Abstract |
Previous studies indicated that long noncoding RNA ( lncRNA) serine peptidase inhibitor, Kunitz type 1 antisense RNA1 (SPINT1-AS1) could function as an oncogenic gene in various human cancers. However, the regulatory mechanisms of SPINT1-AS1 in the tumorigenesis of colorectal cancer (CRC) remain unclear. It was found that SPINT1-AS1 was upregulated in CRC and contributed to the poor prognosis of CRC patients. Silencing of SPINT1-AS1 inhibited proliferation and metastasis but increased apoptosis of CRC cells. Furthermore, we found that SP1 could activate SPINT1-AS1 by acting as a transcription factor. Meanwhile, we identified miR-214 was negatively regulated by SPINT1-AS1. Furthermore, miR-214 repression restored the suppressive effects on malignant biological behaviors of CRC caused by SPINT1-AS1 silencing. In addition, SPINT1-AS1 mediated HDGF expression through targeting miR-214. Finally, overexpressed heparin-binding growth factor (HDGF) overturned the effects on viability, metastasis, and apoptosis of CRC cells induced by SPINT1-AS1 depletion or miR-214 upregulation. In conclusion, our results demonstrated that SP1-induced SPINT1-AS1 could facilitate CRC progression by inhibiting miR-214 and increasing HDGF expression. These findings might provide a new approach for CRC treatment.
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Authors | Ying Fang, Qianqian Yang |
Journal | Bioengineered
(Bioengineered)
Vol. 13
Issue 2
Pg. 3309-3322
(02 2022)
ISSN: 2165-5987 [Electronic] United States |
PMID | 35068341
(Publication Type: Journal Article, Video-Audio Media)
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Chemical References |
- MIRN214 microRNA, human
- MicroRNAs
- Neoplasm Proteins
- RNA, Antisense
- RNA, Neoplasm
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Topics |
- Aged
- Apoptosis
- Caco-2 Cells
- Cell Movement
- Cell Proliferation
- Colorectal Neoplasms
(genetics, metabolism)
- Female
- HCT116 Cells
- Humans
- Male
- MicroRNAs
(genetics, metabolism)
- Middle Aged
- Neoplasm Invasiveness
- Neoplasm Proteins
(genetics, metabolism)
- RNA, Antisense
(genetics, metabolism)
- RNA, Neoplasm
(genetics, metabolism)
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