LncRNA HOXC-AS3 overexpression inhibits TGF-ß2-induced colorectal cancer cell migration and invasion by sponging miR-1269.
Hum Exp Toxicol
; 41: 9603271221093630, 2022.
Article
em En
| MEDLINE
| ID: mdl-35537198
OBJECTIVE: Long non-coding RNA (lncRNA) HOXC-AS3 has been characterized as a cancer-related lncRNA in many types of cancer, while its role in colorectal cancer (CRC) is unknown. METHODS: The expression of HOXC-AS3 and TGF-ß2 were detected by RT-qPCR. Overexpression assays were performed to explore the interaction between HOXC-AS3 and TGF-ß2. A follow-up study was performed to explore the prognostic value of HOXC-AS3 for CRC. The direct interaction between HOXC-AS3 and miR-1269 was assessed with RNA-RNA pulldown assay. Transwell assays were performed to determine the role of HOXC-AS3 and TGF-ß2 in regulating CRC cell invasion and migration. RESULTS: HOXC-AS3 was significantly downregulated in CRC tissues, while TGF-ß2 was significantly upregulated in CRC tissues compared to that in adjacent non-cancer tissues of CRC patients. The follow-up study showed that low expression levels of HOXC-AS3 in CRC tissues were closely correlated with poor survival. Correlation analysis showed that HOXC-AS3 and TGF-ß2 were inversely correlated across CRC tissues but not non-cancer tissues. Overexpression of HOXC-AS3 in the two cell lines resulted in downregulation of TGF-ß2, while the expression of HOXC-AS3 was not affected by TGF-ß2. Transwell migration and invasion assay showed that overexpression of TGF-ß2 increased cell invasion and migration, while overexpression of HOXC-AS3 decreased cell migration and invasion. In addition, overexpression of HOXC-AS3 attenuated the effects of overexpression of TGF-ß2. MiR-1269 increased the expression of TGF-ß2. HOXC-AS3 directly interacted with miR-1269 in CRC cells. CONCLUSIONS: Upregulation of HOXC-AS3 inhibited TGF-ß2-induced colorectal cancer (CRC) cell migration and invasion possibly by sponging miR-1269.
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MEDLINE
Assunto principal:
Neoplasias Colorretais
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MicroRNAs
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RNA Longo não Codificante
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article