Wild-type p53-induced phosphatase 1 (WIP1) regulates the proliferation of swine Sertoli cells through P53.
Wild-type p53-induced phosphatase 1 (WIP1) regulates the proliferation of swine Sertoli cells through P53.
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DOI：
10.1071/rd20215
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发表时间：
2020-12
期刊：
影响因子：
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通讯作者：
Bingyuan Wang;Mingrui Zhang;Jingjing Che;Kui Li;Y. Mu;Zhiguo Liu
中科院分区：
文献类型：
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作者：
Bingyuan Wang;Mingrui Zhang;Jingjing Che;Kui Li;Y. Mu;Zhiguo Liu
野生型p53诱导的磷酸酶1（WIP 1）通过增加各种癌症类型中的细胞增殖而发挥致癌功能。WIP 1表达的缺乏可能通过损害血-睾丸屏障和精子发生而导致男性不育。然而，WIP 1如何在支持细胞中发挥作用以影响男性生殖仍不清楚。因此，在本研究中，我们使用了猪支持细胞系，以调查是否WIP 1调节支持细胞的增殖参与男性生殖。分别用WIP 1抑制剂GSK 2830371、WIP 1-short interference（si）RNA和上游microRNA（miR-16）抑制WIP 1的表达，观察其对支持细胞增殖、P53表达和P53磷酸化水平的影响。抑制WIP 1表达抑制了猪支持细胞增殖，增加了P53表达和P53磷酸化水平。此外，在猪Sertoli细胞中过表达miR-16导致WIP 1表达减少，P53表达和P53磷酸化增加。总之，这些发现表明WIP 1通过抑制P53磷酸化正向调节猪Sertoli细胞的增殖，并且miR-16也可能参与靶向WIP 1。
Wild-type p53-induced phosphatase 1 (WIP1) plays an oncogenic function by increasing cell proliferation in various cancer types. Deficiency in WIP1 expression leads to male infertility, possibly by impairing the blood-testis barrier and spermatogenesis. However, how WIP1 functions in the Sertoli cells to affect male reproduction remains unclear. Thus, in the present study we used a swine Sertoli cell line to investigate whether WIP1 regulated the proliferation of Sertoli cells to participate in male reproduction. The WIP1 inhibitor GSK2830371, WIP1-short interference (si) RNAs and an upstream microRNA (miR-16) were used to inhibit the expression of WIP1, after which the proliferation of swine Sertoli cells, P53 expression and the levels of P53 phosphorylation were determined. Inhibiting WIP1 expression suppressed swine Sertoli cell proliferation, increased P53 expression and increased levels of P53 phosphorylation. In addition, overexpression of miR-16 in swine Sertoli cells resulted in a decrease in WIP1 expression and increases in both P53 expression and P53 phosphorylation. Together, these findings suggest that WIP1 positively regulates the proliferation of swine Sertoli cells by inhibiting P53 phosphorylation, and the miR-16 is likely also involved by targeting WIP1.