MKL-1 regulates the stem cell marker. CD44 in breast cancer cells

CD44, cluster of differentiation 44 is a typical marker of stem cells. At present, it has been found that CD44 is prevalent in various human malignant tumors, but its expression regulation mechanism is still not clear. The initiation of gene expression, the modification of RNA levels, and the regula...

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Main Authors: Dai Zhou-Tong, Yao Ao, Xiang Yuan, Li Jia Peng, Guo Wei, Zhang Hui-Min, Huang Feng, Li Han-Han, Zhang Zi-Jiang, Li Hui, Liao Xing Hua
Format: Article
Language:English
Published: EDP Sciences 2019-01-01
Series:E3S Web of Conferences
Online Access:https://doi.org/10.1051/e3sconf/20197801002
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spelling doaj-4c68fd88bda44731ba73a83d14b2bb752021-03-02T10:16:37ZengEDP SciencesE3S Web of Conferences2267-12422019-01-01780100210.1051/e3sconf/20197801002e3sconf_fsee2018_01002MKL-1 regulates the stem cell marker. CD44 in breast cancer cellsDai Zhou-TongYao AoXiang YuanLi Jia PengGuo WeiZhang Hui-MinZhang Hui-MinHuang FengLi Han-HanZhang Zi-JiangLi HuiLiao Xing HuaCD44, cluster of differentiation 44 is a typical marker of stem cells. At present, it has been found that CD44 is prevalent in various human malignant tumors, but its expression regulation mechanism is still not clear. The initiation of gene expression, the modification of RNA levels, and the regulation of protein levels are the main factors affecting the expression level of genes, and the most critical one is the regulation of gene expression by signaling pathways. Up to now, there has been no report on the role of MKL-1 in the cloning of the cd44 promoter. Therefore, this study intends to clone the cd44 gene promoter, construct its luciferase reporter gene vector, transfect the MKL-1 overexpression vector, and analyze how it affects transcriptional activity, in order to further study the expression regulation of cd44. The mechanism provides a powerful tool in the future.https://doi.org/10.1051/e3sconf/20197801002
collection DOAJ
language English
format Article
sources DOAJ
author Dai Zhou-Tong
Yao Ao
Xiang Yuan
Li Jia Peng
Guo Wei
Zhang Hui-Min
Zhang Hui-Min
Huang Feng
Li Han-Han
Zhang Zi-Jiang
Li Hui
Liao Xing Hua
spellingShingle Dai Zhou-Tong
Yao Ao
Xiang Yuan
Li Jia Peng
Guo Wei
Zhang Hui-Min
Zhang Hui-Min
Huang Feng
Li Han-Han
Zhang Zi-Jiang
Li Hui
Liao Xing Hua
MKL-1 regulates the stem cell marker. CD44 in breast cancer cells
E3S Web of Conferences
author_facet Dai Zhou-Tong
Yao Ao
Xiang Yuan
Li Jia Peng
Guo Wei
Zhang Hui-Min
Zhang Hui-Min
Huang Feng
Li Han-Han
Zhang Zi-Jiang
Li Hui
Liao Xing Hua
author_sort Dai Zhou-Tong
title MKL-1 regulates the stem cell marker. CD44 in breast cancer cells
title_short MKL-1 regulates the stem cell marker. CD44 in breast cancer cells
title_full MKL-1 regulates the stem cell marker. CD44 in breast cancer cells
title_fullStr MKL-1 regulates the stem cell marker. CD44 in breast cancer cells
title_full_unstemmed MKL-1 regulates the stem cell marker. CD44 in breast cancer cells
title_sort mkl-1 regulates the stem cell marker. cd44 in breast cancer cells
publisher EDP Sciences
series E3S Web of Conferences
issn 2267-1242
publishDate 2019-01-01
description CD44, cluster of differentiation 44 is a typical marker of stem cells. At present, it has been found that CD44 is prevalent in various human malignant tumors, but its expression regulation mechanism is still not clear. The initiation of gene expression, the modification of RNA levels, and the regulation of protein levels are the main factors affecting the expression level of genes, and the most critical one is the regulation of gene expression by signaling pathways. Up to now, there has been no report on the role of MKL-1 in the cloning of the cd44 promoter. Therefore, this study intends to clone the cd44 gene promoter, construct its luciferase reporter gene vector, transfect the MKL-1 overexpression vector, and analyze how it affects transcriptional activity, in order to further study the expression regulation of cd44. The mechanism provides a powerful tool in the future.
url https://doi.org/10.1051/e3sconf/20197801002
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