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首页> 外文期刊>Journal of biochemical and molecular toxicology >E4F1 silencing inhibits the cell growth through cell‐cycle arrest in malignant transformed cells induced by hydroquinone
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E4F1 silencing inhibits the cell growth through cell‐cycle arrest in malignant transformed cells induced by hydroquinone

机译：E4F1沉默通过氢醌诱导的恶性转化细胞中的细胞周期停留来抑制细胞生长

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Abstract Hydroquinone (HQ), one of the most significant metabolic activation products of benzene in an organism, can cause hematological toxicity, such as acute myeloid leukemia. It is a clear carcinogen that can cause changes in the disorder of cell cycle and cell growth. However, its molecular mechanisms remain unclear. E4 transcription factor 1 (E4F1), an important transcription factor, participating in the regulation of cell cycle may be related to the occurrence of tumor. Here, we examined the HQ‐induced malignant transformed TK6 cells (TK6‐HT) to illustrate the role of E4F1 in carcinogenesis. The present study showed that both the expressions of E4F1 messenger RNA and protein increased obviously in TK6‐HT, preliminarily indicating that E4F1 is associated with HQ‐induced carcinogenesis. To further explore the role of E4F1, we established E4F1 silencing TK6‐HT (pLVX‐shE4F1) and its control cells (pLVX‐shNC) using lentiviral short hairpin RNA (shRNA) interference expression plasmid vector pLVX‐shRNA. Flow cytometry and cell counting kit‐8 assay were used to determine the effects of E4F1 silencing on cell cycle and cell growth, respectively. E4F1 silencing inhibited cell growth in TK6‐HT. The results from flow cytometry indicated that the inhibitory effect on cell growth may be the results of the E4F1 silencing–induced accumulation in G2/M compared with TK6‐HT‐shNC. Meanwhile, levels of DNA damage (γ‐H2AX), proteins of Rb and phosphorylated Rb, and reactive oxygen species were increased in TK6‐HT‐shRNA2 cells, which is the critical reason of cell‐cycle arrest. In conclusion, E4F1 silencing inhibits the cell growth through cell‐cycle arrest in malignant transformed cells induced by HQ.
机译：摘要氢醌（HQ）是生物体中苯最重要的代谢活化产物之一，可引起血液毒性，如急性髓性白血病。它是一种透明的致癌，可导致细胞周期和细胞生长的疾病变化。然而，其分子机制仍然不清楚。 E4转录因子1（E4F1），参与细胞周期调节的重要转录因子可能与肿瘤发生有关。在这里，我们检查了HQ诱导的恶性转化的TK6细胞（TK6-HT）以说明E4F1在致癌中的作用。本研究表明，E4F1信使RNA和蛋白表达在TK6-HT中显而易见，初步表明E4F1与HQ诱导的致癌作用有关。为了进一步探讨E4F1的作用，我们使用慢病毒短发夹RNA（ShRNA）干扰表达质粒载体PlVX-shRNA建立了E4F1沉默TK6-HT（PLVX-SHE4F1）及其对照细胞（PLVX-SHNC）。流式细胞术和细胞计数试剂盒测定分别用于分别测定E4F1沉默对细胞周期和细胞生长的影响。 E4F1沉默在TK6-HT中抑制细胞生长。流式细胞术的结果表明，与TK6-HT-SHNC相比，对细胞生长的抑制作用可以是G2 / M中的E4F1沉默诱导的积累。同时，在TK6-HT-SHRNA2细胞中增加了DNA损伤（γ-H2AX），RB的蛋白质和磷酸化RB的蛋白质，以及反应性氧物质，这是细胞周期停滞的关键原因。总之，E4F1沉默通过HQ诱导的恶性转化细胞中的细胞周期停留来抑制细胞生长。

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