Melittin can induce apoptosis of human gastric cancer (GC) cells through the mitochondria pathways, and it may be a potent agent in the treatment of human GC.
Aidi injection, a proprietary Chinese medicine, has been widely used for the treatment of cancer. However, its effects and potential mechanism in esophageal squamous cell carcinoma (ESCC) have not yet been characterized. The aim of the present study was to identify the mechanism underlying the anti-metastatic effects of treatment with Aidi. To test the effects and mechanism, EC9706 and KYSE70 cells were selected for in vitro experiments. In vivo, the anti-metastatic effects of Aidi injection on a nude mouse peritoneal metastasis model were examined, and the mechanisms were assessed with immunohistochemical staining. A cell proliferation assay demonstrated that treatment with more than 3 mg/ml Aidi for 24 or 48 h significantly inhibited the proliferation of EC9706 (P<0.01) and KYSE70 cells (P<0.05, P<0.01). Subsequent experiments assessed cell migration, invasion and vasculogenic mimicry (VM) formation, with 5-fluorouracil serving as a positive control. It was observed that treatment with Aidi inhibited cell migration, invasion and VM formation. Furthermore, it was identified that treatment with Aidi inhibited epithelial-mesenchymal transition (EMT) signaling and the expression of vascular endothelial growth factor A (VEGF-A) in EC9706 and KYSE70 cells, using western blotting. In the in vivo experiments, Aidi injection effectively suppressed tumor metastasis in the mouse tumor model. Additionally, the expression of vimentin and vascular endothelial growth factor was decreased, and the expression of cadherin-1 was increased in the tumor tissue. The present results suggested that treatment with Aidi may inhibit tumor metastasis in ESCC through the inhibition of EMT signaling and angiogenesis.
DJ-1, an oncogene, has been reported to be an independent prognostic indicator of poor survival in patients with esophageal squamous cell carcinoma (ESCC). The aim of the present study was to investigate the role of DJ-1 in tumor cell proliferation and invasion in ESCC and its underlying mechanisms. It was observed that the expression level of DJ-1 was upregulated and positively associated with EMT biomarkers in 84 human ESCC tissue specimens. Overexpression and knockdown experiments demonstrated that DJ-1 was involved in proliferation, migration, invasion and EMT in ECA-109 cells in vitro and extensive peritoneal seeding in a peritoneal dissemination mice model. Furthermore, the present data revealed that DJ-1 could activate the Wnt/β-catenin signaling pathway, which mediates the EMT and metastasis in ESCC. In conclusions, DJ-1 promoted proliferation, invasion, metastasis and the EMT in ESCC via activation of the Wnt/β-catenin signal pathway. The present results suggested DJ-1 could represent a promising therapeutic target for the prevention and treatment of ESCC-related metastasis.
Myelolipoma is a kind of rare benign tumour composed of mature adipocytes and hemopoietic elements, and is most often found in the adrenal glands. Primary mediastinal myelolipoma (PMM) more rarely happens and has no definite symptoms, and mediastinal masses are usually found in chest examination. The patients normally receive a surgical resection and have a favorable prognosis after postoperative pathological diagnosis. Here, we present the case of PMM, which was resected via video-assisted thoracic surgery (VATS), and investigate recent correlative literatures to summarize its etiology, histopathology, differential diagnosis and therapeutic method. In this way, we aim to improve clinical doctors' understanding of this disease.
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