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NLK的表达在功能上与结直肠癌(CRC)相关。

The expression of NLK is functionally associated with colorectal cancers (CRC).

作者信息

Chen Xinyan, Zhou Yifan, Wan Yufeng, Chen Tingting, Zhu Huaqing, Cheng Xiaowen

机构信息

Department of Clinical Laboratory, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China.

Department of Pathology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230036, China.

出版信息

J Cancer. 2021 Oct 17;12(23):7088-7100. doi: 10.7150/jca.62526. eCollection 2021.

DOI:10.7150/jca.62526
PMID:34729110
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8558666/
Abstract

The regulatory mechanism of NLK in the carcinomagenesis and progression of colorectal cancer (CRC) remains unclear. Here, we identified a single nucleotide polymorphism (SNP) site of NLK (rs2125846) as a new susceptibility locus for CRC risk located within an intron of the human NLK gene in a Chinese population. NLK downregulation led to a decrease in the ability of proliferation and migration of RKO cells . The proportion of RKO apoptotic cells increased by interfering with the endogenous expression of NLK. We speculate that LncRNA XIST may upregulate NLK expression by downregulating miR-92b-3p, thereby promote the development of CRC. These results provide important information for the identification of novel potential targets for the prevention or treatment of CRC.

摘要

NLK在结直肠癌(CRC)发生发展中的调控机制尚不清楚。在此,我们在中国人群中鉴定出NLK的一个单核苷酸多态性(SNP)位点(rs2125846),它作为一个新的CRC风险易感位点,位于人类NLK基因的一个内含子内。NLK下调导致RKO细胞增殖和迁移能力下降。干扰NLK的内源性表达使RKO凋亡细胞比例增加。我们推测LncRNA XIST可能通过下调miR-92b-3p来上调NLK表达,从而促进CRC的发展。这些结果为识别预防或治疗CRC的新型潜在靶点提供了重要信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/71d4e7c5ff2a/jcav12p7088g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/7e4ad16b53c5/jcav12p7088g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/4b493353a0aa/jcav12p7088g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/4a78770e7777/jcav12p7088g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/15c1f4992cf3/jcav12p7088g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/9553f4641f85/jcav12p7088g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/71d4e7c5ff2a/jcav12p7088g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/7e4ad16b53c5/jcav12p7088g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/4b493353a0aa/jcav12p7088g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/4a78770e7777/jcav12p7088g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/15c1f4992cf3/jcav12p7088g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/9553f4641f85/jcav12p7088g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a800/8558666/71d4e7c5ff2a/jcav12p7088g006.jpg

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