Expression and function of long non-coding RNA DLX6-AS1 in endometrial cancer

被引:0
|
作者
Shi, Wei [1 ,2 ,3 ]
Lin, Jianxia [1 ,2 ,3 ]
Jin, Rong [1 ,2 ,3 ]
Xie, Xianjing [1 ,2 ,3 ]
Liang, Yan [1 ,2 ,3 ]
机构
[1] Shanghai Jiao Tong Univ, Int Peace Matern & Child Hlth Hosp, Sch Med, Dept Gynecol Oncol, Shanghai 200030, Peoples R China
[2] Shanghai Key Lab Embryo Original Dis, Shanghai 200030, Peoples R China
[3] Shanghai Municipal Key Clin Specialty, Shanghai 200030, Peoples R China
关键词
Endometrial cancer; LncRNA DLX6-AS1; MicroRNA-374a-3p; Zinc-finger protein; Biomarker; Invasion; PROGRESSION;
D O I
10.32604/biocell.2023.026037
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background: LncRNA DLX6-AS1 has been uncovered to exert effects on various cancers. Nevertheless, the impacts of DLX6-AS1 on endometrial cancer (EC) development remained obscure. The study explored the influence of DLX6-AS1 on EC progression via the microRNA (miR)-374a-3p/zinc-finger protein (ZFX) axis. Methods: EC cell lines were collected and DLX6-AS1, miR-374a-3p, and ZFX levels in EC cell lines were detected. The EC cells were transfected with DLX6-AS1, miR-374a-3p, and ZFX constructs to examine the biological functions of EC cells. The xenograft model was established for detecting tumor growth. Rescue experiments were conducted to verify the interaction of DLX6-AS1, miR-374a-3p, and ZFX in EC cells. Results: DLX6-AS1 and ZFX levels were elevated, while miR-374a-3p exhibited a reduced level in EC cells. Silencing DLX6-AS1 and elevated miR-374a-3p expressions repressed the biological activities of EC cells. Reduced DLX6-AS1 repressed tumor development. MiR-374a-3p silencing reversed the impacts of DLX6-AS1 silencing, while ZFX overexpression abrogated the impacts of miR-374a-3p elevation on EC cell growth. Mechanically, DLX6-AS1 was found to bind to miR-374a-3p, and miR-374a-3p targeted ZFX. Conclusion: DLX6-AS1 depletion restricts the malignant phenotype of EC cells. The study might provide novel therapeutic biomarkers for EC treatment.
引用
收藏
页码:869 / 877
页数:9
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