTC-1 cells significantly increased cell proliferation and colony formation compared with controls. We observed significant inhibition of cancer cell invasion in cells overexpressing DAPK1, but the opposite effect in KD cells. Tumorsphere formation significantly increased after inhibition of DAPK1 expression in 8505C cells and was significantly suppressed in DAPK1-overexpressing MDA-T32 and BCPAP cells. DAPK1 overexpression inhibited mRNA and protein levels of stem markers (OCT4, Sox2, KLF4, and Nanog). Furthermore, the expression of these markers increased after KD of DAPK1 in 8505C cells. Mechanistic studies suggest that DAPK1 may modulate the expression of stem cell markers through the inhibition of β-catenin pathways. These findings were consistent with the public data and our thyroid tissue analysis, which showed higher DAPK1 expression was associated with advanced-stage papillary thyroid cancer with a higher stemness index and lower disease-free survival.Mi-Hyeon YouWoo Kyung LeeMeihua JinDong Eun SongSheue-yann ChengTae Yong KimWon Bae KimMin Ji JeonWon Gu KimMDPI AGarticle<i>DAPK1</i>thyroid cancerneoplastic stem cellstumor suppressorBiology (General)QH301-705.5ENCells, Vol 10, Iss 2994, p 2994 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	<i>DAPK1</i> thyroid cancer neoplastic stem cells tumor suppressor Biology (General) QH301-705.5
spellingShingle	<i>DAPK1</i> thyroid cancer neoplastic stem cells tumor suppressor Biology (General) QH301-705.5 Mi-Hyeon You Woo Kyung Lee Meihua Jin Dong Eun Song Sheue-yann Cheng Tae Yong Kim Won Bae Kim Min Ji Jeon Won Gu Kim Death-Associated Protein Kinase 1 Inhibits Progression of Thyroid Cancer by Regulating Stem Cell Markers
description	The activation of metastatic reprogramming is vital for cancer metastasis, but little is known about its mechanism. This study investigated the potential role of death-associated protein kinase 1 (DAPK1) in thyroid cancer progression. We generated knockdown (KD) DAPK1 using siRNA or shRNA in 8505C and KTC-1 cell lines, which we transiently or stably overexpressed in MDA-T32 and BCPAP cell lines. DAPK1 KD in 8505C and KTC-1 cells significantly increased cell proliferation and colony formation compared with controls. We observed significant inhibition of cancer cell invasion in cells overexpressing DAPK1, but the opposite effect in KD cells. Tumorsphere formation significantly increased after inhibition of DAPK1 expression in 8505C cells and was significantly suppressed in DAPK1-overexpressing MDA-T32 and BCPAP cells. DAPK1 overexpression inhibited mRNA and protein levels of stem markers (OCT4, Sox2, KLF4, and Nanog). Furthermore, the expression of these markers increased after KD of DAPK1 in 8505C cells. Mechanistic studies suggest that DAPK1 may modulate the expression of stem cell markers through the inhibition of β-catenin pathways. These findings were consistent with the public data and our thyroid tissue analysis, which showed higher DAPK1 expression was associated with advanced-stage papillary thyroid cancer with a higher stemness index and lower disease-free survival.
format	article
author	Mi-Hyeon You Woo Kyung Lee Meihua Jin Dong Eun Song Sheue-yann Cheng Tae Yong Kim Won Bae Kim Min Ji Jeon Won Gu Kim
author_facet	Mi-Hyeon You Woo Kyung Lee Meihua Jin Dong Eun Song Sheue-yann Cheng Tae Yong Kim Won Bae Kim Min Ji Jeon Won Gu Kim
author_sort	Mi-Hyeon You
title	Death-Associated Protein Kinase 1 Inhibits Progression of Thyroid Cancer by Regulating Stem Cell Markers
title_short	Death-Associated Protein Kinase 1 Inhibits Progression of Thyroid Cancer by Regulating Stem Cell Markers
title_full	Death-Associated Protein Kinase 1 Inhibits Progression of Thyroid Cancer by Regulating Stem Cell Markers
title_fullStr	Death-Associated Protein Kinase 1 Inhibits Progression of Thyroid Cancer by Regulating Stem Cell Markers
title_full_unstemmed	Death-Associated Protein Kinase 1 Inhibits Progression of Thyroid Cancer by Regulating Stem Cell Markers
title_sort	death-associated protein kinase 1 inhibits progression of thyroid cancer by regulating stem cell markers
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/7d14c5ee76f3475d887debc1f60cb4d3
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Death-Associated Protein Kinase 1 Inhibits Progression of Thyroid Cancer by Regulating Stem Cell Markers

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