Long non-coding RNA SChLAP1 regulates the proliferation of triple negative breast cancer cells via the miR-524-5p/HMGA2 axis

被引:8
|
作者
Bai, Xiangdong [1 ]
Zhang, Shengxiao [2 ]
Qiao, Jun [2 ]
Xing, Xiaolong [3 ]
Li, Weina [4 ]
Zhang, Huanhu [5 ]
Xie, Jun [6 ]
机构
[1] Shanxi Med Univ, Shanxi Prov Canc Hosp, Dept Breast Surg, Taiyuan 030013, Shanxi, Peoples R China
[2] Shanxi Med Univ, Dept Rheumatism & Immunol, Clin Med Coll 2, Taiyuan 030001, Shanxi, Peoples R China
[3] Shanxi Immune Med Technol Co Ltd, Res & Dev Div, Taiyuan 030001, Shanxi, Peoples R China
[4] Shanxi Med Univ, Shanxi Prov Canc Hosp, Dept Radiotherapy, Taiyuan 030001, Shanxi, Peoples R China
[5] Shanxi Med Univ, Shanxi Prov Canc Hosp, Dept Gastroenterol, 3 New Workers Rd, Taiyuan 030013, Shanxi, Peoples R China
[6] Shanxi Med Univ, Shanxi Prov Canc Hosp, Dept Biochem & Mol Biol, 56 Xinjian South Rd, Taiyuan 030001, Shanxi, Peoples R China
关键词
triple negative breast cancer; second chromosome locus associated with prostate-1; microRNA-524-5p; High Mobility Group AT-Hook 2;
D O I
10.3892/mmr.2021.12085
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Long non-coding RNA (lncRNA) second chromosome locus associated with prostate-1 (SChLAP1), also named LINC00913, has been reported to accelerate the carcinogenesis of prostate cancer. The aim of this study was to explore the role and mechanism of SChLAP1 in triple negative breast cancer (TNBC). The expression of SChLAP1 in TNBC tissues and cells was determined by reverse transcription quantitative PCR. The effects of SChLAP1 on the growth of TNBC cells was evaluated by detecting cell viability, colony formation and apoptosis. The present study determined that SChLAP1 was upregulated in TNBC tissues and was associated with the long-distant lymph node metastasis of patients with TNBC. Knockdown of SChLAP1 significantly inhibited cell viability and colony formation, and triggered apoptosis of TNBC cells. Bioinformatics analysis suggested that SChLAP1 acted as a sponge of microRNA (miR)-524-5p and negatively modulated the expression of miR-524-5p. An inverse correlation was also identified between the expression levels of SChLAP1 and miR-524-5p in TNBC tissues. Furthermore, the results demonstrated that SChLAP1 interacted with miR-524-5p, and subsequently regulated the expression level of High Mobility Group AT-Hook 2 (HMGA2) in TNBC cells. It was also found that the overexpression of HMGA2 rescued the suppressed viability of TNBC cells induced by SChLAP1 knockdown. In conclusion, the present findings demonstrated that SChLAP1 modulated the malignant tumor behaviors of TNBC cells by regulating HMGA2 and subsequently restraining miR-524-5p.
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页数:10
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