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Updated: Feb 1, 2026

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
Published on: June 15, 2016
MicroRNA-148a inhibits cell proliferation and cell cycle progression in lung adenocarcinoma via directly targeting
Jianwei Liu1,2, Libo Si1, Hui Tian1
1Department of Thoracic Surgery, Qilu Hospital of Shandong University, Jinan, Shandong 250012, P.R. China.
Abstract:
MicroRNAs (miRs) serve important roles in various human cancers, including lung adenocarcinoma. Exploring the function and regulatory mechanism of miRs underlying lung adenocarcinoma progression may contribute to identifying novel therapeutic targets and candidates. The present study aimed to examine miR-148a expression and investigate the molecular mechanisms of miR-148a in lung adenocarcinomas. The data from the current study indicated that miR-148a was significantly downregulated in lung adenocarcinoma tissues and cell lines, and low miR-148a expression was significantly associated with advanced Tumor, Node, Metastasis stages and lymph node metastasis, as well as the shorter survival time of patients. Increased miR-148a expression markedly decreased the cell proliferation, colony formation and cell cycle progression of H23 and H1975 cells. Transcription factor E2F3 (E2F3) was identified as a target of miR-148a in H23 and H1975 cells. The expression of E2F3 was negatively mediated by miR-148a in H23 and H1975 cells. In addition, E2F3 was significantly upregulated in lung adenocarcinoma tissues and cell lines, and the expression of miR-148a was inversely correlated with E2F3 expression in lung adenocarcinoma tissues. Additional experiments demonstrated that increased E2F3 expression counteracted the inhibitory effects on lung adenocarcinoma cells caused by miR-148a overexpression. In summary, the findings of the current study suggest that miR-148a may have suppressive effects on the proliferation of lung adenocarcinoma cells at least in part through directly targeting E2F3. Therefore, miR-148a may be used as a potential candidate for the treatment of lung adenocarcinoma.
Insights
MicroRNA-148a (miR-148a) is downregulated in lung adenocarcinoma, suppressing tumor growth by targeting E2F3. Restoring miR-148a shows potential for treating lung cancer.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- MicroRNAs (miRs) play critical roles in human cancers, including lung adenocarcinoma.
- Understanding miR function in lung cancer progression can reveal novel therapeutic targets.
Purpose of the Study:
- To investigate the expression and molecular mechanisms of miR-148a in lung adenocarcinomas.
- To explore miR-148a's potential as a therapeutic candidate for lung cancer.
Main Methods:
- Analysis of miR-148a and E2F3 expression in lung adenocarcinoma tissues and cell lines.
- Assessment of miR-148a's functional effects on lung adenocarcinoma cell proliferation, colony formation, and cell cycle.
- Identification and validation of E2F3 as a direct target of miR-148a.
Main Results:
- miR-148a was significantly downregulated in lung adenocarcinoma, correlating with advanced stages and poor prognosis.
- Overexpression of miR-148a inhibited lung adenocarcinoma cell proliferation, colony formation, and cell cycle progression.
- E2F3 was identified as a direct target of miR-148a, with inverse expression correlation in tumor tissues. E2F3 overexpression counteracted miR-148a's inhibitory effects.
Conclusions:
- miR-148a suppresses lung adenocarcinoma cell proliferation, potentially by directly targeting E2F3.
- miR-148a represents a promising therapeutic candidate for lung adenocarcinoma treatment.
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