Abstract
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.
Highlights
CD44, cluster of differentiation 44 is a typical stem cell marker
Gastric adenocarcinoma highly expresses CD44, and multiple human gastric cancer cell lines (NCI-N87, AGS, MKN-28, MKN-45, MKN-74), it was found that CD44 is expressed in gastric cancer cells and used as a surface of gastric cancer stem cells Marker [12]
Some research has found that CD44+ and CD24+ cells were isolated from cancer tissues of 5 patients with gastric cancer
Summary
In the study of breast cancer, CD44 was first discovered and confirmed to be a solid tumor stem cell surface marker molecule [1]. CD44+/CD24+ can be used as markers for gastric cancer stem cells by comparing the self-renewal, differentiation and tumorigenicity of different phenotype tumor cells [13]. MKL-1 (MRTF-A, Myocardinrelated transcriptional factor) is a transcriptional regulator originally discovered as a transcriptional cofactor for the Serum response factor (SRF). It is involved in regulating the expression of smooth muscle cell-specific genes [14; 15]. In Prostate Cancer Cells, some research identified that one compound could block MKL transcription to inhibit prostate cancer cell invasion [18]. This study demonstrates that MKL-1 can promote the promoter activity of CD44 and lay the foundation for subsequent research
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