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We studied the involvement of CD5L in liver cancer. Immunohistochemistry (IHC) of CD5L in 60 hepatocellular carcinomas and 34 adjacent nontumor livers, showed that CD5L staining was higher in tumor than in nontumor tissue (Mann\u2010Whitney test;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.0039). High CD5L correlated with elevated proliferation (Ki67, linear regression;\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.0001) and lower patient event\u2010free survival (log\u2010rank;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.0185). Accordingly, CD5L expression was detected in the liver cancer cell lines Huh7, HepG2, and SNU\u2010398.\n                    <jats:italic>In vitro<\/jats:italic>\n                    technologies using these cell lines, including small interfering RNA (siRN\n                    <jats:italic>A<\/jats:italic>\n                    ) and cDNA transfection, showed that CD5L promoted colony formation and cell proliferation and protected against cisplatin\u2010induced apoptosis. To find a molecular explanation for these roles, novel CD5L\u2010interacting protein ligands in liver cancer cells were identified by immunoprecipitation followed by mass spectrometry. Among these, the molecular chaperone of the unfolded protein response (UPR), heat shock protein (HSP)\u2010A5, was selected for validation. The interaction was confirmed by confocal microscopy in the Huh7 and HepG2 cell lines. Furthermore, functional experiments revealed that CD5L activates the UPR and autophagy mechanisms in Huh7 cells, thereby providing a novel molecular link between the UPR and autophagy in liver cancer.\u2014Aran, G., Sanjurjo, L., Barcena, C., Simon\u2010Coma, M., Tellez, E., Vazquez\u2010Vitali, M., Garrido, M., Guerra, L., D\u00edaz, E., Ojanguren, I., Elortza, F., Planas, R., Sala, M., Armengol, C., Sarrias, M.\u2010R. CD5L is upregulated in hepatocellular carcinoma and promotes liver cancer cell proliferation and antiapoptotic responses by binding to HSPA5 (GRP78). FASEB J. 32, 3878\u20133891 (2018).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201700941rr","type":"journal-article","created":{"date-parts":[[2018,2,20]],"date-time":"2018-02-20T16:31:56Z","timestamp":1519144316000},"page":"3878-3891","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["CD5L is upregulated in hepatocellular carcinoma and promotes liver cancer cell proliferation and antiapoptotic responses by binding to HSPA5 (GRP78)"],"prefix":"10.1096","volume":"32","author":[{"given":"Gemma","family":"Aran","sequence":"first","affiliation":[{"name":"Innate Immunity Group Health Sciences Research Institute Germans Trias i Pujol (IGTP) Badalona 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