Related Experiment Video
Updated: Oct 31, 2025

The Soft Agar Colony Formation Assay
Published on: October 27, 2014
Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis
Qingling Kong1, Guangcai Li2, Gang Yin3
1Hospital Infection Control Office, Rizhao People's Hospital, Rizhao 276800, China.
Background:
Understanding the role of lncRNAs in the development of human malignancies is necessary for the targeted therapy of malignant tumors, including esophageal cancer (EC). Nevertheless, the specific role and regulatory mechanism of lncRNA WDFY3-AS2 in EC are still unclear. Here, we examined the functional role and regulatory mechanism of WDFY3-AS2 in EC.
Materials And Methods:
RT-qPCR assay was applied to measure the expression of WDFY3-AS2 and miR-18a in EC samples and cells. The luciferase reporter and RIP assays were used to check the relationship between WDFY3-AS2, miR-18a, and PTEN. Counting Clock Kit-8 (CCK-8) assay was carried out to detect cell viability, and transwell assays were used for measuring cell migration and invasion.
Results:
Underexpression of WDFY3-AS2 was found in EC specimens and cells, which predicted a poor prognosis of EC patients. Reexpression of WDFY3-AS2 repressed the progression of EC via inhibiting cell proliferation, migration, and invasion. Additionally, WDFY3-AS2 was negatively correlated with miR-18a and positively with PTEN. Furthermore, we discovered that the expression of PTEN decreased by miR-18a mimic was rescued by WDFY3-AS2 overexpression.
Conclusions:
WDFY3-AS2 modulates the expressional level of PTEN as a competitive endogenous RNA via sponging miR-18a in EC, which suggests that the WDFY3-AS2/miR-18a/PTEN pathway might be involved in the progression of EC.
Insights
Long non-coding RNA WDFY3-AS2 is underexpressed in esophageal cancer (EC), inhibiting tumor progression. WDFY3-AS2 acts as a ceRNA by sponging miR-18a to regulate PTEN, suggesting a novel therapeutic target for EC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are crucial in human cancer development, necessitating research into their roles in esophageal cancer (EC).
- The specific function and regulatory mechanisms of lncRNA WDFY3-AS2 in EC remain largely unknown.
- This study investigates the functional role and regulatory mechanism of WDFY3-AS2 in EC progression.
Purpose of the Study:
- To elucidate the functional role of lncRNA WDFY3-AS2 in esophageal cancer.
- To investigate the regulatory mechanism of WDFY3-AS2 in EC.
- To explore the potential of WDFY3-AS2 as a therapeutic target for EC.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) to assess WDFY3-AS2 and miR-18a expression levels in EC tissues and cells.
- Luciferase reporter and RNA immunoprecipitation (RIP) assays to determine the interaction between WDFY3-AS2, miR-18a, and PTEN.
- Cell Counting Kit-8 (CCK-8) and Transwell assays to evaluate cell viability, migration, and invasion.
Main Results:
- WDFY3-AS2 was found to be underexpressed in EC specimens and cells, correlating with poor patient prognosis.
- Re-expression of WDFY3-AS2 significantly inhibited EC cell proliferation, migration, and invasion.
- WDFY3-AS2 negatively correlated with miR-18a and positively with PTEN, with WDFY3-AS2 overexpression rescuing PTEN levels suppressed by miR-18a mimic.
Conclusions:
- WDFY3-AS2 functions as a competing endogenous RNA (ceRNA) by sponging miR-18a, thereby modulating PTEN expression in EC.
- The WDFY3-AS2/miR-18a/PTEN pathway is implicated in the progression of esophageal cancer.
- WDFY3-AS2 represents a potential therapeutic target for esophageal cancer treatment.
Related Concept Videos
MicroRNAs
MicroRNAs
lncRNA - Long Non-coding RNAs
lncRNA - Long Non-coding RNAs
Experimental RNAi
Abnormal Proliferation
