ArticleBioengineered2022
Specificity protein 1-induced serine peptidase inhibitor, Kunitz Type 1 antisense RNA1 regulates colorectal cancer cell proliferation, migration, invasion and apoptosis through targeting heparin binding growth factor via sponging microRNA-214.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Long non‑coding RNAs as diagnostic and prognostic biomarkers for colorectal cancer (Review).Oncology letters · 2024Review
- Disulfidptosis-associated LncRNA signature predicts prognosis and immune response in kidney renal clear cell carcinoma.Biology direct · 2024Article
- Exploitation of porphyrin-based titanium-rich porous organic polymers for targeted phosphopeptide enrichment from the serum of colorectal cancer individuals.Mikrochimica acta · 2024Article
- The functions and mechanisms of long non-coding RNA in colorectal cancer.Frontiers in oncology · 2024Review
- Knockdown of miR-214 Alleviates Renal Interstitial Fibrosis by Targeting the Regulation of the PTEN/PI3K/AKT Signalling Pathway.Oxidative medicine and cellular longevity · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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