p145 expression during the cell cycle in HL-60 cell line and normal human lymphocytes: effects of camptothecin, vinblastine, cycloheximide, actinomycin D, retinoic acid and DMSO.
Bivariate flow cytometric analysis of nucleolar antigen p145 was performed on quiescent and phytohemagglutinin-stimulated human lymphocytes and on a promyelocytic cell line (HL-60). Data were acquired on a FACScan flow cytometer and analyzed using LYSYS II. Quiescent lymphocytes did not express p145. PHA-stimulated proliferating lymphocytes expressed p145 maximally after 48 h, similarly to HL-60 cells in exponential growth. Antigen expression in G1 was notably heterogeneous in both cell types. The ratio of p145/DNA was highest in early S and decreased during mid and late S and remained low in G2M. p145 expression was lowest in M-phase cells treated for 6 h with vinblastine. Cycloheximide and actinomycin D had similar effects on p145 in HL-60 cells: expression of p145 gradually decreased from 1 to 6 h incubation in all phases of the cell cycle. Camptothecin did not decrease p145 expression and apoptotic cells from CAM-treated cultures still expressed p145. Retinoic acid and DMSO induced differentiation in HL-60 cells, and as this process progressed, p145 levels gradually fell until they approached isotype antibody control levels at 9 and 6 days, respectively. However, after 5 days treatment with 2 nM retinoic acid apoptotic cells appeared which still expressed p145. The data on drug treatment suggest that p145 exists in undifferentiated and proliferating cells and may not be a specific marker for malignancy, but may prove useful as a monitor of chemotherapeutic effects in cancer treatment.
Qiao
L
L
New York Medical College, Department of Pathology, Valhalla 10595.
Pizzolo
J G
JG
Gorczyca
W
W
Melamed
M R
MR
D034961:Antigens, Nuclear; D000970:Antineoplastic Agents / Q000494:pharmacology*; D002166:Camptothecin / Q000494:pharmacology; D002453:Cell Cycle; D002454:Cell Differentiation / Q000187:drug effects; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D005434:Flow Cytometry; D006801:Humans; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000276:immunology*; D009687:Nuclear Proteins / Q000032:analysis*; D014212:Tretinoin / Q000494:pharmacology; D014407:Tumor Cells, Cultured; D014747:Vinblastine / Q000494:pharmacology
D034961:Antigens, Nuclear; D000970:Antineoplastic Agents; D009687:Nuclear Proteins; D003609:Dactinomycin; D014212:Tretinoin; D014747:Vinblastine; D003513:Cycloheximide; D002166:Camptothecin; D004121:Dimethyl Sulfoxide