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Published on: March 30, 2019
LncRNA SNHG14 accelerates breast cancer progression through sponging miR-543 and regulating KLF7 expression
Daoping Zhang1, Xu Ding1, Meirong Peng2
1Department of Laboratory Medicine, Jingmen No. 1 People's Hospital, No.6 Zhongtian Street, Dongbao District, Jingmen, 448000, Hubei, China.
Purpose:
Dysregulation of long non-coding RNAs (lncRNAs) is being found to have relevance to human cancers, including breast cancer (BC). The aim of this study was to further explore the functional role and molecular mechanisms of small nucleolar RNA host gene 14 (SNHG14) on BC progression.
Methods:
The expression levels of SNHG14, miR-543, and krüppel-like factor 7 (KLF7) mRNA were determined by quantitative real-time PCR. Western blot analysis was used to evaluate KLF7 protein level. Cell proliferation, apoptosis, and migration and invasion abilities were detected by Cell Counting kit-8 assay, flow cytometry, and transwell assay, respectively. The direct interactions between miR-543 and SNHG14 or KLF7 were confirmed using dual-luciferase reporter assays.
Results:
Our data indicated that SNHG14 expression was increased in BC tissues and cells, and SNHG14 knockdown mitigated the proliferation, migration, and invasion and facilitated apoptosis of BC cells. SNHG14 directly interacted with miR-543. MiR-543 mediated the regulatory effects of SNHG14 silencing on BC cell behaviors. Moreover, KLF7 was a direct target of miR-543. Overexpressed miR-543-mediated anti-proliferation, anti-migration, anti-invasion, and pro-apoptosis effects were mediated by KLF7. Furthermore, SNHG14 modulated KFL7 expression through acting as a competing endogenous RNA (ceRNA) of miR-543 in BC cells.
Conclusion:
Our study suggested that SNHG14 knockdown hindered BC progression in vitro at least partly through acting as a ceRNA of miR-543 and modulating KLF7 expression, providing evidence for SNHG14 as a potential target for BC therapy.
Insights
Small nucleolar RNA host gene 14 (SNHG14) promotes breast cancer (BC) progression by regulating miR-543 and KLF7. Silencing SNHG14 inhibits BC cell proliferation, migration, and invasion, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are implicated in human cancers, including breast cancer (BC).
- Dysregulation of lncRNAs plays a significant role in cancer development and progression.
- Understanding the specific roles of lncRNAs like SNHG14 in BC is crucial for therapeutic development.
Purpose of the Study:
- To investigate the functional role of small nucleolar RNA host gene 14 (SNHG14) in breast cancer (BC) progression.
- To elucidate the molecular mechanisms underlying SNHG14's involvement in BC.
- To explore SNHG14 as a potential therapeutic target for breast cancer.
Main Methods:
- Quantitative real-time PCR and Western blot analysis to assess gene and protein expression levels.
- Cell Counting kit-8, flow cytometry, and transwell assays to evaluate cell proliferation, apoptosis, migration, and invasion.
- Dual-luciferase reporter assays to confirm direct interactions between SNHG14, miR-543, and KLF7.
Main Results:
- SNHG14 expression was elevated in BC tissues and cells.
- SNHG14 knockdown suppressed BC cell proliferation, migration, and invasion, while promoting apoptosis.
- SNHG14 acts as a competing endogenous RNA (ceRNA) for miR-543, thereby modulating KLF7 expression and influencing BC cell behaviors.
Conclusions:
- SNHG14 knockdown inhibits breast cancer progression in vitro.
- SNHG14's mechanism involves acting as a ceRNA for miR-543 and regulating KLF7 expression.
- SNHG14 presents a promising potential therapeutic target for breast cancer treatment.
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