LncRNA PCAT6 promotes occurrence and development of ovarian cancer by inhibiting PTEN.

OBJECTIVE: The purpose of this study was to explore the expression and function of long non-coding RNA (lncRNA) PCAT6 in ovarian cancer. PATIENTS AND METHODS: Quantitative Real-Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of lncRNA PCAT6 in 42 pairs of ovarian cancer tissues and adjacent normal tissues. Then, the relationship between PCAT6 expression and pathological indicators of ovarian cancer was analyzed. Subsequently, the transfection efficiency of PCAT6 in ovarian cancer cells was verified, and the PCAT6 knockdown model was constructed using lentiviruses in SKOV3 and CAOV3 ovarian cancer cell lines. In addition, Cell Counting Kit-8 (CCK-8) test, wound healing assay and transwell invasion and migration experiments were performed to estimate the effect of PCAT6 on the biological function of ovarian cancer cells, to further explore the possible potential mechanisms. RESULTS: QRT-PCR results showed that the expression level of PCAT6 in ovarian cancer was higher than that in the adjacent normal tissues. The incidence of distant metastasis and lymph node metastasis in patients with high expression of PCAT6 was higher than those with low PCAT6 expression. Compared with the NC group, the proliferation, metastasis and invasion ability of ovarian cancer cells in si-PCAT6 group decreased significantly. QRT-PCR results demonstrated that the PTEN expression was increased after the knockdown of PCAT6. In addition, the recovery experiment also revealed that PCAT6 and PTEN have a mutual regulation, which can jointly regulate the development of ovarian cancer. CONCLUSIONS: LncRNA PCAT6 was up-regulated in ovarian cancer tissues and was closely related to distant metastasis or lymph node metastasis. Additionally, lncRNA PCAT6 might promote the proliferation, migration and invasion of ovarian tumor cells by inhibiting PTEN.

Low plasma miR-25 expression is a favorite prognosis factor in non-small cell lung cancer.

OBJECTIVE: Circulating microRNAs (miRNAs) are promising biomarkers for the diagnosis and prognosis prediction of cancer. In the study, we aimed to investigate the potential clinical significance of the plasma miR-25 in non-small cell lung carcinoma (NSCLC). PATIENTS AND METHODS: We first compared the miRNAs expression pattern between NSCLC tissues and adjacent normal tissues then, bioinformatic analysis of the downstream targets of miR-25 was performed. The diagnostic and prognostic value of the plasma miR-25 in NSCLC was then evaluated. RESULTS: The expression level of miR-25 was increased in NSCLC tissues compared to the adjacent normal tissues. In addition, bioinformatic analysis of the downstream-targeted genes of miR-25 revealed that many gene ontology functions and pathways were associated with cancer progression. The levels of plasma miR-25 were significantly upregulated in NSCLC patients compared to normal controls. In addition, the plasma miR-25 levels were especially higher in NSCLC patients with positive lymph node metastasis, poorly differentiation or advanced clinical stage. Subsequently, we found that the plasma miR-25 expression levels were dramatically decreased in 45 NSCLC patients after receiving surgical treatment. The receiver operating characteristic (ROC) curve analysis indicated that the plasma miR-25 exhibited high diagnostic sensitivity and specificity to discriminate NSCLC cases from healthy subjects. More interestingly, the combination of the plasma miR-25 and carcinoembryonic antigen (CEA) could effectively enhance the accuracy for distinguishing NSCLC patients from normal controls. Moreover, the plasma miR-25 overexpression was closely correlated with aggressive clinical characteristics and poor survival. Finally, the plasma miR-25 was identified as an independent prognostic marker for the overall survival of NSCLC. CONCLUSIONS: Collectively, our findings demonstrated that the plasma miR-25 might serve as a novel promising biomarker in the diagnosis and prognosis prediction of NSCLC.

[Effects of apigenin on lipopolysaccharide induced proliferation of rat aortic vascular smooth muscle cells].

Objective: To investigate the effect of natural active compounds apigenin (API) on the proliferation of rat aortic vascular smooth muscle cells (VSMCs) induced by lipopolysaccharide (LPS) and related mechanisms. Methods: VSMCs of primary cultured SD rats were obtained and the cytotoxic effects of API (0, 10, 20, 40 and 80 µmol/L) was explored by CCK-8 method. Impact of LPS (0, 0.1, 1, 10 and 100 µg/ml) on VSMCs proliferation and the impact of API (0, 10, 20, 40 µmol/L) on LPS (10 µmol)-induced VSMCs proliferation by CCK-8 methods. Using EdU and FCM method, we observed the effect of API on proliferation of VSMCs induced by LPS. VSMCs proliferation and cell cycle were also assessed by EdU method and FACS in 10 µg/ml LPS, 10 µg/ml LPS+ 40 µmol/L API and equal volume DMSO treated VSMCs. Results: (1) CCK-8 cell vitality test showed that cell vitality was not affected by 0-40 µmol/L API, while cell vitality was significantly reduced by 80 µmol/L API (57%), which was significantly lower than in blank group (P<0.05). (2) VSMCs proliferation was significantly promoted by 0.1, 1 and 10 µg/ml LPS and peaked in 10 µg/ml LPS stimulated VSMCs group, while VSMCs proliferation was significantly reduced in 100 µg/ml LPS stimulated group (P<0.05 vs. blank group). (3) LPS (10 µm/ml) induced VSMCs proliferation was not affected by 10 µmol/L API, which was significantly inhibited by 20 and 40 µmol/L API (both P<0.05 vs. LPS). (4) VSMCs proliferation assessed by EdU was significantly higher in LPS group than in blank group (P<0.01), which could be significantly reduced by cotreatment with API (P<0.01). (5) FACS results showed that percent of VSMCs in G0/G1 stage was significantly lower in LPS group compared to blank group (P<0.05), which could be significantly increased post API treatment (P<0.05 vs. LPS), while percent of VSMCs in S stage was significantly lower post API treatment in comparison with LPS group. Conclusion: API can significantly inhibit LPS-induced proliferation of VSMCs, partly through inhibiting mitosis and inducing G0/G1 cell cycle arrest.

[Finite element analysis of different load mode on tooth movement for space closure in patient with bimaxillary protrusion].

OBJECTIVE: To investigate the stress distribution on the maxillary anterior teeth retracted with sliding mechanics and micro-implant anchorage using different retraction hook heights and positions. METHODS: DICOM image data including maxilla and upper teeth were obtained with cone-beam CT. The three-dimensional finite element model was constructed using Mimics software. Brackets and archwire model were constructed using Creo software. The models were instantiated using Pro/Engineer software. Abaqus software was used to simulate the sliding mechanics by loading 2 N force on 0, 2, 4, 6, 8, 10 mm retraction hooks and three different positions, repectively. Rotation of the occlusal plane, the initial displacement and stress distribution of teeth were analyzed. RESULTS: Lingual rotation of maxillary central incisor(0.021°), gingival movement of the maxillary first molar(0.005 mm), and clockwise rotation of the maxillary occlusal plane(0.012°) were observed when the force application point located at the archwire level (0 mm). In contrast, 0.235° labial rotation of the maxillary central incisor, 0.015 mm occlusal movement of the maxillary first molar, and 0.075° anti-clockwise rotation of the maxillary occlusal plane were observed when the force application point located at the higher level(10 mm retraction hook). The more the force application point was located posteriorly at the archwire level, the less lingual rotation of the maxillary central incisor and the more buccal displacement of maxillary first molar was observed. CONCLUSIONS: Maxillary anterior tooth rotation and retraction, vertical displacement of posterior segment, and rotation of the occlusal plane could be controlled by adjusting the height and position of the retraction hook in space closure using miniscrew and sliding mechanics.

Permanent hepatic artery embolization with dextran microspheres in 131 patients with unresectable hepatocellular carcinoma.

One hundred thirty-one patients with hepatocellular carcinoma were subjected to permanent hepatic artery embolization with dextran microspheres (G-25, 50-150 mu). Dextran hepatic artery embolization is indicated for massive, nodular or multinodular hepatocellular carcinoma with total bilirubin less than 3 mg/dl, serum albumin greater than 3.0 g/dl, tumor involvement area less than 50% or without involvement of the main portal vein. Following hepatic angiography a catheter was inserted superselectively into the hepatic artery feeding the tumor. Adriamycin (60-80 mg) or cisplatin (60-100 mg) was infused immediately before embolization. Under fluoroscopic guidance, 0.3-0.5 g of dextran microsphere embolizer permeated with 10 mg of mitomycin C was infused into the feeding artery through the catheter. Dextran microspheres caused marked homogeneous and distal micro-arterial embolization, especially in the arteriole with a caliber of about 100 mu. Dextran microspheres were not resorbed in a period of 16 weeks in humans, thus reducing or preventing the formation of intrahepatic and extrahepatic collaterals after hepatic artery embolization. Dextran hepatic artery embolization was very effective for not only main tumor but also daughter foci or metastatic nodules, as was confirmed histologically in 8 cases. The 1-year, 2-year and 3-year survival rates were 57.0%, 31.4% and 24.2% respectively.