Abstract
Traditional Chinese medicine (TCM) is widely used as an alternative therapy for cancer treatment in China. Glutamine catabolism plays an important role in cancer development. Qici Sanling decoction (QCSL) suppresses bladder cancer growth. However, the association between QCSL and glutamine catabolism remains unknown. In this study, different doses of QCSL were applied to T24 cells, followed by the measurements of cell viability and apoptosis using CCK-8 and Annexin V/PI assay, respectively. Furthermore, glutamine consumption was detected using the glutamine assay kit. QCSL was observed to inhibit cell growth and induced cell apoptosis in a dose-dependent manner. Analysis of glutamine consumption revealed that QCSL suppressed glutamine consumption in T24 cells. Furthermore, QCSL decreased the mRNA and protein levels of c-Myc, GLS1, and SLC1A5. All these effects induced by QCSL could be alleviated by c-Myc overexpression, indicating c-Myc was involved in the protective role of QCSL in bladder cancer. In addition, QCSL was found to inhibit tumor growth in the xenograft tumor model. The similar results were obtained in tumor samples that protein levels of c-Myc, GLS1, and SLC1A5 were decreased upon treatment with QCSL. In conclusion, QCSL suppresses glutamine consumption and bladder cancer cell growth through inhibiting c-Myc expression.
Highlights
Bladder cancer (BC) is one of the most common malignancies, which accounts for an estimated 500,000 new cases and 200,000 deaths each year throughout the world [1]. e high recurrence rate is the main cause of death
Glutaminase 1 (GLS1), frequently upregulated in tumors, is regulated by the transcription factor c-Myc [6]. c-Myc is a member of Journal of Oncology the Myc family which plays critical roles in numerous cellular processes [7]. c-Myc has been reported to activate the expression of glutaminase, GLS, and SLC1A5, resulting in the regulation of glutamine uptake and catabolism [8]
To explore the function of Qici Sanling decoction (QCSL) in BC, different doses (0, 0.05, 0.1, 0.2, 0.5, 1, and 2 mg/ml) of QCSL were applied to BC cell line, T24 cells
Summary
Bladder cancer (BC) is one of the most common malignancies, which accounts for an estimated 500,000 new cases and 200,000 deaths each year throughout the world [1]. e high recurrence rate is the main cause of death. The tumor microenvironment (TME) attracts researchers’ attentions as playing a key role in tumor development, including BC. E diverse TME observed in tumor indicates that adequate nutrients are needed for growth of tumor cells. One of the most abundant amino acids in the TME, is of great importance in the cancer cell metabolism and proliferation [3]. To fulfill the rapid proliferation of cancer cells, enhancing the carbon flux through glutaminolysis is observed [4]. Glutaminolysis is the process of glutamine catabolism. C-Myc is a member of Journal of Oncology the Myc family which plays critical roles in numerous cellular processes [7]. C-Myc has been reported to activate the expression of glutaminase, GLS, and SLC1A5 (solute carrier family 1 member 5), resulting in the regulation of glutamine uptake and catabolism [8] GLS1, frequently upregulated in tumors, is regulated by the transcription factor c-Myc [6]. c-Myc is a member of Journal of Oncology the Myc family which plays critical roles in numerous cellular processes [7]. c-Myc has been reported to activate the expression of glutaminase, GLS, and SLC1A5 (solute carrier family 1 member 5), resulting in the regulation of glutamine uptake and catabolism [8]
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