ABSTRACT
Objective To explore the mechanism of gastric carcinoma cell SGC-7901 apoptosis induced by chlorogenic acid-like compounds extracted from Broussonetia papyrifera (CALCBP) bark. Methods The SGC-7901 cells were used to evaluate the anti-tumour activity of the extract in vivo, and the proliferation of cells was examined by MTT assay. The cell morphological changes of cells were observed by DAPI staining; The cell apoptosis and the cell cycle were detected respectively by flow cytometry after PI and Annexin V/PI staining; The intracellular ROS were determined under the fluorescence microscope using DCHF-DA probe, the changes of mitochondrial membrane potential were observed by JC-1 staining. The protein expression of p53, Bcl-2, Bax, and Cytochrome C, p-p38, p-JNK, JNK, p-ERK, ERK were analyzed by Western blotting. Results The proliferation of SGC-7901 cells was inhibited significantly by CALCBP in dose-dependent and time-dependent manner, the condensed chromosome and apoptotic body can be observed in the treated cells and the cell cycle was arrested in G2/M phase, the mitochondrial membrane potential was significantly decreased, whereas the cellular ROS levels of the treated cells were significantly increased. Moreover, the protein expression of p53, Bax, Cytochrome C, and p-p38 were significantly up-regulated and p-ERK and Bcl-2 expression were significantly down-regulated. Conclusion The apoptosis of gastric cancer cell SGC-7901 induced by CALCBP was probably related to oxidative stress of the cell mitochondrial via p38-MAPK and ERK-MAPK signal pathways.
ABSTRACT
<p><b>Background</b>MicroRNAs (miRNAs) have been reported to play vital roles in liver regeneration. Previous studies mainly focused on the functions of intracellular miRNAs, while the functions of circulating exosomal miRNAs in liver regeneration remain largely unknown. The aim of this study was to identify the key exosomal miRNA that played vital roles in liver regeneration.</p><p><b>Methods</b>The Sprague-Dawley male rats were assigned to 70% partially hepatectomized group (n = 6) and sham surgery group (n = 6). The peripheral blood of both groups was collected 24 h after surgery. The exosomal miRNAs were extracted, and microarray was used to find out the key miRNA implicated in liver regeneration. Adenovirus was used to overexpress the key miRNA in rats, and proliferating cell nuclear antigen (PCNA) staining was applied to study the effect of key miRNA overexpression on liver regeneration. Western blotting was used to validate the predicted target of the key miRNA.</p><p><b>Results</b>Exosomal miR-10a was upregulated more than nine times in hepatectomized rats. The level of miR-10a was increased in the early phase of liver regeneration, reached the top at 72 h postsurgery, and decreased to perioperative level 168 h after surgery. Moreover, enforced expression of miR-10a by adenovirus facilitated the process of liver regeneration as evidenced by immunohistochemical staining of PCNA. Erythropoietin-producing hepatocellular receptor A4 (EphA4) has been predicted to be a target of miR-10a. The protein level of EphA4 was decreased in the early phase of liver regeneration, reached the bottom at 72 h postsurgery, and rose to perioperative level 168 h after surgery, which was negatively correlated with miR-10a, confirming that EphA4 served as a downstream target of miR-10a. Moreover, inhibition of EphA4 by rhynchophylline could promote the proliferation of hepatocytes by regulating the cell cycle.</p><p><b>Conclusion</b>Exosomal miR-10a might accelerate liver regeneration through downregulation of EphA4.</p>
ABSTRACT
OBJECTIVE: The aim of the study was to compare transcatheter arterial chemoembolization (TACE) plus ¹³¹I-labelled metuximab with TACE alone for hepatocellular carcinoma (HCC). MATERIALS AND METHODS: A comprehensive search was conducted in PubMed, Embase, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, and Chinese BioMedical Literature Database with published date from the earliest to February 29th, 2016. No language restrictions were applied, but only prospective randomized controlled trials (RCTs) or non-RCTs were eligible for a full-text review. The primary outcome was the overall survival (OS) and effective rate (the rate of partial atrophy or complete clearance of the tumor lesion). The odds ratios (ORs) were combined using either the fixed-effects model or random-effects model. RESULTS: Eight trials (3 RCTs and 5 non-RCTs) were included, involving a total of 1121 patients. Patients receiving combined therapy of TACE plus ¹³¹I-labelled metuximab showed significant improvement in effective rate {OR = 4.00, (95% confidence interval [CI]: 2.40–6.66), p < 0.001}, 1-year OS (OR = 2.03 [95% CI: 1.55–2.67], p < 0.001) and 2-year OS (OR = 2.57 [95% CI: 1.41–4.66], p = 0.002]. CONCLUSION: TACE plus ¹³¹I-labelled metuximab is more beneficial for treating advanced HCCs than TACE alone in terms of tumor response and OS. Large, multi-center, and blinded randomized trials are required to confirm these findings.