miR-148a inhibits early relapsed colorectal cancers and the secretion of VEGF by indirectly targeting HIF-1α under non-hypoxia/hypoxia conditions
| Autor: | Hsiang-Lin Tsai, Wei-Chih Su, Jaw-Yuan Wang, Che-Jen Huang, K.-L. Li |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Tube formation
business.industry Colorectal cancer Angiogenesis Hematology Hypoxia (medical) medicine.disease digestive system diseases Vascular endothelial growth factor Blot chemistry.chemical_compound Vascular endothelial growth factor A Oncology Downregulation and upregulation chemistry Cancer research Medicine medicine.symptom business |
| Zdroj: | Annals of Oncology. 30:v239 |
| ISSN: | 0923-7534 |
| DOI: | 10.1093/annonc/mdz246.111 |
| Popis: | Background Vascular endothelial growth factor (VEGF) is correlated with angiogenesis and early relapse of colorectal cancer (CRC). This study investigated the role of miR-148a in the regulation of VEGF/angiogenesis and early relapse of CRC. Methods We established a stable clone with miR-148a expression in HCT116 and HT29 cell lines and created a hypoxic condition by using CoCl2 to determine the underlying mechanism of miR-148a. The effects of miR-148a on the pERK/HIF-1α/VEGF pathway were evaluated through western blotting, and the inhibitory effect of miR-148a on angiogenesis was demonstrated through a tube formation assay. Sixty-three CRC tissues (28 early relapse and 35 non–early relapse) were analyzed to assess the relationship between miR-148a and HIF-1α/VEGF. Results The protein expression of pERK/HIF-1α/VEGF in HCT116 and HT29 cells was significantly decreased by miR-148a (all P Conclusions miR-148a suppresses VEGF through downregulation of the pERK/HIF-1α/VEGF pathway and might lead to the inhibition of angiogenesis; miR-148a downregulation increased the early relapse rate of CRC. This demonstrates that miR-148a is a potential diagnostic and therapeutic target. Legal entity responsible for the study The authors. Funding Has not received any funding. Disclosure All authors have declared no conflicts of interest. |
| Databáze: | OpenAIRE |
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