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Long non-coding RNA UCA1 regulates the proliferation, migration and invasion of human lung cancer cells by modulating
1Department of The First Thoracic Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China. zhaojz@sj-hospital.org.
Objective:
Accounting for 25% of all the cancers and 20% of the cancer-related mortality, lung cancer is one of the devastating types of cancers. Due to an increase in the incidence of lung cancer and limited treatment options, there is a pressing need to look for novel drug options and to identify potential therapeutic targets. Long non-coding RNAs (LncRNAs) have been considered to be important therapeutic targets due to their plethora of cellular roles. Herein, we investigated the therapeutic potential of UCA1 in lung cancer and also attempted to examine the underlying mechanism through UCA1 exerts its growth inhibitory effects on cancer cells.
Materials And Methods:
The quantitative Reverse-Transcriptase Polymerase Chain Reaction (qRT-PCR) was used to perform the expression analysis. The CCK-8 assay was used to monitor the growth of the cells. The AO/EB assay was used to check apoptosis and flow cytometry was used for cell cycle distribution. The wound heal and transwell assays were used to monitor the cell migration and invasion.
Results:
It was found that the lncRNA UCA was significantly (p < 0.05) upregulated in the lung cancer cells and silencing of UCA1 could inhibit the proliferation of the SK-MES-1 lung cancer cells via induction of G2/M cell cycle arrest and apoptosis. Moreover, UCA1 silencing could also suppress the migration and invasion of the SK-MES-1 cells. The LncRNA UCA1 was also found to upregulate the expression of miR-143, and overexpression of miR-143 could also suppress the proliferation, migration, and invasion of the SK-MES-1 lung cancer cells. Both UCA1 silencing and miR-143 overexpression could cause a significant decrease in the expression of mitogen-activated protein kinase 1 (MAPK1). Therefore, it is concluded that UCA1 regulates the growth of the SK-MES-1 lung cancer by inhibition of MAPK1 via miR-143 upregulation.
Conclusions:
UCA1, as well as miR-143, may be essential therapeutic targets for the management of lung cancer and warrant further investigations.
Insights
Long non-coding RNA UCA1 is upregulated in lung cancer. Silencing UCA1 inhibits cancer cell growth, migration, and invasion by downregulating MAPK1 through miR-143, suggesting UCA1 as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Lung cancer accounts for 25% of all cancers and 20% of cancer mortality.
- Limited treatment options necessitate novel therapeutic targets.
- Long non-coding RNAs (LncRNAs) play crucial roles in cellular functions and are potential therapeutic targets.
Purpose of the Study:
- Investigate the therapeutic potential of UCA1 in lung cancer.
- Elucidate the mechanism by which UCA1 affects cancer cell growth.
Main Methods:
- Quantitative Reverse-Transcriptase Polymerase Chain Reaction (qRT-PCR) for expression analysis.
- Cell Counting Kit-8 (CCK-8) assay for cell proliferation.
- Apoptosis assays (AO/EB) and flow cytometry for cell cycle analysis.
- Wound healing and Transwell assays for cell migration and invasion.
Main Results:
- UCA1 was significantly upregulated in lung cancer cells.
- UCA1 silencing inhibited proliferation, induced G2/M cell cycle arrest and apoptosis in SK-MES-1 cells.
- UCA1 silencing suppressed migration and invasion.
- UCA1 upregulated miR-143, which also suppressed proliferation, migration, and invasion.
- Both UCA1 silencing and miR-143 overexpression decreased MAPK1 expression.
Conclusions:
- UCA1 regulates lung cancer cell growth by inhibiting MAPK1 via miR-143 upregulation.
- UCA1 and miR-143 are potential therapeutic targets for lung cancer management.
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