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

Cell Death Dis. 2021 Jun 9;12(6):595. doi: 10.1038/s41419-021-03879-2.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • HEK293 Cells
  • Humans
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / physiopathology*
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs / physiology
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Long Noncoding / physiology*
  • Rats
  • Repressor Proteins / physiology
  • Signal Transduction / genetics
  • Wound Healing / genetics*

Substances

  • MicroRNAs
  • Mirn128 microRNA, mouse
  • Phf6 protein, mouse
  • RNA, Long Noncoding
  • Repressor Proteins
  • Proto-Oncogene Proteins c-akt

Grants and funding