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J 亚群禽白血病病毒株通过负调控鸡成纤维细胞中 14-3-3σ 的表达促进细胞增殖。

J Subgroup Avian Leukosis Virus Strain Promotes Cell Proliferation by Negatively Regulating 14-3-3σ Expressions in Chicken Fibroblast Cells.

机构信息

Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai'an 271018, China.

出版信息

Viruses. 2023 Jan 31;15(2):404. doi: 10.3390/v15020404.

Abstract

This study focuses on clarifying the regulation of chicken 14-3-3σ protein on the fibrous histiocyte proliferation caused by ALV-J-SD1005 strain infection. DF-1 cells were inoculated with 10 TCID of ALV-J-SD1005 strain; the cell proliferation viability was dramatically increased and 14-3-3σ expressions were dramatically decreased within 48 h after inoculation. Chicken over-expression could significantly decrease the cell proliferation and the ratio of S-phase cells, but increase the ratio of G2/M-phase cells in ALV-J-infected DF-1 cells; by contrast, chicken knockdown expression could cause the opposite effects. Additionally, chicken over-expression could also dramatically down-regulate the expressions of CDK2/CDC2, but up-regulate p53 expressions in the DF-1 cells; in contrast, the knockdown expression could significantly increase the expressions of CDK2/CDC2 and decrease p53 expressions. It can be concluded that chicken 14-3-3σ can inhibit cell proliferation and cell cycle by regulating CDK2/CDC2/p53 expressions in ALV-J-infected DF1 cells. ALV-J-SD1005 strain can promote cell proliferation by reducing expressions. This study helps to clarify the forming mechanism of acute fibrosarcoma induced by ALV-J infection.

摘要

本研究旨在阐明鸡 14-3-3σ蛋白对 ALV-J-SD1005 株感染引起的纤维组织细胞增殖的调节作用。用 10 TCID 的 ALV-J-SD1005 株接种 DF-1 细胞,接种后 48 h 内细胞增殖活力显著增加,14-3-3σ表达显著降低。鸡 14-3-3σ过表达可显著降低 ALV-J 感染 DF-1 细胞的细胞增殖和 S 期细胞比例,但增加 G2/M 期细胞比例;相反,鸡 14-3-3σ 敲低表达则会产生相反的效果。此外,鸡 14-3-3σ过表达还可显著下调 CDK2/CDC2 的表达,但上调 DF-1 细胞中 p53 的表达;相反,敲低表达可显著增加 CDK2/CDC2 的表达并降低 p53 的表达。综上所述,鸡 14-3-3σ 可以通过调节 CDK2/CDC2/p53 的表达抑制 ALV-J 感染的 DF1 细胞的增殖和细胞周期。ALV-J-SD1005 株通过降低 14-3-3σ 的表达来促进细胞增殖。本研究有助于阐明 ALV-J 感染引起的急性纤维肉瘤的形成机制。

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