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Cellular Adhesion Promotes Prostate Cancer Cells Escape from Dormancy

Fig 4

Constitutive activation of MLCK promotes proliferation of LuCaP PDX cells via upregulation of CDK6.

A) LuCaP cells were infected with lentivirus containing A-tMK (constitutively activate MLCK) showed positive Ki67 staining, whereas cells transduced with an empty vector did not. B) In LuCaP 86.2, 92, and 93, ectopic expression of A-tMK induced an upregulation of CDK6 and a concurrent downregulation of E2F4 when compared to that of the empty vector-transduced cells. Inhibition of MLCK with the MLCK inhibitor ML-7 suppressed proliferation by C) abolishing Ki67 expression, D) decreasing cell viability assessed by WST-1 assay and E) downregulating CDK6 expression. E2F4 expression was not altered by the ML-7. Green, EpCAM; Red, Ki67; Blue, DAPI. Magnification: 200x. Scale bar: 20 μm. **p< 0.01 as compared to the DMSO control. CDK6: cyclin-dependent kinase 6; E2F4: E2F transcription factor 4.

Fig 4

doi: https://doi.org/10.1371/journal.pone.0130565.g004