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NKX2-1 的重新表达通过细胞凋亡和坏死诱导去分化甲状腺癌细胞死亡。

NKX2-1 re-expression induces cell death through apoptosis and necrosis in dedifferentiated thyroid carcinoma cells.

机构信息

Department of Laboratory Medicine, School of Medicine, Fukushima Medical University, Fukushima, Fukushima, Japan.

Third Department of Internal Medicine, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, Japan.

出版信息

PLoS One. 2021 Nov 8;16(11):e0259558. doi: 10.1371/journal.pone.0259558. eCollection 2021.

DOI:10.1371/journal.pone.0259558
PMID:34748583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8575255/
Abstract

NK2 homeobox 1 (NKX2-1) is a thyroid transcription factor essential for proper thyroid formation and maintaining its physiological function. In thyroid cancer, NKX2-1 expression decreases in parallel with declined differentiation. However, the molecular pathways and mechanisms connecting NKX2-1 to thyroid cancer phenotypes are largely unknown. This study aimed to examine the effects of NKX2-1 re-expression on dedifferentiated thyroid cancer cell death and explore the underlying mechanisms. A human papillary thyroid carcinoma cell line lacking NKX2-1 expression was infected with an adenoviral vector containing Nkx2-1. Cell viability decreased after Nkx2-1 transduction and apoptosis and necrosis were detected. Arginase 2 (ARG2), regulator of G protein signaling 4 (RGS4), and RGS5 mRNA expression was greatly increased in Nkx2-1-transducted cells. After suppressing these genes by siRNA, cell death, apoptosis, and necrosis decreased in RGS4 knockdown cells. These findings demonstrated that cell death was induced via apoptosis and necrosis by NKX2-1 re-expression and involves RGS4.

摘要

NK2 同源盒 1（NKX2-1）是甲状腺转录因子，对于甲状腺的正常形成和维持其生理功能至关重要。在甲状腺癌中，NKX2-1 的表达随着分化程度的降低而平行下降。然而，NKX2-1 与甲状腺癌表型之间的分子途径和机制在很大程度上尚不清楚。本研究旨在探讨 NKX2-1 再表达对去分化甲状腺癌细胞死亡的影响，并探讨其潜在机制。用人乳头状甲状腺癌细胞系感染含有 Nkx2-1 的腺病毒载体，使该细胞系缺乏 NKX2-1 的表达。Nkx2-1 转导后细胞活力下降，并检测到细胞凋亡和坏死。Nkx2-1 转导细胞中 ARG2、RGS4 和 RGS5 的 mRNA 表达显著增加。用 siRNA 抑制这些基因后，RGS4 敲低细胞中的细胞死亡、凋亡和坏死减少。这些发现表明，通过 NKX2-1 的再表达诱导细胞死亡，涉及 RGS4 导致细胞凋亡和坏死。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/33f189280f7a/pone.0259558.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/41ec4662898c/pone.0259558.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/56d1451f18a6/pone.0259558.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/8397a6320a6d/pone.0259558.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/54e1a66a12ca/pone.0259558.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/233f5d9fccf7/pone.0259558.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/33f189280f7a/pone.0259558.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/41ec4662898c/pone.0259558.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/56d1451f18a6/pone.0259558.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/8397a6320a6d/pone.0259558.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/54e1a66a12ca/pone.0259558.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/233f5d9fccf7/pone.0259558.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a6/8575255/33f189280f7a/pone.0259558.g006.jpg

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