Journal
ONCOTARGET
Volume 8, Issue 22, Pages 36266-36278Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.16742
Keywords
colorectal cancer; miR-22; Sp1; PTEN; AKT
Categories
Funding
- Scientific Research Project of Sichuan Medical Association [S15024]
- Sichuan Youth Science and Technology Foundation [2017JQ0039]
- Scientific Research Project of Nanchong Municipal Science and Technology Bureau [16YFZJ0128]
- Scientific Research Project of Sichuan Provincial Health and Family Planning Commission [16ZD037]
- Scientific Research Fund of Sichuan Provincial Education Department of China [14ZA0184, 13ZA0230]
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MicroRNAs have recently emerged as regulators of many biological processes including cell proliferation, development and differentiation. This study identified that miR-22 was statistically decreased in colorectal cancer clinical specimens and highly metastatic cell lines. Moreover, low miR-22 expression was associated with tumor metastasis, advanced clinical stage and relapse. Consistent with clinical observations, miR-22 significantly suppressed the ability of colorectal cancer cells to growth and metastasize in vitro and in vivo. Sp1 was validated as a target of miR-22, and ectopic expression of Sp1 compromised the inhibitory effects of miR-22. In addition, Sp1 repressed miR-22 transcription by binding to the miR-22 promoter, hence forming a negative feedback loop. Further study has shown that miR-22 suppresses the activity of PTEN/AKT pathway by Sp1. Our present results implicate the newly indentified miR-22/ Sp1/PTEN/AKT axis might represent a potential therapeutic target for colorectal cancer.
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