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Long non-coding RNA MIR205HG regulates KRT17 and tumor processes in cervical cancer via interaction with SRSF1
Mingli Dong1, Zhennan Dong2, Xinyu Zhu3
1Department of Obstetrics and Gynecology, Chinese PLA General Hospital, Beijing 100853, China.
Abstract:
Abnormal expression of long non-coding RNAs (lncRNAs) has been demonstrated to be a vital regulatory factor in a large number of malignancies. The investigation in cervical cancer and the associated modulation mechanisms are yet to be probed. The aim of this study is to specifically investigate the expression pattern and modulatory mechanism of MIR205HG in cervical cancer. Our paper firstly revealed the up-regulation of KRT17 in cervical cancer. Function assays further displayed that KRT17 silencing impaired the proliferation and migration, and activated the apoptosis of cervical cancer cells. Based on the finding that MIR205HG could regulate KRT17 expression, we further probed the detailed mechanism between MIR205HG and KRT17. It was observed from mechanism experiments that MIR205HG depleted SRSF1 to increase KRT17 expression. The whole mechanism of MIR205HG/SRSF1/KRT17 axis affecting cell proliferation, apoptosis and migration in cervical cancer was validated using rescue assays. In conclusion, MIR205HG modulated the biological activities of cervical cancer cells via targeting SRSF1 and regulating KRT17, which better understood the pathogenesis of cervical carcinoma and excavated a novel therapeutic target.
Insights
Long non-coding RNA MIR205HG is upregulated in cervical cancer, promoting cancer cell proliferation and migration by regulating KRT17 expression via SRSF1. This finding offers a potential new therapeutic target for cervical cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Aberrant expression of long non-coding RNAs (lncRNAs) is implicated in various cancers.
- The specific role and regulatory mechanisms of MIR205HG in cervical cancer remain largely unexplored.
Purpose of the Study:
- To investigate the expression pattern and functional role of MIR205HG in cervical cancer.
- To elucidate the underlying molecular mechanism by which MIR205HG influences cervical cancer progression.
Main Methods:
- Quantitative real-time PCR to assess MIR205HG and KRT17 expression levels.
- Cell proliferation, migration, and apoptosis assays following KRT17 or MIR205HG manipulation.
- Western blotting and RNA immunoprecipitation assays to determine the interaction between MIR205HG, SRSF1, and KRT17.
Main Results:
- MIR205HG and KRT17 were found to be significantly upregulated in cervical cancer tissues and cell lines.
- Silencing KRT17 inhibited cervical cancer cell proliferation and migration while promoting apoptosis.
- MIR205HG depletion suppressed cancer progression, and rescue experiments confirmed MIR205HG targets SRSF1 to upregulate KRT17, impacting cell proliferation, migration, and apoptosis.
Conclusions:
- MIR205HG acts as an oncogenic lncRNA in cervical cancer by modulating the MIR205HG/SRSF1/KRT17 axis.
- This pathway influences key cellular processes including proliferation, migration, and apoptosis in cervical cancer.
- MIR205HG represents a potential therapeutic target for cervical cancer intervention.
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