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Additional Supporting Information may be found in the online version of this article.

FilenameFormatSizeDescription
hep26597-sup-0001-suppfig1.tif4300KSupporting Fig. 1. Overactivation of the TGF-β pathway in HCC cells that show a mesenchymal-like phenotype. Correlation with higher production of TGF-β. (Complement to Fig. 1).
hep26597-sup-0002-suppfig2.tif1253KSupporting Fig. 2. CXCL12 increases the migratory capacity of SNU449 cells, whereas has no effect on HepG2 cells. (Complement to Fig. 2).
hep26597-sup-0003-suppfig3.tif4767KSupporting Fig. 3. Stable silencing of TGFBRI in PLC/PRF/5 induces reorganization of the cytoskeleton and attenuates expression and asymmetric distribution of CXCR4. (Complement to Fig. 3).
hep26597-sup-0004-suppfig4.tif951KSupporting Fig. 4. Effect of pharmacological inhibition of TGFBR1 kinase in the mesenchymal HCC cell lines. (Complement to Fig. 4).
hep26597-sup-0005-suppfig5.tif4171KSupporting Fig. 5. DEN treatment was used to induce HCC in mice. (Complement to Fig. 5).
hep26597-sup-0006-suppfig6.tif12580KSupporting Fig. 6. Higher expression of both TGFB1 and CXCR4 in tumor tissues correlates with differentiation stages III/IV (less differentiated phenotype) and a cirrhotic background in HCC patients. (Complement to Fig. 6).
hep26597-sup-0007-suppinfo1.doc51KSupporting Information
hep26597-sup-0008-suppinfo2.doc29KSupporting Information
hep26597-sup-0009-supptab1.doc37KSupplementary Table 1. Molecular characteristics of the human HCC cell lines used in this study.

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