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Propofol, a commonly used intravenous anesthetic during cancer resection surgery, has been found to exhibit tumor inhibitory effects in vitro and in vivo. The role of propofol in lung cancer has been previously reported, whereas its action mechanism remains unclear. This study further investigated the effects of propofol on lung cancer A549 cell growth, migration and invasion, as well as the underlying mechanisms. Cell viability, proliferation, migration, invasion and apoptosis were assessed by CCK-8 assay, BrdU assay, two chamber transwell assay and flow cytometry, respectively. The regulatory effect of propofol on microRNA-372 (miR-372) expression in A549 cells was analyzed by qRT-PCR. Cell transfection was used to change the expression of miR-372. The protein expression of key factors involving in cell proliferation, apoptosis, migration and invasion, as well as Wnt/β-catenin and mTOR pathways were analyzed by western blotting. Propofol inhibited lung cancer A549 cell viability, proliferation, migration, and invasion, but promoted cell apoptosis. Moreover, miR-372 was down-regulated in propofol-treated A549 cells. Overexpression of miR-372 abrogated the effects of propofol on proliferation, migration, invasion and apoptosis of A549 cells. Knockdown of miR-372 had opposite effects. Furthermore, propofol suppressed Wnt/β-catenin and mTOR signaling pathways by down-regulating miR-372. Propofol inhibits growth, migration and invasion of lung cancer A549 cells at least in part by down-regulating miR-372 and then inactivating Wnt/β-catenin and mTOR pathways.

Dysregulation of microRNA (miRNA) expression in various cancers and their role in cancer progression is well documented. The purpose of this study was to investigate the biological role of miR‐372 in human pancreatic adenocarcinoma (HPAC). We collected 20 pairs of HPAC tissues and adjacent non‐cancerous tissues to detect miR‐372 expression levels. We transfected BXPC‐3 and PANC‐1 cells with miR‐372 inhibitor/mimics to study their effect on cell proliferation, apoptosis, invasion, migration and autophagy. In addition, miR‐372 mimics and a tumor protein UNC51‐like kinase 1 (ULK1) siRNA were co‐transfected into BXPC‐3 and PANC‐1 cells to explore the mechanism of miR‐372 and ULK1 on HPAC tumorigenesis. We found that the expression of miR‐372 was markedly downregulated in HPAC cells compared to adjacent normal tissues. Furthermore, functional assays showed that miR‐372 inhibited cell proliferation, invasion, migration and autophagy in BXPC‐3 and PANC‐1 cells. An inverse correlation between miR‐372 expression and ULK1 expression was observed in HPAC tissues. Downregulation of ULK1 inhibited the overexpression effects of miR‐372, and upregulation of ULK1 reversed the effects of overexpressed miR‐372. Finally, we found that silencing ULK1 or inhibiting autophagy partly rescued the effects of miR‐372 knockdown in HPAC cells, which may explain the influence of miR‐372/ULK1 in HPAC development. Taken together, these results revealed a significant role of the miR‐372/ULK1 axis in suppressing HPAC cell proliferation, migration, invasion and autophagy. Human pancreatic adenocarcinoma tissue downregulated miR‐372, and miR‐372 plays a negative role on HPAC cell growth. ULK1 as a direct target of miR‐372, and a reversed correlation existed between miR‐372 expression levels and ULK1 mRNA levels in HPAC. The loss of phosphorylation of ULK1 on Ser 555 induced by miR‐372 inhibits HPAC cell autophagy.

Today, researchers have succeeded in achieving oocyte-like cells through the in vitro differentiation of stem cells. MicroRNAs are key regulators of oocyte development. In this study we decided to evaluate the expression pattern of microRNA-21, microRNA-15a, and microRNA-372 in oocyte-like cells, to determine the maturation stage of oocyte-like cells. Human follicular fluid samples were collected and centrifuged, and their cells were divided into 3 groups; day 7 as control group, days 14 and 21. During this period, the cells were evaluated for their morphological appearance and viability by inverted microscopy. RNA isolation was performed and cDNA was reversely transcribed by specific stem-loop RT primers. Real-time RT-PCR was used to detect microRNA expression. The relative expression of microRNA-21 and microRNA-15a on day 21 was significantly down-regulated compared to the control group (day 7), but microRNA-372 did not show a significant difference. Also, on day 14 compared to the control group (day 7), microRNA-21 did not show a significant difference; but microRNA-15a and microRNA-372 were significantly down-regulated. MicroRNA-21 and microRNA-15a on day 21 compared to day 14 revealed down-regulated levels, but microRNA-372 revealed up-regulated levels. Our results showed significant decreases in the expression of microRNA-21 and microRNA-15a in oocyte-like cells, as well as in oocytes, which may lead to cytoplasmic maturation, germinal vesicle break down and the completion of meiosis І. In addition, down-regulation expression of microRNA-372 maybe a confirmation that mesenchymal stem cells have differentiated into germ cells, and these cells were differentiated into oocyte-like cells.

Background Recent studies have shown that miR-372 plays important roles in hepatocellular carcinoma (HCC) progression. However, results have been conflicting regarding its expression levels and role in HCC. Methods RT-PCR and in situ hybridization was used to evaluate miR-372 expression in HCC tissues and cell lines. The methylation status of neighboring CpG islands upstream of the miR-372 promoter was analyzed by methylation-specific PCR (MSP). Transfection of miR-372 mimic into HCC cell lines was used to evaluate cellular proliferation and invasion. Prognostic significance was analyzed by the Kaplan–Meier survival method and Cox regression. Results miR-372 was expressed at lower levels in HCC tissues compared with controls and was related to tumor metastasis and poor prognosis. Hypermethylation of miR-372 was detected in HCC cell lines and tissues, and miR-372 expression was restored upon 5-aza-dCyd treatment. Upregulated expression by mir-372 mimic transfection inhibited proliferation and invasion capacity in HCC cells. Conclusions miR-372 may play an important role in hepatic carcinogenesis and may serve as a new target or method to detect and treat HCC in the future.

MicroRNA-372 (miR-372) has been demonstrated to play a crucial role in cellular proliferation and apoptosis of cancer cells. However, its effects in hepatocellular carcinoma (HCC) have not been explored. The aim of this study was to investigate the clinical significance of miR-372 in human HCC. Quantitative RT-PCR was performed to detect miR-372 expression in HCC clinical samples and cell lines. Then, Kaplan–Meier and Cox proportional regression analyses were performed to determine the association of miR-372 expression with survival of HCC patients. Moreover, the effects of miR-372 on tumorigenicity of HCC cell lines were evaluated by in vitro assays. miR-372 expression in HCC tissues was significantly higher than in the corresponding normal adjacent liver tissues ( P  < 0.001). There was a correlation between miR-372 upregulation and advanced TNM stage of HCC patients ( P  = 0.02). In addition, HCC patients with higher miR-372 expression had significantly poorer recurrence-free survival ( P  = 0.006) and overall survival ( P  = 0.001). Multivariate analysis revealed that high miR-372 expression was an independent predictor of poor prognosis (for recurrence-free survival: Hazard Ratio [HR] 6.826, P  = 0.01; for overall survival: HR 9.533, P  = 0.008). Moreover, in vitro assays demonstrated that the ectopic expression of miR-372 may significantly promote the cellular proliferation, invasion, and migration of HCC cell lines. Our findings showed that miR-372 may serve as a potent prognostic marker for tumor recurrence and survival of HCC patients. Furthermore, miR-372 has been identified as a promoter for tumorigenicity of HCC cells, suggesting that it might be a prospective therapeutic target for HCC.

Nasopharyngeal carcinoma (NPC) is a common cancer found in the nasopharynx, which plagues countless NPC patients. MicroRNA‐372 (miR‐372) has been reported to be involved in various tumors. Here, we explored the important role of miR‐372 in radiosensitivity, invasion, and metastasis of NPC. Microarray analysis was conducted to search the NPC‐related differentially expressed genes (DEGs) and predict the miRs regulating PBK, which suggested that miR‐372 could influence the development of NPC via PBK and the p53 signaling pathway. Importantly, miR‐372 was observed to target PBK, thus down‐regulating its expression. Then, NPC 5‐8F and C666‐1 cells were selected, and treated with ionization radiation and alteration of miR‐372 and PBK expression to explore the functional role of miR‐372 in NPC. The expression of miR‐372, PBK, Bcl‐2, p53, and Bax as well as the extent of Akt phosphorylation were measured. In addition, cell colony formation, cell cycle, proliferation, apoptosis, migration, and invasion were detected. At last, tumor growth and the effect of miR‐372 on radiosensitivity of NPC were evaluated. Besides, over‐expressed miR‐372 down‐regulated Bcl‐2 and PBK expression and the extent of Akt phosphorylation while up‐regulated the expression of p53 and Bax. Additionally, miR‐372 over‐expression and radiotherapy inhibited cell clone formation, proliferation, tumor growth, migration, invasion, and cell cycle entry, but promoted cell apoptosis. However, the restoration of PBK in NPC cells expressing miR‐372 reversed the anti‐tumor effect of miR‐372 and activation of the p53 signaling pathway. In conclusion, the study shows that up‐regulated miR‐372 promotes radiosensitivity by activating the p53 signaling pathway via inhibition of PBK. In conclusion, the study shows that up‐regulated miR‐372 promotes radiosensitivity by activating the p53 signaling pathway via inhibition of PBK.

The aim of the present study was to investigate the expression of microRNA (miRNA)-372 in the serum of patients with hyperlipidemic acute pancreatitis (HTGAP), and its clinical significance. Patients with a serum lipid concentration ≥11.3 or 5.65-11.3 mmol/l with chylous serum were included in group A (n=40). The remaining patients did not have HTGAP and were included in group B (B). A further 25 patients with hyperlipidemia, but not AP (group C), and 30 healthy volunteers (group D) were recruited as controls. The level of miR-372 in the serum of group A (4.76±2.60) was significantly increased compared with groups B (0.98±0.80), C (0.85±0.62) and D (0.76±0.44); however, there was no significant difference in the expression of miR-372 between groups B, C and D. The expression level of miR-372 was significantly increased in the severe HTGAP group (6.45±2.20) compared with the mild HTGAP group (3.08±1.74). Further experiments suggested that the expression level of miR-372 was positively correlated with the level of triacylglycerol (r=0.666; P<0.001) but not with the level of amylase (r=-0.145; P>0.05). ROC analysis indicated that the combined use of miR-372 expression levels and Acute Physiology and Chronic Health Evaluation II scoring improved the diagnostic value for HTGAP. In summary, the expression of miR-372 in HTGAP was significantly upregulated and increased with the severity of the disease. The results of the present study may provide a novel strategy for the diagnosis and severity assessment of HTGAP in the clinic.

The present study aimed to investigate the expression pattern and underlying mechanism of microRNA-372 (miR-372) in the progression of ulcerative colitis (UC). Reverse transcription-quantitative polymerase chain reaction was used to measure miR-372 expression levels in the blood and colonic mucosa tissue samples from patients with UC. The present study demonstrated that levels of miR-372 were significantly increased in the blood and colonic mucosa tissue samples from patients with UC compared with healthy controls. Furthermore, the level of serum miR-372 was positively correlated with the level of serum c-reactive protein. Receiver operating characteristic analysis indicated that levels of miR-372 detected in serum and tissue samples could be used to screen for patients with UC from healthy controls. These results indicated a potential role of miR-372 as a diagnostic marker and therapeutic target for patients with UC. Furthermore, a conserved miR-372 binding site in the 3′untranslated region of the NLR family pyrin domain containing 12 (NLRP12) was identified. Dual luciferase assay demonstrated that overexpression of miR-372 significantly reduced the relative luciferase activity of pmirGLO-NLRP12-3′UTR compared with control pmirGLO. In addition, western blot analysis indicated that overexpression of miR-372 significantly decreased the protein expression level of NLRP12. Therefore it was hypothesized that miR-372 may promote the progression of UC by suppressing NLRP12 protein expression and thereby inducing the excessive production of inflammatory cytokines. In conclusion, high levels of miR-372 detected in peripheral blood samples may serve a role as a potential biomarker to screen potential patients with UC from healthy controls.

Aberrant microRNA (miRNA) expression has been investigated in gastric cancer, which is one of the most common malignancies. However, the roles of miRNAs in gastric cancer remain largely unknown. In the present study, we found that microRNA-372 (miR-372) directly targets tumor necrosis factor, α-induced protein 1 (TNFAIP1), and is involved in the regulation of the NFκB signaling pathway. Furthermore, over-expression of TNFAIP1 induced changes in AGS cells similar to those in AGS cells treated with miR-372-ASO. Collectively, these findings demonstrate an oncogenic role for miR-372 in controlling cell growth and apoptosis through downregulation of TNFAIP1. This novel molecular basis provides new insights into the etiology of gastric cancer.

It has been reported that hsa-microRNA (miRNA/miR)-372 functions as a tumor suppressor or oncogene in various digestive system tumors, however, its roles in gallbladder cancer (GBC) are yet to be established. The present study aimed to determine the expression and clinical relevance of hsa-miR-372 in GBC. The expression of hsa-miR-372 in 80 pairs of human GBC tissues and adjacent normal gallbladder tissues was measured by reverse transcription-quantitative polymerase chain reaction. Subsequently, the associations between hsa-miR-372 expression levels and the clinicopathological characteristics of patients with GBC were determined using χ2 test. Furthermore, Kaplan-Meier method and Cox regression analysis were performed to evaluate the association between hsa-miR-372 expression and the prognosis of patients with GBC. Furthermore, a dual-luciferase reporter assay and western blot analysis were performed to predict and verify the target gene of hsa-miR-372. The results demonstrated that markedly lower hsa-miR-372 expression was observed in GBC tissues, which was associated with poor prognosis in patients with GBC. Downregulated expression of hsa-miR-372 was negatively associated with tumor histological grade, tumor-node-metastasis stage, lymph node metastasis and distant metastasis, however, no association was observed between reduced hsa-miR-372 expression and patient gender, age, tumor size and gallbladder stones. Multivariate Cox regression analysis revealed that hsa-miR-372 expression, histological grade and lymph node metastasis were independent prognostic factors for overall survival in patients with GBC. Chloride intracellular channel 1 (CLIC1) was previously reported to be an effective biomarker for predicting the prognosis of GBC. Notably, the results of the present study indicated that CLIC1 may be a direct target gene of hsa-miR-372. In conclusion, the current study provides the first statistically convincing evidence that downregulation of hsa-miR-372 may occur in GBC tissues, which may be associated with aggressive and progressive tumor behavior by affecting CLIC1 expression.