Malignant melanoma is a highly metastatic cancer, and has a poor prognosis once metastasis has occurred. E-cadherin downregulation is associated with a poorer prognosis in various types of cancer, including lung, ovarian, cervical and prostate. In the majority of cancer cell lines, E-cadherin upregulation inhibits cell motility, migration and invasiveness, and reduces tumor metastasis in models. In the present study, the inhibitory effects of metformin on the motility, invasion and migration of the B16F10 murine melanoma cell line, and the possible molecular mechanisms underlying this effect were investigated. B16F10 cells were treated with various concentrations of metformin for 24 h and their motility, migration and invasion were tested using a wound-healing assay, a migration assay and a matrigel invasion assay, respectively. Furthermore, the expression of E-cadherin was measured by immunocytochemistry, western blotting and reverse transcription-quantitative polymerase chain reaction. The results showed that metformin effectively upregulated the expression of E-cadherin, and inhibited B16F10 cell motility, migration and invasion, in a dose-dependent manner. This suggested that the inhibition of motility, migration and invasion of B16F10 cells by metformin may be associated with the upregulation of E-cadherin expression, indicating that metformin may have a role in the treatment of melanoma.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4533732 | PMC |
| http://dx.doi.org/10.3892/ol.2015.3475 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Tegaserod maleate exerts anti-tumor effects on prostate cancer via repressing sonic hedgehog signaling pathway.
Mol Med
January 2025
Department of Urology, The Fifth Affiliated Hospital of Southern Medical University, Guangzhou, 510920, Guangdong, People's Republic of China.
Prostate cancer (PCa) is a highly common type of malignancy and affects millions of men in the world since it is easy to recur or emerge therapy resistance. Therefore, it is urgent to find novel treatments for PCa patients. In the current study, we found that tegaserod maleate (TM), an FDA-approved agent, inhibited proliferation, colony formation, migration as well as invasion, caused the arrest of the cell cycle, and promoted apoptosis of PCa cells in vitro.
View Article and Find Full Text PDFGemistocytic tumor cells programmed for glial scarring characterize T cell confinement in IDH-mutant astrocytoma.
Nat Commun
January 2025
Department of Medical Oncology, Laboratory of Tumor Immunology, Erasmus MC Cancer Institute, Rotterdam, The Netherlands.
Isocitrate dehydrogenase 1/2 mutant (IDHmt) astrocytoma is considered a T cell-deprived tumor, yet little is known regarding the phenotypes underlying T cell exclusion. Using bulk, single nucleus and spatial RNA and protein profiling, we demonstrate that a distinct spatial organization underlies T cell confinement to the perivascular space (T cell cuff) in IDHmt astrocytoma. T cell cuffs are uniquely characterized by a high abundance of gemistocytic tumor cells (GTC) in the surrounding stroma.
View Article and Find Full Text PDFPD-L1-CD80 interactions are required for intracellular signaling necessary for dendritic cell migration.
Sci Adv
January 2025
Department of Medicine, Division of Gastroenterology and Hepatology, University of Colorado School of Medicine, Aurora, CO, USA.
Programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1) interactions are targets for immunotherapies aimed to reinvigorate T cell function. Recently, it was documented that PD-L1 regulates dendritic cell (DC) migration through intracellular signaling events. In this study, we find that both preclinical murine and clinically available human PD-L1 antibodies limit DC migration.
View Article and Find Full Text PDFInotodiol induces hepatocellular carcinoma apoptosis by activation of MAPK/ERK pathway.
PLoS One
January 2025
Heilongjiang University of Traditional Chinese Medicine, Harbin, Heilongjiang, China.
Hepatocellular carcinoma(HCC) has a high mortality and morbidity rate and seriously jeopardizes human life. Chemicals and chemotherapeutic agents have been experiencing problems such as side effects and drug resistance in the treatment of HCC, which cannot meet the needs of clinical treatment. Therefore, finding novel low-toxicity and high-efficiency anti-hepatocellular carcinoma drugs and exploring their mechanisms of action have become the current problems to be solved in the treatment of HCC.
View Article and Find Full Text PDFSHP2 promotes the epithelial-mesenchymal transition in triple negative breast cancer cells by regulating β-catenin.
J Cancer Res Clin Oncol
January 2025
Key Laboratory of Laboratory Medicine, Ministry of Education of China, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Purpose: Growing evidence suggests that the tyrosine phosphatase SHP2 is pivotal for tumor progression. Triple-negative breast cancer (TNBC) is the most lethal subtype of breast cancer, characterized by its high recurrence rate, aggressive metastasis, and resistance to chemotherapy. Understanding the mechanisms of tumorigenesis and the underlying molecular pathways in TNBC could aid in identifying new therapeutic targets.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!