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The ATF2/miR-3913-5p/CREB5 axis is involved in the cell proliferation and metastasis of colorectal cancer.

Weiyu DaiLinjie HongWushuang XiaoLuyu ZhangWeihong ShaZhen YuXuehua LiuSide LiuYizhi XiaoPing YangYing PengJieming ZhangJianjiao LinXiaosheng WuWeimei TangZhizhao LinLi XiangJiaying LiMiaomiao PeiJide Wang
Published in: Communications biology (2023)
Various miRNAs have been shown to participate in the tumor progression and development of colorectal cancer (CRC). However, the role of miR-3913-5p in CRC are yet to be clearly defined. In the present study, we determine that miR-3913-5p is downregulated in CRC cell lines and CRC tissues. Exogenous miR-3913-5p expression weakens the CRC cells growth, migration and invasion. Mechanistically, miR-3913-5p directly targets the 3'UTR of CREB5. Overexpression of CREB5 reverses the suppression of CRC cells proliferation, migration and invasion induced by miR-3913-5p. Furthermore, ATF2 negatively regulates the transcription of miR-3913-5p by binding to its promoter. CREB5 can cooperate with ATF2. CREB5 is required for ATF2 in regulating miR-3913-5p. Finally, inverse correlations can be found between the expressions of miR-3913-5p and CREB5 or ATF2 in CRC tissues. Thus, a plausible mechanism of ATF2/miR-3913-5p/CREB5 axis regulating CRC progression is elucidated. Our findings suggest that miR-3913-5p functions as a tumor suppressor in CRC. ATF2/miR-3913-5p/CREB5 axis might be a potential therapeutic target against CRC progression.
Keyphrases
  • transcription factor
  • endoplasmic reticulum stress
  • induced apoptosis
  • cell proliferation
  • poor prognosis
  • gene expression
  • cell cycle arrest
  • dna methylation
  • signaling pathway
  • long non coding rna
  • climate change