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Updated: Dec 8, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
LncRNA STARD13-AS blocks lung squamous carcinoma cells growth and movement by targeting miR-1248/C3A
1Queen Mary School of Medical College, Jiangxi Medical College, Qianhu Campus, Nanchang University, No. 1299 Xuefu Street, Nanchang, Jiangxi, China.
Background:
This research aims to illustrate the effect of lncRNA StAR Related Lipid Transfer Domain Containing 13 antisense RN (STARD13-AS)/miR-1248/C3A on lung squamous carcinoma cells growth and metastasis.
Methods:
Bioinformatics analysis was applied to detect the expression of STARD13-AS/miR-1248/C3A in lung cancer samples and establish the ceRNA network. Transfection was performed to construct over-expression or knockdown models. PCR was implemented to examine the transfection efficiency. The biological function including growth, invasion and migration of LUSC cells were estimated by CCK-8 analysis, colony formation assay and transwell assay. Luciferase assay was executed to analyze the relationship between C3A and miR-1248, as well as miR-1248 and STARD13-AS.
Results:
By consulting the TCGA database and GEPIA website, we found that C3A expression was significantly reduced in LUSC samples. Additionally, we also discovered that miR-1248, which was a downstream target of STARD13-AS, was presented as an upstream regulator of C3A. Moreover, STARD13-AS was under expressed in LUSC cells and has a negative effect on LUSC cells growth ability. C3A expression was co-regulated by miR-1248 and STARD13-AS. Importantly, the inhibitory effect of C3A or the promoting effect of miR-1248 on LUSC cells growth, invasion and migration abilities can be regulated by STARD13-AS.
Conclusions:
Our findings revealed that overexpression of STARD13-AS restricted the growth and aggressiveness of LUSC cells via regulating miR-1248/C3A.
Insights
Overexpression of long non-coding RNA STARD13-AS inhibits lung squamous cell carcinoma growth and metastasis by regulating the miR-1248/C3A axis. This finding offers a potential therapeutic target for LUSC. Keywords: STARD13-AS, miR-1248, C3A, lung squamous cell carcinoma, metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Lung squamous cell carcinoma (LUSC) is a major subtype of lung cancer with complex molecular underpinnings.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development and progression.
- The specific roles of lncRNA STARD13-AS, miR-1248, and C3A in LUSC remain to be fully elucidated.
Purpose of the Study:
- To investigate the regulatory network involving lncRNA STARD13-AS, miR-1248, and C3A in lung squamous cell carcinoma.
- To determine the effect of STARD13-AS on the biological functions of LUSC cells, including growth, invasion, and migration.
- To explore the potential of the STARD13-AS/miR-1248/C3A axis as a therapeutic target for LUSC.
Main Methods:
- Bioinformatic analysis of TCGA and GEPIA databases to assess STARD13-AS, miR-1248, and C3A expression in LUSC.
- Construction of overexpression and knockdown models using cell transfection.
- Quantitative PCR (qPCR) to confirm transfection efficiency.
- In vitro assays including CCK-8, colony formation, and Transwell assays to evaluate cell growth, invasion, and migration.
- Luciferase reporter assays to validate the interactions between STARD13-AS, miR-1248, and C3A.
Main Results:
- C3A expression was significantly downregulated in LUSC tissues.
- STARD13-AS was underexpressed in LUSC cells and negatively impacted cell growth.
- miR-1248 was identified as a downstream target of STARD13-AS and an upstream regulator of C3A.
- STARD13-AS was found to co-regulate C3A expression and modulate the effects of miR-1248 on LUSC cell proliferation, invasion, and migration.
Conclusions:
- Overexpression of STARD13-AS effectively inhibited the growth and aggressiveness of LUSC cells.
- The STARD13-AS/miR-1248/C3A axis plays a crucial role in LUSC progression.
- Targeting the STARD13-AS/miR-1248/C3A pathway represents a promising therapeutic strategy for LUSC.
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