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Carcinoma invasion kinase - Europe PMC

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Last Updated: 03 February 2022

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Knockdown of STK39 suppressed cell proliferation, migration, and invasion in hepatocellular carcinoma by repressing the phosphorylation of mitogen-activated protein kinase p38.

Hepatocellular carcinoma is a common malignant tumor of the liver. STK39 expression was also increased in HCC patients and tissues, according to the qRT-PCR and western blot assay in this research. In addition, CCK-8 and colony formation assays reported that STK39's knockdown has stopped CCK-HEP-1 and Huh7 cell proliferation, which is also reported by CCK-8 and colony formation assays. In addition, wound healing assay and transwell assay confirmed that STK39's knockdown of SK-HEP-1 and Huh7 cells migration and invasion stopped. HCC tumor formation in vivo was slowed by the STK39's downfall in vivo.

Source link: https://europepmc.org/article/MED/34519635


Transcription factor specificity protein 1-mediated Serine/threonine kinase 39 upregulation promotes the proliferation, migration, invasion and epithelial-mesenchymal transition of hepatocellular carcinoma cells by activating the transforming growth factor-β1 /Smad2/3 pathway.

This study was designed to see if STK39 could be controlled by specificity protein 1 to influence HCC cells' malignant processes. Firstly, the expression of STK39 in tissues of HCC patients and several cell lines was determined. Cell proliferation was determined by methyl thiazolyl tetrazolium and colony formation assay after STK39 silencing, according to methyl thiazolyl tetrazolium and colony formation assay. Cell apoptosis was detected by Tunel staining. The increased expression of STK39, which was found in both HHC patients and HCC cell lines, was seen in poor HCC cell lines, causing poor HCC prognosis, according to the results. Cell proliferation, migration, emigration, migration, TIG, and TGF-1/Smad2/3 expressions were reduced by silencing but not cell apoptosis. In addition, SP1 could bind to the STK39 promoter and promote STK39 expression, as well as STK39 expression. SP1 overexpression blocked the effects of STK39 silencing on Hep3b cells, according to new reports. HCC progression can be reduced by therapies targeting SP1 to knock down STK39 expressions.

Source link: https://europepmc.org/article/MED/34281492

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions