LINC00657 Promotes Malignant Progression of Cervical Cancer by Sponging miR-30a-5p to Regulate Skp2 Expression
10.3971/j.issn.1000-8578.2026.25.0660
- VernacularTitle:LINC00657通过吸附miR-30a-5p调控Skp2表达促进宫颈癌恶性进展
- Author:
Changhui ZHOU
1
;
Jingqin REN
1
;
Zhen CHEN
1
;
Qi YAN
1
;
Nan YANG
1
;
Jiaqi ZHAO
1
;
Rong LI
2
Author Information
1. College of Public Health, Xinjiang Medical University, Urumqi 830054, China.
2. College of Public Health, Xinjiang Medical University, Urumqi 830054, China;State Key Laboratory of Pathogenesis, Prevention and Treatment of High-Incidence Diseases in Central Asia, Urumqi 830054, China.
- Publication Type:BASICRESEARCH
- Keywords:
LINC00657;
miR-30a-5p;
Skp2;
Molecular sponge;
Cervical cancer
- From:
Cancer Research on Prevention and Treatment
2026;53(2):103-111
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role and regulatory mechanism of LINC00657 in the progression of cervical cancer. Methods Bioinformatics analysis predicted potential binding sites between LINC00657 and miR-30a-5p and between miR-30a-5p and Skp2. These sites were verified by using RNA immunoprecipitation and dual-luciferase reporter experiments. LINC00657, miR-30a-5p, and Skp2 mRNA expression levels in cervical cancer tissues and cell lines were assessed by utilizing RT-qPCR. Western blot analysis was employed to examine the protein levels of Skp2 in cells and subcutaneous xenograft tumor models in nude mice. Immunohistochemistry was applied to analyze Skp2 expression in animal tissues. The cellular processes of cervical cancer cell lines were evaluated through CCK-8, scratch, and Transwell assays. Results LINC00657 and Skp2 presented binding sites for miR-30a-5p. In cervical cancer, LINC00657 and Skp2 showed high expression levels (P<0.05), whereas miR-30a-5p displayed low expression (P<0.05). Functional experiments demonstrated that linc00657 upregulates Skp2 expression, a process that is dependent on its sequestration of miR-30a-5p. Conclusion LINC00657 promoted the malignant progression of cervical cancer by upregulating Skp2 expression through specifically sequestering miR-30a-5p, thereby relieving its inhibitory effect on the target gene Skp2.
