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Objective: We aimed to investigate the mechanism of the regulatory axis of miR-196b/AQP4 underlying the invasion and migration of lung adenocarcinoma (LUAD) cells.
Methods: LUAD miRNA and mRNA expression profiles were downloaded from TCGA database and then differential analysis was used to identify the target miRNA. Target gene for the miRNA was obtained via prediction using 3 bioinformatics databases and intersection with the differentially expressed mRNAs searched from TCGA-LUAD. Then, qRT-PCR and western blot were used to validate the expression of miR-196b and AQP4. Dual-luciferase reporter assay was performed to confirm the targeting relationship between miR-196b and AQP4. Transwell assay was used to investigate the migration and invasion of LUAD cells.
Results: MiR-196b was screened out by differential and survival analyses, and the downstream target gene AQP4 was identified. In LUAD, miR-196b was highly expressed while AQP4 was poorly expressed. Besides, overexpression of miR-196b promoted cell invasion and migration, while overexpression of AQP4 had negative effects. Moreover, the results of the dual-luciferase reporter assay suggested that AQP4 was a direct target of miR-196b. In addition, we also found that overexpressing AQP4 could suppress the promotive effect of miR-196b on cancer cell invasion and migration.
Conclusion: MiR-196b promotes the invasion and migration of LUAD cells by down-regulating AQP4, which helps us find new molecular targeted therapies for LUAD.
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http://dx.doi.org/10.1177/1533033820985868 | DOI Listing |
PLoS One
September 2025
Biobank of Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu, PR China.
Heart failure (HF) and lung cancer (LC) often coexist, yet their shared molecular mechanisms are unclear. We analyzed transcriptome data from the NCBI Gene Expression Omnibus (GEO) database (GSE141910, GSE57338) to identify 346 HF‑related differentially expressed genes (DEGs), then combined weighted gene co-expression network analysis (WGCNA) pinpointed 70 hub candidates. Further screening of these 70 hub candidates in TCGA lung cancer cohorts via LASSO, Random Forest, and multivariate Cox regression suggested CYP4B1 as the only independent prognostic marker.
View Article and Find Full Text PDFIn Vitro Cell Dev Biol Anim
September 2025
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama-shi, Okayama, 700-8558, Japan.
S100 protein family members S100A8 and S100A9 function primarily as a heterodimer complex (S100A8/A9) in vivo. This complex has been implicated in various cancers, including gastric cancer (GC). Recent studies suggest that these proteins play significant roles in tumor progression, inflammation, and metastasis.
View Article and Find Full Text PDFBiochem Genet
September 2025
Department of General Surgery, The Second People's Hospital & Nantong Rehabilitation Hospital, No. 298, Xinhua Road, Nantong, 226001, Jiangsu, China.
To evaluate the expression of hsa_circ_0077007 in the serum of colorectal cancer (CRC) patients and offer a foundational theory for the prognosis of CRC. The present study focuses on investigating the biological function and therapeutic target of hsa_circ_0077007 in colorectal cancer CRC. Retrieve the GEO database and use the GEO2R tool to analyze the GSE dataset (GSE223001 and GSE159669) to obtain aberrantly expressed circRNAs.
View Article and Find Full Text PDFCancer Med
September 2025
The Key Laboratory of Tumor Stem Cell Research of Liaoning Province, Dalian Medical University, Dalian, China.
Background: Prostate cancer is one of the principal malignancies threatening human health, and the development of castration resistance often constitutes a major cause of treatment failure in its management.
Methods: To elucidate the potential association between programmed death-ligand 1 (PD-L1) and castration resistance in prostate cancer, we analyzed the expression levels of PD-L1 in both primary prostate cancer tissues and castration-resistant prostate cancer (CRPC) specimens as well as in corresponding cell lines by using western blots and immunohistochemistry. Then, we explored the specific mechanisms through transcriptomic sequencing technology.
Cancer Biol Med
September 2025
Department of Urology, First Affiliated Hospital of Jiujiang Medical University, Jiujiang 332000, China.
Prostate cancer is a significant global health issue with inflammation emerging as a critical driver of progression. The prostate tumor microenvironment (TME) is comprised of tumor cells, mesenchymal stem cells, immune cells, cancer-associated fibroblasts, adipocytes, and the extracellular matrix. All of these TME components interact soluble factors, such as growth factors, cytokines, and chemokines.
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