Objective: To construct an adenovirus vector expressing TIP30 gene (Ad-TIP30) and investigate its tumor suppressive effect in vitro and in vivo.
Methods: Ad-Easy system was used to construct Ad-TIP30 by recombination in E. coli. The virus was packaged in 293 cells and subsequently identified valid. Human HCC (hepatocellular carcinoma) cell lines HepG(2) (p53-wt), PLC/PRL/5 (p53-mut), and osteosarcoma cell line Saos-2 (p53-null) with different p53 genotype were infected with Ad-TIP30 and control virus with Ad-GFP, respectively. The tumor suppressive effect of TIP30 in vitro was examined by trypan blue exclusion method. The expression level of p53 was determined by RT-PCR before and after Ad-TIP30 infection. The in vivo tumor suppressive effect was detected in nude mice with human HCC xenograft.
Results: The expression of TIP30 significantly inhibited the in vitro proliferation of tumor cells, among which HepG(2) with wild type p53 gene was most susceptible to Ad-TIP30 induced growth inhibition. The expression of p53 was significantly up-regulated in HepG(2) after Ad-TIP30 infection as determined by RT-PCR. The growth in nude mice of HCC infected with Ad-TIP30 was significantly inhibited with an inhibition rate of 62.9%.
Conclusion: The expression of TIP30 could inhibit the proliferation of tumor cell lines through both p53-dependent and p53-independent pathways, and may be used as a potential tool for cancer therapy.
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Clinics (Sao Paulo)
January 2025
Department of Otolaryngology and Head and Neck Surgery, The First Affiliated Hospital of Bengbu Medical College, Anhui Province, China. Electronic address:
Objective: TRIB3 has been confirmed to participate in and regulate biological metabolic activities in head and neck tumors such as nasopharyngeal carcinoma and oropharyngeal carcinoma, so the purpose of this study was to explore whether there is a correlation between TRIB3 and Laryngeal Squamous Cell Carcinoma (LSCC) and to preliminarily explore the biological characteristics of TRIB3 in LSCC.
Methods: TRIB3 expression in the LSCC was analyzed based on The Cancer Genome Atlas (TCGA) database. CCK-8 assay, Colony Formation Assay, wound healing assay, and Transwell assay were performed to investigate the roles of TRIB3 in the proliferation, invasion and metastasis of LSCC.
Chem Biodivers
January 2025
Faculty of Chemistry and Life Sciences, Department of Chemistry, Government College University Lahore, Lahore, Pakistan.
Macrophages are heterogeneous cells that are the mediators of tissue homeostasis. These immune cells originated from monocytes and are classified into two basic categories, M1 and M2 macrophages. M1 macrophages exhibit anti-tumorous inflammatory reactions due to the behavior of phagocytosis.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, United States of America.
Dysregulated eIF4E-dependent translation is a central driver of tumorigenesis and therapy resistance. eIF4E binding proteins (4E-BP1/2/3) are major negative regulators of eIF4E-dependent translation that are inactivated in tumors through inhibitory phosphorylation or downregulation. Previous studies have linked PP2A phosphatase(s) to activation of 4E-BP1.
View Article and Find Full Text PDFJ Mol Endocrinol
January 2025
L Maletinska, Biochemistry, Czech Academy of Sciences, Praha, Czech Republic.
Lipopolysaccharides (LPS) are major components of Gram-negative bacteria. LPS not only induce endotoxemia and inflammation, but also contribute to various diseases. In experimental settings, LPS administration serves as a model for acute inflammatory responses.
View Article and Find Full Text PDFMol Cancer Res
January 2025
Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Malignant neoplasms arise within a region of chronic inflammation caused by tissue injuries. Inflammation is a key factor involved in all aspects of tumorigenesis including initiation, proliferation, invasion, angiogenesis, and metastasis. Interleukin-1 (IL-1) plays critical functions in tumor development with influencing the tumor microenvironment and promoting cancer progression.
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