For HT29-D4 cell line, we confirmed the interaction between c-Myc protein and microtubules by immunoprecipitation. We then studied the effect of antimitotic agents, nocodazole and the taxoids [paclitaxel (taxol) and docetaxel (taxotere)] on c-myc oncogene expression. The expression was analyzed by RT-PCR and Western blot. Taxol (1 microM), taxotere (1 microM) and nocodazole (3 microM) inhibited by 30-50% the c-myc induction produced by growth factors in culture medium. According to the flow cytometry analysis, the inhibition is not linked to the mitotic block. These results observed for both stabilizing and depolymerizing agents suggest that microtubular system is involved in c-myc expression more through its dynamic properties which influence signal transduction and intracellular transports than through its direct interaction with c-Myc protein.
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http://dx.doi.org/10.1006/bbrc.1997.6187 | DOI Listing |
Adv Pharmacol Pharm Sci
November 2024
Cancer Chemoprevention Research Center, Faculty of Pharmacy, Universitas Gadjah Mada, Yogyakarta, Indonesia.
Hepatocellular carcinoma (HCC) is one of the most aggressive types of liver cancer, and it is frequently associated with upregulated c-Myc expression. Sorafenib (Sor) is commonly used to treat HCC, but many patients experienced mild to severe side effects due to prolonged Sor treatment during therapy. It has been known that Pentagamavunone-1 (PGV-1) exhibits a remarkable antiproliferative effect on several cancer cells, yet limited studies have reported its cellular activities in HCC.
View Article and Find Full Text PDFFront Immunol
December 2024
National and Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China.
Introduction: Portal hypertension combined with hypersplenism (PHcH) is the main cause of hypocytosis and esophagogastric variceal hemorrhage in patients with liver cirrhosis. Activated macrophages that destroy excess blood cells are the main cause of hypersplenism, but the activating pathway is not very clear. This study aims to investigate the activation types of splenic macrophages and their activation mechanisms, to provide experimental evidence for the biological treatment of splenomegaly, and to find a strategy to improve liver fibrosis and inflammation by intervening in splenic immune cells.
View Article and Find Full Text PDFJ Biol Chem
November 2024
State Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing, China. Electronic address:
Understanding the mechanisms behind MYC-driven oncogenic transformation could pave the way for identifying novel drug targets. This study explored the role of CREPT in MYC-induced malignancy by generating MYC-transformed mouse embryonic fibroblasts (MEFs) with conditional CREPT deletion. Our results demonstrated that the loss of CREPT significantly impaired MYC-induced colony formation and cell proliferation, indicating that CREPT is essential for the malignant transformation of MEFs.
View Article and Find Full Text PDFCell Death Dis
November 2024
Early Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, UK.
Oncogenic transformation and Oct4, Sox2, Klf4 and c-Myc (OSKM)-mediated induction of pluripotency are two independent and incompatible cellular fates. While continuous expression of OSKM can convert normal somatic cells into teratogenic pluripotent cells, it remains speculative what is the impact of transient OSKM expression in cancer cells. Here, we find that OSKM expression limits the growth of transformed lung cells by inducing apoptosis and senescence.
View Article and Find Full Text PDFMol Biol Rep
November 2024
Cellular and Molecular Research Center, Gerash University of Medical Sciences, Gerash, Iran.
Background: Chronic Myeloid Leukemia (CML), accounting for 15-20% of adult leukemia cases, is marked by the Philadelphia chromosome, resulting from the t(9;22)(q34;q11) translocation. This leads to uncontrolled cell proliferation and survival. Imatinib therapy lowers BCR-ABL levels, influencing telomere-associated proteins and increasing telomerase accessibility, indirectly boosting its activity.
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