Related Experiment Video
Updated: Dec 22, 2025

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
Published on: May 21, 2019
Restoration of UPK1A-AS1 Expression Suppresses Cell Proliferation, Migration, and Invasion in Esophageal Squamous
Fang Du1, Tao Guo2, Chenghua Cao3
1Department of Hematology and Oncology, No. 988 Hospital of Joint Logistic Support Force of the Chinese People's Liberation Army, Zhengzhou, Henan Province, People's Republic of China.
Background:
Recent evidence suggests that long non-coding RNAs (lncRNAs) are emerging as key determinants of esophageal squamous cell carcinoma (ESCC) progression. This study aimed to investigate the role of lncRNA UPK1A antisense RNA 1 (UPK1A-AS1) in ESCC cell proliferation, invasion, and migration.
Methods:
The expression levels of UPK1A-AS1 and miR-1248 were determined using quantitative reverse transcriptase-polymerase chain reaction. The functional role of UPK1A-AS1 in ESCC was investigated using subcellular localization assay, Cell Counting Kit-8 assay, colony formation assay, scratch-healing assay, and transwell invasion assay. The functional interaction between UPK1A-AS1 and miR-1248 was assessed using luciferase reporter and RNA pull-down assays.
Results:
Twenty dysregulated lncRNAs were detected in ESCC. Downregulation of UPK1A-AS1 was observed in ESCC tissues and cell lines. Functionally, upregulation of UPK1A-AS1 suppressed the proliferation, migration, and invasion of ESCC cells. Moreover, an inverse correlation between UPK1A-AS1 and miR-1248 expression was observed in ESCC specimens, and miR-1248 was identified as a direct target of UPK1A-AS1. Furthermore, we found that UPK1A-AS1 exerts its anti-cancer effects partially through sponging miR-1248 in ESCC cells.
Conclusion:
UPK1A-AS1 suppressed the proliferation, migration, and invasion of ESCC cells partially by sponging miR-1248. Hence, our findings provide novel insights into the regulatory pathway involved in ESCC development.
Insights
Long non-coding RNA UPK1A antisense RNA 1 (UPK1A-AS1) suppresses esophageal squamous cell carcinoma (ESCC) progression. UPK1A-AS1 inhibits ESCC cell proliferation, invasion, and migration by sponging miR-1248.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are increasingly recognized as critical regulators in cancer development.
- Esophageal squamous cell carcinoma (ESCC) is a significant global health concern with complex molecular underpinnings.
- The specific roles of many lncRNAs in ESCC pathogenesis remain to be elucidated.
Purpose of the Study:
- To investigate the expression and function of lncRNA UPK1A antisense RNA 1 (UPK1A-AS1) in ESCC.
- To determine the impact of UPK1A-AS1 on ESCC cell proliferation, invasion, and migration.
- To elucidate the molecular mechanism involving UPK1A-AS1 and its interaction with miR-1248 in ESCC.
Main Methods:
- Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) for gene expression analysis.
- Cell-based assays including CCK-8, colony formation, scratch-healing, and transwell invasion assays to assess cell behavior.
- Luciferase reporter and RNA pull-down assays to confirm the interaction between UPK1A-AS1 and miR-1248.
Main Results:
- UPK1A-AS1 was found to be downregulated in ESCC tissues and cell lines.
- Overexpression of UPK1A-AS1 significantly inhibited ESCC cell proliferation, migration, and invasion.
- UPK1A-AS1 directly targets and sponges miR-1248, indicating a regulatory feedback loop.
Conclusions:
- UPK1A-AS1 functions as a tumor suppressor in ESCC.
- The anti-cancer effects of UPK1A-AS1 are partially mediated through its interaction with miR-1248.
- These findings offer new insights into the regulatory mechanisms governing ESCC progression and potential therapeutic targets.
Related Concept Videos
MicroRNAs
MicroRNAs
Abnormal Proliferation
Role Of Notch Signalling In Intestinal Stem Cell Renewal
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

