Previous studies have suggested that metformin, a biguanide family member widely used as an oral antidiabetic drug, may inhibit proliferation and induce apoptosis in certain types of cancer cell. However, the molecular mechanisms underlying metformin-associated anticancer effects, and in particular antimetastatic effects, remain to be fully understood. The present study assessed the efficacy of metformin in inhibiting the migration and invasion of the esophageal carcinoma cell line EC109, and evaluated the effect of metformin on the protein kinase B (AKT) signaling pathway. EC109 cells were treated with 0, 5, 10 or 20 mM metformin during the logarithmic growth phase. A Transwell assay and western blot analysis revealed that metformin inhibited the migration and invasion of EC109 cells, nuclear factor-κB activation, matrix metallopeptidase 9 and N-cadherin expression in a phosphorylated-AKT dependent manner. These results suggested that metformin inhibits the migration and invasion of human esophageal carcinoma cells by suppressing AKT phosphorylation and regulating the expression of migration- and invasion-associated genes.
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http://dx.doi.org/10.3892/ol.2017.7699 | DOI Listing |
J Transl Med
January 2025
Department of Radiation Oncology, State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Background: Drug resistance constitutes one of the principal causes of poor prognosis in breast cancer patients. Although cancer cells can maintain viability independently of mitochondrial energy metabolism, they remain reliant on mitochondrial functions for the synthesis of new DNA strands. This dependency underscores a potential link between mitochondrial energy metabolism and drug resistance.
View Article and Find Full Text PDFCell Mol Biol Lett
January 2025
Clinical Research Center, Jiading District Central Hospital Affiliated to Shanghai University of Medicine and Health Sciences, Shanghai, 201800, China.
Background: Circular (circ)RNAs have emerged as crucial contributors to cancer progression. Nonetheless, the expression regulation, biological functions, and underlying mechanisms of circRNAs in mediating hepatocellular carcinoma (HCC) progression remain insufficiently elucidated.
Methods: We identified circUCK2(2,3) through circRNA sequencing, RT-PCR, and Sanger sequencing.
BMC Complement Med Ther
January 2025
Division of Pharmacology and Biopharmaceutical Sciences, Faculty of Pharmaceutical Sciences, Burapha University, Chonburi, Thailand.
Background: Plant flavonoids such as quercetin are useful for both the therapeutic and preventive care of a variety of illnesses. Nevertheless, their antitumor efficacy against KON oral cancer is still unknown. Therefore, the aim of this investigation was to examine quercetin's anti-growth, anti-migrative, and anti-invasive characteristics.
View Article and Find Full Text PDFEur J Med Res
January 2025
Department of Surgical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, 277 West Yanta Road, Xi'an, 710061, Shaanxi, China.
Objective: The effect of coiled-coil domain-containing 154 (CCDC154) in liver cancer (LC) remains unexplored. The objective of this study was to investigate the role of CCDC154 in LC and its underlying mechanism.
Methods: The analysis of CCDC154 expression and prognosis was performed using UALCAN, Human Protein Atlas and Kaplan-Meier plotter websites.
Sci Rep
January 2025
Department of Gastroenterological Surgery, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Sympathetic nerves regulate nearly all human organs. Their peripheral nerves are present in tumor tissue. Activation of the sympathetic nervous system promotes malignant transformation in several cancers.
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