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Background: Teicoplanin is a member of vancomycin-ristocetin family of glycopeptide antibiotics. It mediated wound healing by increasing neovascularization possibly through activation of MAP kinase signaling pathway. The aim of this study is an evaluation of c-myc and c-fos genes expression after treatment of cells by teicoplanin and determines whether this glycopeptide antibiotic exerts its proliferation effects by influencing the expression of these genes. Hence, this study was designed to elucidate one possible mechanism underlying teicoplanin effects on cell proliferation using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay.
Materials And Methods: Breast cancer cell line, MCF-7, was cultured, and three different concentrations of teicoplanin were added to the plates. We measured the cell proliferation rate by MTT assay. After cell harvesting, total RNA was extracted to synthesize single-stranded cDNA. Real-time polymerase chain reaction was performed, and the data were analyzed.
Results: It was observed that the level of c-fos and c-myc genes' expressions was decreased at all three different concentrations of teicoplanin.
Conclusion: it could be concluded that although teicoplanin is considered as an enhancing cell growth and proliferation, but probably its effect is not through MAP kinase signaling pathway or perhaps even has inhibitory effect on the expression of some genes such as c-myc and c-fos in this pathway. Hence, the mechanism of action of teicoplanin for increasing cell propagation, through cell signaling pathways or chromosomal abnormalities, remains unclear, and further studies should be conducted.
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http://dx.doi.org/10.4103/2277-9175.190984 | DOI Listing |
Genes Genomics
August 2025
Department of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Qiqihar Medical University, 3 Taishun Street, Tiefeng District, Qiqihar, 161000, Heilongjiang, China.
Background: Our previous research revealed that PRDI-BF1 and RIZ homology domain containing protein 14 (PRDM14) accelerated human non-small cell lung cancer (NSCLC) cell migration. However, the internal mechanism remains unclear.
Objective: Herein, we aimed to explore whether PRDM14 modulates NSCLS cell growth and metastasis via H3K27me3-mediated phosphatidylethanolamine-binding protein 1 (PEBP1)/Raf-1/MEK/ERK signaling.
Sci Rep
August 2025
Department of Pathology, The Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, China.
Neuroblastoma (NB) is the most common extracranial solid tumor in early childhood and frequently presents with bone marrow (BM) metastasis, particularly in high-risk cases. Metastatic NB cells residing in the BM exhibit distinct biological behaviors and are closely associated with treatment resistance and poor prognosis. Emerging evidence suggests that metabolic reprogramming is a hallmark of NB progression; however, its regulatory landscape within the bone marrow microenvironment remains poorly understood.
View Article and Find Full Text PDFBackground: Pulmonary hypertension is a pathophysiological condition characterized by multiple forms of regulated cell death. PANoptosis, which is an inflammation-driven mode of regulated cell death, is regulated by the PANoptosome. Super-enhancers (SEs) have been implicated in the pathology of pulmonary hypertension by modulating the transcriptional regulation of target genes.
View Article and Find Full Text PDFBiomed Pharmacother
July 2025
Institute of Natural Products, Korea Institute of Science and Technology, Republic of Korea. Electronic address:
Notoginsenoside Ft1 (NFt1) is a bioactive compound derived from Panax notoginseng, a traditional medicinal herb that exhibits various pharmacological properties, including anti-inflammatory and anticancer effects. However, its effects on hepatocellular carcinoma (HCC) remain poorly understood. This study sought to investigate the anticancer effects of NFt1 and uncover its fundamental mechanisms in HCC cells.
View Article and Find Full Text PDFNat Commun
May 2025
Department of Molecular and Cellular Biology, University of California, Davis, CA, USA.
The RAS/ERK pathway plays a central role in diagnosis and therapy for many cancers. ERK activity is highly dynamic within individual cells and drives cell proliferation, metabolism, and other processes through effector proteins including c-Myc, c-Fos, Fra-1, and Egr-1. These proteins are sensitive to the dynamics of ERK activity, but it is not clear to what extent the pattern of ERK activity in an individual cell determines effector protein expression, or how much information about ERK dynamics is embedded in the pattern of effector expression.
View Article and Find Full Text PDF