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首页> 外文期刊>Molecular Carcinogenesis >Resistance of primary cultured mouse hepatic tumor cells to cellular senescence despite expression of p16(Ink4a), p19(Arf), p53, and p21(Waf1/Cip1).
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Resistance of primary cultured mouse hepatic tumor cells to cellular senescence despite expression of p16(Ink4a), p19(Arf), p53, and p21(Waf1/Cip1).

机译：尽管表达了p16（Ink4a），p19（Arf），p53和p21（Waf1 / Cip1），但原代培养的小鼠肝肿瘤细胞对细胞衰老具有抗性。

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摘要

Primary cultured mouse hepatic cells become senescent within a short period, although rare cells form colonies from which continuously proliferating cell lines can be established. In contrast, hepatic tumor (HT) cells show little senescence and higher colony-forming capacity. To assess this difference, we investigated p16(Ink4a)/p19(Arf)/p53/p21(Waf1/Cip1) expression in primary normal and HT cells, together with cell lines established from both. In primary normal cells, p16(Ink4a)/p19(Arf) were expressed only in association with senescence and disappeared at later stages of colony formation. In contrast, primary HT cells showed sustained p16(Ink4a)/p19(Arf) expression from the beginning. No p16(Ink4a)/p19(Arf) alterations, such as deletion, mutations, or hypermethylation, were detected in the primary HT cells, although most cell lines derived from either normal or HT cell colonies lost p16(Ink4a) or p19(Arf) expression owing to hypermethylation or homozygous deletion of p16(Ink4a)/p19(Arf). On the other hand, primary normal and HT cells and most cell lines showed constitutively elevated expression of p53/p21(Waf1/Cip1), with a further increment after ultraviolet ir-radiation, indicating a functionally normal p53 pathway. These results indicate that primary HT cells are resistant to senescence despite retaining p16(Ink4a)/p19(Arf)/p53/p21(Waf1/Cip1) expression and that loss of p16(Ink4a)/p19(Arf) function is associated only with establishment of the cell lines.
机译：原代培养的小鼠肝细胞会在短时间内衰老，尽管稀有细胞会形成菌落，从中可以建立持续增殖的细胞系。相反，肝肿瘤（HT）细胞显示出很少的衰老和较高的集落形成能力。为了评估这种差异，我们调查了原代正常细胞和HT细胞以及从两者建立的细胞系中的p16（Ink4a）/ p19（Arf）/ p53 / p21（Waf1 / Cip1）表达。在原代正常细胞中，仅与衰老相关地表达p16（Ink4a）/ p19（Arf），并在菌落形成的后期消失。相反，初级HT细胞从一开始就显示持续的p16（Ink4a）/ p19（Arf）表达。在原代HT细胞中未检测到p16（Ink4a）/ p19（Arf）改变，如缺失，突变或甲基化过高，尽管大多数源自正常或HT细胞集落的细胞系都丢失了p16（Ink4a）或p19（Arf） ）的表达是由于p16（Ink4a）/ p19（Arf）的高度甲基化或纯合缺失所致。另一方面，原代正常细胞和HT细胞以及大多数细胞系显示p53 / p21（Waf1 / Cip1）的组成性表达升高，在紫外线照射后进一步增加，表明功能正常的p53途径。这些结果表明，尽管保留了p16（Ink4a）/ p19（Arf）/ p53 / p21（Waf1 / Cip1）表达，但原代HT细胞仍具有抗衰老作用，而p16（Ink4a）/ p19（Arf）功能的丧失仅与细胞系的建立。

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