Epithelial-Mesenchymal Molecular Interactions in Prostatic Tumor Cell Plasticity

Hendrix, Mary J.C.; Luo, Jun; Seftor, Elisabeth A.; Sharma, Navesh K.; HeidgerJr., Paul M.; Cohen, Michael B.; Bhatty, Robert; Chungthapong, Jirapat; Seftor, Richard E.B.; Lubaroff, David M.

doi:10.1007/978-1-4020-5847-9_7

Cited by 2 publications

(2 citation statements)

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“…ccRCC cells were treated with four final concentrations of Ukrain (5,10,20, and 40 mmol/l) for 24 and 48 h in serum-free medium. Untreated cultures served as controls.…”

Section: Ukrain Preparation and Treatmentmentioning

confidence: 99%

“…The de-novo expression of vimentin is a molecular marker frequently associated with EMT and the metastatic conversion of epithelial cells. Moreover, a correlation between vimentin expression and a perturbation of E-cadherin-mediated cell adhesion has been evidenced [5]. EMT plays a pivotal role rendering tumor cells invasive and metastatic [3,4].…”

Section: Introductionmentioning

confidence: 99%

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Malignant phenotype of renal cell carcinoma cells is switched by Ukrain administration in vitro

Gagliano¹,

Pettinari²,

Aureli³

et al. 2011

Anti-Cancer Drugs

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aWe investigated whether Ukrain modulates the malignant phenotype of clear cell renal cell carcinoma (ccRCC) cells Caki-1, Caki-2, and ACHN treated with four doses (5, 10, 20, and 40 lmol/l) for 24 and 48 h. The epithelial-tomesenchymal transition markers E-cadherin, b-catenin, and vimentin were analyzed by immunofluorescence as well as actin and tubulin; matrix metalloproteinase-2 and matrix metalloproteinase-9 activity was analyzed by SDS-zymography, intracellular and secreted SPARC levels by western blot, and cell cycle by flow cytometry. Ukrain did not induce E-cadherin/b-catenin immunoreactivity at the cell-cell boundary, although it determined the actin cortical expression in Caki-2 and ACHN, and did not affect vimentin organization; however, in some Caki-1 and ACHN cells the perinuclear concentration of vimentin was consistent with its downregulation. Matrix metalloproteinase-2 and matrix metalloproteinase-9 activity was significantly downregulated 48 h after 20 lmol/l Ukrain administration. At this time point, Ukrain significantly decreased migration and invasion, and downregulated SPARC levels in cell supernatants at all doses in Caki-2, and at 20 lmol/l in Caki-1 and ACHN cells. Concomitantly, SPARC was upregulated in all ccRCC cells, suggesting that Ukrain could also affect cell proliferation by cell cycle inhibition, as supported by the cell cycle analysis, as SPARC also acts as a cell cycle inhibitor. Our results suggest that Ukrain may switch the epithelial-to-mesenchymal transition-related phenotype of ccRCC cells, and targets the two major aspects involved in RCC progression, such as tumor invasion/microenvironment remodeling and cell proliferation.

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“…ccRCC cells were treated with four final concentrations of Ukrain (5,10,20, and 40 mmol/l) for 24 and 48 h in serum-free medium. Untreated cultures served as controls.…”

Section: Ukrain Preparation and Treatmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%