LncRNA HOXC-AS3 overexpression inhibits TGF-β2-induced colorectal cancer cell migration and invasion by sponging miR-1269

被引：7
|
作者：
Zhang, Tong-tong [1 ]
Chen, Hai-peng [2 ]
Yu, Su-yang [1 ]
Zhao, Shi-peng [1 ]
机构：
[1] Hebei Med Univ, Hosp 3, Dept Gastrointestinal Surg, 139 Ziqiang Rd, Shijiazhuang 050000, Hebei, Peoples R China
[2] Natl Clin Res Ctr Canc, Canc Hosp, Natl Canc Ctr, Dept Colorectal Surg, Beijing, Peoples R China
来源：
HUMAN & EXPERIMENTAL TOXICOLOGY | 2022年 / 41卷
关键词：
colorectal cancer; lncRNA HOXC-AS3; TGF-beta; 2; prognosis; LONG NONCODING RNA; MESENCHYMAL-TRANSITION;
D O I：
10.1177/09603271221093630
中图分类号：
R99 [毒物学（毒理学）];
学科分类号：
100405 ;
摘要：
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-beta 2 were detected by RT-qPCR. Overexpression assays were performed to explore the interaction between HOXC-AS3 and TGF-beta 2. 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-beta 2 in regulating CRC cell invasion and migration. Results: HOXC-AS3 was significantly downregulated in CRC tissues, while TGF-beta 2 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-beta 2 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-beta 2, while the expression of HOXC-AS3 was not affected by TGF beta 2. Transwell migration and invasion assay showed that overexpression of TGF-beta 2 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-beta 2. MiR-1269 increased the expression of TGF-beta 2. HOXC-AS3 directly interacted with miR-1269 in CRC cells. Conclusions: Upregulation of HOXC-AS3 inhibited TGF-beta 2-induced colorectal cancer (CRC) cell migration and invasion possibly by sponging nniR-1269.
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页数：8
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