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首页> 外文OA文献 >Continuous suppression of globin gene expression and differentiation of Friend erythroleukemia cells by phorbol 12-myristate 13-acetate (PMA) despite the loss of PMA binding sites by down regulation.
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Continuous suppression of globin gene expression and differentiation of Friend erythroleukemia cells by phorbol 12-myristate 13-acetate (PMA) despite the loss of PMA binding sites by down regulation.

机译：佛波醇12-肉豆蔻酸酯13-醋酸酯（PMA）持续抑制球蛋白基因表达和Friend红白血病细胞分化，尽管下调导致PMA结合位点丢失。

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The tumor promoter phorbol 12-myristate 13-acetate (PMA) reversibly inhibits hexamethylene bisacetamide-induced terminal differentiation of Friend erythroleukemia cells (FELC). We were successful in continuously inhibiting FELC differentiation by PMA up to 125 weeks (about 240 serial passages of cells in the presence of PMA). During that period, FELC can be induced to differentiate and enter terminal cell division upon removal of PMA. PMA-mediated suppression of FELC differentiation was associated with only a low level of globin mRNA accumulation. However, a rapid accumulation of globin mRNA in the cytoplasm followed by hemoglobin accumulation occurred upon removal of PMA. A specific, saturable, high-affinity receptor for phorbol esters is present in FELC, as was shown by binding studies with [3H]phorbol 12,13-dibutyrate. A significant (80%) loss in the number of phorbol ester receptors of FELC was observed after a continuous inhibition of differentiation by PMA for as much as 125 weeks. Despite such a down regulation of phorbol ester receptors, these cells respond to PMA with a dose-response similar to that of their parent cells, which have the normal number of phorbol ester receptors. Thus, PMA can suppress reversibly the accumulation of globin-specific mRNA and terminal differentiation of FELC during prolonged periods, despite loss of receptor sites, and our results suggest that only few phorbol ester receptors may be necessary for complete inhibition of FELC differentiation by PMA.
机译：肿瘤启动子佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）可逆地抑制六亚甲基双乙酰胺诱导的Friend红白血病细胞（FELC）的终末分化。我们成功地通过PMA持续抑制FELC分化长达125周（在PMA存在的情况下，约有240次连续细胞传代）。在此期间，可在去除PMA后诱导FELC分化并进入终末细胞分裂。 PMA介导的FELC分化抑制仅与低水平的珠蛋白mRNA积累有关。然而，在去除PMA后发生了珠蛋白mRNA在细胞质中的快速积累，随后是血红蛋白的积累。如[3H] phorbol 12,13-dibutyrate与[3H] phorbol 12,13-dibutyrate的结合研究所示，FELC中存在一种特定的，可饱和的，大分子佛波酯的高亲和力受体。在PMA持续抑制分化长达125周后，观察到FELC的佛波酯受体数量大量减少（80％）。尽管佛波酯受体的这种下调，但这些细胞对PMA的反应与剂量相似，其亲代细胞具有佛波酯受体的正常数量。因此，尽管受体位点丢失，但PMA可以在较长时期内可逆性抑制球蛋白特异性mRNA的积累和FELC的终末分化，并且我们的结果表明，只有很少的佛波酯受体才能完全抑制PMA对FELC的分化。

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