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This study investigates the mRNA expression levels of E-Cadherin and Vimentin in the context of CK2β deletion across various cell lines, including HaCaT, MCF10A, ACHN, and MCF7. Using mock, wild type (WT), and ΔCK2β variants, alongside TGFβ1 treatment, we analyze how these genetic manipulations influence cellular adhesion and epithelial-mesenchymal transition markers. Our results highlight the significant role of CK2β in the regulation of key mRNA levels, potentially linking it to cancer metastasis and the epithelial phenotype.
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10µm 10µm A HaCaT Fig.S3 E-Cadherin WT ΔCK2β Mock WT+TGFβ1 N-Cadherin WT ΔCK2β ΔCK2β /HA Mock WT+TGFβ1
B: HaCaT C: MCF10A Fig. S3 1.2 E-cadherin mRNA level E-cadherin mRNA level 1.0 1.2 1.0 0.8 0.8 0.6 0.6 0.4 0.4 0.2 0.2 0 0 WT ΔCK2β Mock WT ΔCK2β Mock 5 14 12 4 10 3 8 6 2 4 1 2 0 1.2 1.2 CK2β mRNA level CK2β mRNA level 1.0 1.0 0.8 0.8 0.6 0.6 0.4 0.4 0.2 0.2 0 0 WT ΔCK2β Mock WT ΔCK2β Mock Vimentin mRNA level Vimentin mRNA level 0 WT ΔCK2β Mock WT ΔCK2β Mock
D: ACHN E: MCF7 Fig. S3 2.5 2.0 1.5 1.0 0.5 0 WT Mock ΔCK2β 1.2 1.2 CK2β mRNA level CK2β mRNA level 1.0 1.0 0.8 0.8 0.6 0.6 0.4 0.4 0.2 0.2 0 0 WT ΔCK2β Mock WT ΔCK2β Mock 1.4 1.2 E-cadherin mRNA level E-cadherin mRNA level 1.2 1.0 1.0 0.8 0.8 0.6 0.6 0.4 0.4 0.2 0.2 0 0 WT ΔCK2β Mock WT ΔCK2β Mock Vimentin mRNA level Vimentin mRNA level 2.2 2.0 1.8 1.6 1.4 1.2 1.0 0.8 0.6 0.4 0.2 0 WT ΔCK2β Mock
