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Updated: Nov 27, 2025

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
Published on: February 9, 2024
MIR155HG Knockdown Inhibited the Progression of Cervical Cancer by Binding SRSF1
Ling Shen1, Yuancheng Li2, Guiying Hu3
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, People's Republic of China.
Background:
As the fourth most common cancer among women worldwide, cervical cancer lead to 311,000 deaths in 2018. Although the treatments have been developed, the survival rate of cervical cancer remains unsatisfactory. In this study, we aimed to identify differentially expressed lncRNAs (DEIncRNAs) between cervical cancer and adjacent normal tissues using bioinformatics analysis, and further to investigate the biological function of the DEIncRNAs in vitro and in vivo.
Methods:
The expression profiles from two microarray datasets (GSE6791 and GSE63514) were downloaded from GEO for analysis of DEIncRNAs between cervical cancer and adjacent normal cervical tissues. Among all DEIncRNAs, MIR155HG upregulation was identified and selected for further investigation. The effect of MIR155HG knockdown on proliferation, apoptosis and invasion in SiHa and Hela cells were evaluated. In addition, Western blot, RNA immunoprecipitation (RIP) and cell cycle assays were performed to determine the binding target of MIR155HG. Furthermore, the effect of MIR155HG knockdown on tumor growth in vivo was investigated.
Results:
The level of MIR155HG was found to be significantly upregulated in cervical cancer tissue compared with adjacent cervical tissue. Knockdown of MIR155HG notably inhibited the proliferation of SiHa and Hela cells by inducing apoptosis. In addition, MIR155HG knockdown decreased cell invasion. Moreover, tumor growth in xenograft was significantly inhibited by MIR155HG knockdown in vivo. Additionally, SRSF1 was identified as the binding protein of MIR155HG.
Conclusion:
Our findings demonstrated that MIR155HG knockdown inhibited the progression of cervical cancer by binding SRSF1, inspiring the usage of MIR155HG as a potential novel therapy target for the treatment of cervical cancer.
Insights
This study identified MIR155HG as a key player in cervical cancer progression. Knocking down MIR155HG inhibited cancer cell proliferation and invasion, offering a potential new therapeutic target for cervical cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Bioinformatics
Background:
- Cervical cancer is a significant global health issue with unsatisfactory survival rates despite treatment advancements.
- Identifying novel therapeutic targets is crucial for improving patient outcomes.
Purpose of the Study:
- To identify differentially expressed long non-coding RNAs (DEIncRNAs) in cervical cancer tissues.
- To investigate the functional role of MIR155HG in cervical cancer progression.
- To explore MIR155HG as a potential therapeutic target.
Main Methods:
- Bioinformatic analysis of microarray datasets (GSE6791, GSE63514) to identify DEIncRNAs.
- In vitro studies involving MIR155HG knockdown in SiHa and Hela cells to assess proliferation, apoptosis, and invasion.
- In vivo xenograft models to evaluate the effect of MIR155HG knockdown on tumor growth.
- Western blot and RNA immunoprecipitation (RIP) assays to identify MIR155HG binding proteins.
Main Results:
- MIR155HG was significantly upregulated in cervical cancer tissues compared to normal tissues.
- MIR155HG knockdown inhibited cell proliferation and invasion while inducing apoptosis in vitro.
- MIR155HG knockdown significantly suppressed tumor growth in vivo.
- SRSF1 was identified as a binding protein of MIR155HG.
Conclusions:
- MIR155HG plays a crucial role in promoting cervical cancer progression.
- MIR155HG knockdown inhibits cervical cancer growth by interacting with SRSF1.
- MIR155HG represents a promising novel therapeutic target for cervical cancer treatment.
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