LncRNA Bmp1 promotes the healing of intestinal mucosal lesions via the miR-128-3p/PHF6/PI3K/AKT pathway.

LncRNA Bmp1 promotes the healing of intestinal mucosal lesions via the miR-128-3p/PHF6/PI3K/AKT pathway.
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LncRNA Bmp1 通过 miR-128-3p/PHF6/PI3K/AKT 通路促进肠粘膜病变的愈合。

DOI:
10.1038/s41419-021-03879-2
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发表时间:
2021-06-09
影响因子:
9
通讯作者:
Sun Y
Sun Y
中科院分区:
生物学1区
文献类型:
--
作者:
Zhuang M;Deng Y;Zhang W;Zhu B;Yan H;Lou J;Zhang P;Cui Q;Tang H;Sun H;Sun Y

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肠粘膜损伤与许多常见的急、慢性疾病有直接或间接的关系。长链非编码RNA(lncRNA)在包括肠粘膜损伤在内的许多疾病中表达。然而,lncRNA与肠粘膜损伤之间的关系尚未确定。在此,我们研究了lncRNA Bmp 1对受损肠粘膜的功能和作用机制。我们发现Bmp 1在受损的肠粘膜组织中表达增加,并且Bmp 1过表达能够减轻肠粘膜损伤。Bmp 1过表达被发现影响IEC-6或HIEC-6细胞的细胞增殖、集落形成和迁移。此外,miR-128- 3 p在Bmp 1过表达后下调,并且miR-128- 3 p的上调逆转了Bmp 1过表达对IEC-6细胞的影响。观察到Phf 6是miR-128- 3 p的靶标。此外,PHF 6过表达通过激活由miR-128- 3 p/PHF 6轴介导的PI 3 K/AKT信号传导影响IEC-6细胞。综上所述,Bmp 1通过海绵miR-128- 3 p促进PHF 6的表达,激活PI 3 K/AKT信号通路,促进细胞迁移和增殖。
Intestinal mucosal injuries are directly or indirectly related to many common acute and chronic diseases. Long non-coding RNAs (lncRNAs) are expressed in many diseases, including intestinal mucosal injury. However, the relationship between lncRNAs and intestinal mucosal injury has not been determined. Here, we investigated the functions and mechanisms of action of lncRNA Bmp1 on damaged intestinal mucosa. We found that Bmp1 was increased in damaged intestinal mucosal tissue and Bmp1 overexpression was able to alleviate intestinal mucosal injury. Bmp1 overexpression was found to influence cell proliferation, colony formation, and migration in IEC-6 or HIEC-6 cells. Moreover, miR-128-3p was downregulated after Bmp1 overexpression, and upregulation of miR-128-3p reversed the effects of Bmp1 overexpression in IEC-6 cells. Phf6 was observed to be a target of miR-128-3p. Furthermore, PHF6 overexpression affected IEC-6 cells by activating PI3K/AKT signaling which was mediated by the miR-128-3p/PHF6 axis. In conclusion, Bmp1 was found to promote the expression of PHF6 through the sponge miR-128-3p, activating the PI3K/AKT signaling pathway to promote cell migration and proliferation.
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