» Articles » PMID: 38515708

EP300 Regulates the SLC16A1-AS1-AS1/TCF3 Axis to Promote Lung Cancer Malignancies Through the Wnt Signaling Pathway

Overview
Journal Heliyon
Specialty Social Sciences
Date 2024 Mar 22
PMID 38515708
Authors
Affiliations
Soon will be listed here.
Abstract

Objective: To investigate the regulatory mechanism of EP300 in the interaction between SLC16A1-AS1 and TCF3 to activate the Wnt pathway, thereby promoting malignant progression in lung cancer.

Methods: In lung cancer cell lines, SLC16A1-AS1 was knocked down, and the impact of this knockdown on the malignant progression of lung cancer cells was assessed through clonogenic assays, Transwell assays, and apoptosis experiments. The regulatory relationship between EP300 and SLC16A1-AS1 was investigated through bioinformatic analysis and ChIP experiments. The expression of SLC16A1-AS1 and TCF3 in 56 paired lung cancer tissues was examined using RT-qPCR, and their correlation was analyzed. The interaction between TCF3 and SLC16A1-AS1 was explored through bioinformatic analysis and CoIP experiments. Activation of the Wnt/β-catenin pathway was assessed by detecting the accumulation of β-catenin in the nucleus through Western blotting. The role of EP300 in regulating the effect of SLC16A1-AS1/TCF3-mediated Wnt/β-catenin signaling on lung cancer malignant progression was validated through in vitro and in vivo experiments.

Results: SLC16A1-AS1 is highly expressed in lung cancer and regulates its malignant progression. EP300 mediates histone modifications on the SLC16A1-AS1 promoter, thus controlling its expression. SLC16A1-AS1 exhibits specific interactions with TCF3, and the SLC16A1-AS1/TCF3 complex activates the Wnt/β-catenin pathway. EP300 plays a critical role in regulating the impact of SLC16A1-AS1/TCF3-mediated Wnt/β-catenin signaling on lung cancer malignant progression.

Conclusion: EP300 regulates the SLC16A1-AS1/TCF3-mediated Wnt/β-catenin signaling pathway, influencing the malignant progression of lung cancer.

Citing Articles

Epigenetic modifications in early stage lung cancer: pathogenesis, biomarkers, and early diagnosis.

Bi L, Wang X, Li J, Li W, Wang Z MedComm (2020). 2025; 6(3):e70080.

PMID: 39991629 PMC: 11843169. DOI: 10.1002/mco2.70080.

References
1.
Liu H, Lu S, Guo Z, Zhang Z, Ye X, Du Q . lncRNA SLC16A1-AS1 as a novel prognostic biomarker in non-small cell lung cancer. J Investig Med. 2019; 68(1):52-59. PMC: 6996107. DOI: 10.1136/jim-2019-001080. View

2.
Huang L, Li L, Cheng B, Xing T . SLC38A6, regulated by EP300-mediated modifications of H3K27ac, promotes cell proliferation, glutamine metabolism and mitochondrial respiration in hepatocellular carcinoma. Carcinogenesis. 2022; 43(9):885-894. DOI: 10.1093/carcin/bgac061. View

3.
Thangudu S, Yu C, Lee C, Liao M, Su C . Magnetic, biocompatible FeCO nanoparticles for T2-weighted magnetic resonance imaging of in vivo lung tumors. J Nanobiotechnology. 2022; 20(1):157. PMC: 8952886. DOI: 10.1186/s12951-022-01355-3. View

4.
de Almeida Nagata D, Chiang E, Jhunjhunwala S, Caplazi P, Arumugam V, Modrusan Z . Regulation of Tumor-Associated Myeloid Cell Activity by CBP/EP300 Bromodomain Modulation of H3K27 Acetylation. Cell Rep. 2019; 27(1):269-281.e4. DOI: 10.1016/j.celrep.2019.03.008. View

5.
Feng H, Zhang X, Lai W, Wang J . Long non-coding RNA SLC16A1-AS1: its multiple tumorigenesis features and regulatory role in cell cycle in oral squamous cell carcinoma. Cell Cycle. 2020; 19(13):1641-1653. PMC: 7469610. DOI: 10.1080/15384101.2020.1762048. View