Journal
BIOENGINEERED
Volume 13, Issue 2, Pages 3309-3322Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2022.2026859
Keywords
Serine peptidase inhibitor; Kunitz type 1 antisense RNA1 (SPINT1-AS1); microRNA (miR)-214; heparin-binding growth factor (HDGF); colorectal cancer
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This study found that the upregulation of lncRNA SPINT1-AS1 promotes the progression of colorectal cancer by inhibiting miR-214 and increasing HDGF expression.
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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