title: A newly characterized human endometrial adenocarcinoma cell line (CAC-1) differentiates in response to retinoic acid treatment.
abstract: A new cell line of poorly differentiated human endometrial adenocarcinoma cells termed "CAC-1" cells has been established. These cells are epithelial, as indicated by positive cytokeratin and negative vimentin staining. They are rounded and possess a high nuclear-to-cytoplasmic ratio, desmosomes, surface microvilli, intercelular lumens, and pleomorphic nuclei containing multiple nucleoli. These cells have been in long-term culture for 2 years. Our previous studies demonstrated that moderately differentiated (RL95-2) cells differentiated in response to retinoic acid treatment, illustrated by their reorganization of actin filaments and cell enlargement (Carter et al., 1996; Anticancer Res. 16, 17-24). CAC-1 cells exhibited a similar response because they also organized actin filaments and enlarged in response to retinoic acid treatment. Concurrently, retinoic acid treatment caused a 40% decrease in cell detachment in an in vitro detachment assay compared to controls. A slight lag in cell growth was observed when CAC-1 cells were treated with 1 microM 13-cis or all-trans retinoic acid during a 12-day growth curve. In addition, we examined the effects of retinoic acid on protein kinase C-alpha (PKC-alpha) and myristoylated alanine-rich C-kinase substrate (MARCKS). Treatment with retinoic acid caused cytoplasmic PKC-alpha to increase concomitant with a decrease in PKC-alpha in the membrane. In contrast, MARCKS increased in the membrane in response to retinoic acid treatment. These data indicate that retinoid treatment causes inactivation of PKC-alpha, allowing MARCKS to relocalize to the membrane, where it can cross-link actin filaments. CAC-1 cells represent an ideal model for investigating the effects of retinoids on differentiation induction concomitant with actin reorganization.
authors: Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA. charleatacarter@yahoo.com
authors: C A
authors: CA
authors: Carter
authors: V J
authors: VJ
authors: Madden
mesh_terms: D000199:Actins / Q000032:analysis; D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D015153:Blotting, Western; D002454:Cell Differentiation / Q000187:drug effects*; D048429:Cell Size; D002869:Chromosome Aberrations; D016889:Endometrial Neoplasms / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D004847:Epithelial Cells / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D047908:Intracellular Signaling Peptides and Proteins; D007527:Isoenzymes / Q000187:drug effects / Q000378:metabolism; D007621:Karyotyping; D008565:Membrane Proteins; D008854:Microscopy, Electron; D000076250:Myristoylated Alanine-Rich C Kinase Substrate; D011493:Protein Kinase C / Q000187:drug effects / Q000378:metabolism; D051571:Protein Kinase C-alpha; D011506:Proteins / Q000187:drug effects / Q000378:metabolism; D014212:Tretinoin / Q000494:pharmacology*; D014314:Trisomy; D014407:Tumor Cells, Cultured / Q000166:cytology / Q000187:drug effects* / Q000648:ultrastructure
chemical_list: D000199:Actins; D047908:Intracellular Signaling Peptides and Proteins; D007527:Isoenzymes; C000619710:MARCKS protein, human; D008565:Membrane Proteins; D011506:Proteins; D000076250:Myristoylated Alanine-Rich C Kinase Substrate; D014212:Tretinoin; C496628:PRKCA protein, human; D011493:Protein Kinase C; D051571:Protein Kinase C-alpha