Study on LncRNA01004 Promoting Epithelial-mesenchymal Transformation and Accelerating Malignant Progression of Breast Cancer Cells through Up-regulation of CPSF1 Protein Expression
10.3969/j.issn.1671-7414.2025.01.06
- VernacularTitle:LncRNA01004通过上调CPSF1蛋白表达促进上皮-间质转化加速乳腺癌细胞恶性进展的研究
- Author:
Hongguo GUO
1
;
Nan WU
;
Wanling LU
;
Jun LIU
;
Cai CHENG
Author Information
1. 中国人民解放军空军第九八六医院肿瘤血液科,西安710054
- Publication Type:Journal Article
- Keywords:
breast cancer;
long non-coding RNA 01004;
cleavage and polyadenylation specific factor 1;
epithelial-mesenchymal transition;
proliferation;
invade;
apoptosis
- From:
Journal of Modern Laboratory Medicine
2025;40(1):32-37,47
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of long non-coding RNA 01004 (LncRNA01004) in accelerating the malignant progression of breast cancer cells and its potential regulatory mechanism. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression level of LncRNA01004 in breast cancer tissues and cells. The Starbase online database predicted the binding of LncRNA01004 to CPSF1 and verified it through RNA binding protein immunoprecipitation(RIP) analysis. MCF-7 cells were transfected with LncRNA01004 interference sequence (sh-LncRNA01004) or overexpressed vector (LncRNA01004),or co-transfected with Cleavage and Polyadenylation Specific Factor 1 (CPSF1) interference sequence (sh-CPSF1). Cell viability,invasion and apoptosis were detected with CCK-8,Transwell and flow cytometry (FCM). The overexpression and silencing efficiency of LINC01004 and CPSF1 were detected by qPCR. Western blot (WB) analysis of CPSF1 protein,apoptosis-related protein[B cell lymphoma/leukemia-2(Bcl-2),Bcl-2 Associated X(Bax)]and Epithelial-Mesenchymal transition (EMT) related protein[Epitheia-cadherin(E-cadherin),Nerve-cadherin(N-cadherin),Vimentin,zinc-finger transcription factor(Snail)],and the activity of Cysteinyl aspartate-specific proteinase-3 (Caspase-3) was determined by enzyme-linked immunosorbent assay. Results LncRNA01004 was significantly up-regulated in breast cancer tissues (5.14±0.33) compared with paracancer tissues (1.02±0.03),with the statistically significant difference (t=-78.637,P<0.001);LncRNA01004 expression in breast cancer cells was significantly higher than that in normal breast epithelial cells,the difference between groups is statistically significant (F=142.248,P<0.001). Compared with the Control group,LncRNA01004 significantly inhibited the proliferation (42.15±2.11 vs 100.02±0.65) and invasion (18.65％±1.44％ vs 41.36％±1.57％) of MCF-7 cells,induced apoptosis (16.58％±1.52％ vs 5.24％±1.12％),increased the activity of Caspase-3 (2.93±0.711. vs 51±0.43) and the expression of Bax (2.74±0.39 vs 1.01±0.02) protein,and inhibited the expression of BcL-2 (0.32±0.07 vs 1.02±0.03) protein,with the statistically significant difference (t=3.075～19.332,all P<0.05). Significantly increased compared with Control group,the silent LncRNA01004 E-cadherin (3.06±0.37 vs 1.01±0.02) protein levels,lower N-cadherin (0.44±0.11 vs 1.00±0.01),Vimentin (0.39±0.13 vs 1.02±0.03) and Snail(0.30±0.08 vs 1.01±0.03) protein levels,with the statistically significant difference (t=9.989～17.164,all P<0.05).LncRNA01004 binds to CPSF1 and promotes CPSF1 protein expression.Silencing CPSF1 inhibited the proliferation and invasion of MCF-7 cells,induced cell apoptosis,and counteracted the effect of LncRNA01004 overexpression on MCF-7 cells. Conclusion LncRNA01004 may promote EMT through up-regulation of CPSF1,and then promote proliferation and invasion of breast cancer cells,inhibit cell apoptosis,and participate in the malignant progression of breast cancer.
