In recent years, the incidence of colorectal cancer (CRC) has increased and research into new treatment methods for CRC has become a hot topic. Naringin has an inhibitory effect on the PI3k/AKT/mTOR signaling pathway in various tumor cell types and the effect of naringin is closely related to the occurrence and proliferation of tumor cells. The aim of this present study was to investigate whether naringin could inhibit the proliferation of CRC cells by inhibiting the PI3K/AKT/mTOR signaling pathway. This could provide a more mechanism-based treatment for CRC. MTT assays were used to detect the proliferation of CRC cells treated with various concentrations of naringin. The degree of apoptosis and the expression of apoptosis-related proteins (Bcl-2 and Bax) in CRC cells stimulated by naringin was detected using flow cytometry and western blot assays, respectively. The expression levels of PI3K/AKT/mTOR-related proteins [PI3K, AKT, mTOR, phosphorylated (p)-PI3K, p-AKT and p-mTOR] after naringin stimulation in CRC cells were detected using western blot assays. Naringin inhibited the proliferation of CRC cells in a dose-dependent manner. Naringin promoted the apoptosis of CRC cells and inhibited the activation of the PI3K/AKT/mTOR signaling pathway in a dose-dependent manner. The results demonstrated that naringin may be a promising therapeutic agent for the treatment of CRC, which may inhibit the proliferation of CRC cells and induce apoptosis by inhibiting the PI3K/AKT/mTOR signaling pathway.
Background Dysregulation of the splicing activator, RNA-binding motif 4 (RBM4), has recently been reported to be involved in the progression of several cancers. However, the mechanisms that underpin the activity of RBM4 in gastric cancer (GC) remain unknown. The purpose of our study was to explore how RBM4 affects the biological behavior of GC through in vivo and in vitro experiments. Material/Methods Western blot and flow cytometry analyses were used to investigate the RBM4 protein levels in normal gastric epithelial cells and 5 types of GC cells. Cell Counting Kit-8 assay, flow cytometry analysis, wound-healing, and migration and invasion assays were evaluated in vitro in BGC823 and MGC803 GC cells. A xenograft tumor model was used to assess whether RBM4 inhibits GC growth in vivo . Mitogen-activated protein kinase (MAPK) protein levels were determined using western blot analyses. Results Our study revealed that RBM4 protein was downregulated in GC cells. Re-expression of RBM4 inhibited the proliferation, migration, and invasion of GC cells, while promoting apoptosis. Thus, the overexpression of RBM4 can inhibit tumor growth in GC mouse models. We also report that RBM4 was involved in the activation of MAPK-dependent signaling pathways in human GC. Conclusions It is hoped that these findings will improve our understanding of GC pathogenesis while also helping us to explore the feasibility of RBM4-targeted therapy for GC treatment.
The present study investigated the effect of combined sorafenib chemotherapy on hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) expression and survival time of patients with advanced gastric cancer. From January 2010 to December 2011, 92 patients diagnosed with advanced gastric cancer were selected and randomly divided into the treatment group and control group. The treatment group was treated with sorafenib chemotherapy combined with 5-fluorouracil (5-FU), and the control group received 5-FU. The treatment course was 3–4 cycles. During the same period, 46 healthy persons admitted to the Second People's Hospital of Huaian were selected as the controls. A volume of 3–4 ml peripheral blood from each patient and control was collected before and after treatment. The expression levels of HIF-1α and VEGF in peripheral blood were measured by ELISA. The survival time of patients with advanced gastric cancer was followed and analyzed. Compared with healthy controls, serum levels of HIF-1α and VEGF were significantly higher in patients with advanced gastric cancer (P<0.05). After chemotherapy combined with sorafenib, the peripheral blood levels of HIF-1α and VEGF decreased significantly in the treatment group (P<0.05). The 5-year survival rate of patients in the two groups was followed. Compared with the control group, the 1-year survival rate of the treatment group was significantly higher (P<0.05). In conclusion, chemotherapy combined with sorafenib can effectively reduce serum levels of HIF-1α and VEGF in patients with advanced gastric cancer, and improve their 1-year survival rate and prognosis. Therefore, it has significant clinical application value.
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