{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T02:23:04Z","timestamp":1784600584920,"version":"3.55.0"},"reference-count":58,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2012,1,1]],"date-time":"2012-01-01T00:00:00Z","timestamp":1325376000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Investigative Medicine"],"published-print":{"date-parts":[[2012,1]]},"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Acquired immunodeficiency syndrome (AIDS)-related non-Hodgkin lymphoma (NHL) constitutes an aggressive variety of lymphomas characterized by increased extranodal involvement, relapse rate, and resistance to chemotherapy. Protein kinase C-beta (PKC\u03b2) targeting showed promising results in preclinical and clinical studies involving a wide variety of cancers, but studies describing the role of PKC\u03b2 in AIDS-NHL are primitive if not lacking.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In the present study, 3 AIDS-NHL cell lines were examined: 2F7 (AIDS\u2013Burkitt lymphoma), BCBL-1 (AIDS\u2013primary effusion lymphoma), and UMCL01-101 (AIDS\u2013diffuse large B-cell lymphoma).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Immunoblot analysis demonstrated expression of PKC\u03b21 and PKC\u03b22 in 2F7 and UMCL01-101 cells, and PKC\u03b21 alone in BCBL-1 cells. The viability of 2F7 and BCBL-1 cells decreased significantly in the presence of PKC\u03b2-selective inhibitor at half-maximal inhibitory concentration of 14 and 15 \u03bcmol\/L, respectively, as measured by tetrazolium dye reduction assay. In contrast, UMCL01-101 cells were relatively resistant. As determined using flow cytometric deoxynucleotidyl transferase dUTP nick-end labeling assay with propidium iodide staining, the responsiveness of sensitive cells was associated with apoptotic induction and cell cycle inhibition. Protein kinase C-beta\u2013selective inhibition was observed not to affect AKT phosphorylation but to induce a rapid and sustained reduction in the phosphorylation of glycogen synthase kinase-3 beta, ribosomal protein S6, and mammalian target of rapamycin in sensitive cell lines.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The results indicate that PKC\u03b2 plays an important role in AIDS-related NHL survival and suggest that PKC\u03b2 targeting should be considered in a broader spectrum of NHL. The observations in BCBL-1 were unexpected in the absence of PKC\u03b22 expression and implicate PKC\u03b21 as a regulator in those cells.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2310\/jim.0b013e318237eb55","type":"journal-article","created":{"date-parts":[[2016,5,11]],"date-time":"2016-05-11T09:10:57Z","timestamp":1462957857000},"page":"29-38","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":8,"title":["Protein Kinase C-Beta Inhibition Induces Apoptosis and Inhibits Cell Cycle Progression in Acquired Immunodeficiency Syndrome\u2013Related Non-Hodgkin Lymphoma Cells"],"prefix":"10.1177","volume":"60","author":[{"given":"Nakhle S.","family":"Saba","sequence":"first","affiliation":[{"name":"Section of Hematology and Medical Oncology, Department of Medicine"},{"name":"Tulane Cancer Center, Tulane University School of Medicine, New Orleans, 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