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ITGB4 as a novel solution analysis biomarker and potential restorative focus on pertaining to digestive tract cancer malignancy.
Western blot assay was used to detect the expression of PLCD1 in cells of each group. Results Compared with RWPE-2 cells, the expression level of miRNA-191 in human prostate cancer cells was significantly higher (P ＜0.05), and the expression level of miRNA191 in PC-3 was significantly higher than that in other three cell lines (P＜0.05). After inhibiting the expression of miRNA-191, the expression levels of PLCD1 was significantly higher while PC-3 cells' proliferation ability was inhibited, and their migration and invasion ability were significantly lower than those of blank control group and miRNA-191 NC group (P＜ 0.05). The results of double luciferase reporter gene assay showed that PLCD1 gene was a target gene of miRNA-191. Conclusion miRNA-191 promote the proliferation, migration and invasion of prostate cancer PC-3 cells by targeting PLCD1.Objective To investigate the relationship between toosendanin(TSN) and CTP synthase(CTPS) cytoophidium formation in gastric cancer MKN-45 cells. Methods In this study, the experimental material is MKN-45 human gastric cancer cells. It contains 7 treatment groups of 0, 20, 40, 60, 80, 100, and 120 nmol/L TSN. Each group was treated in triplex privately for 24、48 and 72 hours. Cell counting kit-8 (CCK8) was used to detect the inhibitory effect of TSN on the proliferation of MKN-45 cells. After immunofluorescence detection, the morphology of CTPS cells was observed by a laser confocal microscope. The effect of TSN on MYC gene expression was detected by qRT-PCR. In addition, it contains 2 treatment groups of 1 mmol/L DON and 1 mmol/L MPA, each group was treated in triplex privately for 6 hours and then the cytoophidium morphology was detected by immunofluorescence. Results The results of immunofluorescence showed that CTPS formed a filamentous cytoophidium structure after treating MKN-45 cells with 1 mmol/L DON and 1 mmol/L MPA, which means that the cells have the ability to form CTPS cytoophidium; The cell proliferation rate of TSN treatment group was significantly lower than that of 0 nmol / L TSN group (P＜0.01); Immunofluorescence results showed that CTPS cytoophidium was the most abundant in MKN-45 cells after treated with 80 nmol/L TSN for 72 h. The results of qRT-PCR showed that MYC expression in cells was significantly decreased after treated with 80 nmol/L TSN for 24 h (P＜0.05), and MYC expression was significantly increased after 48 h (P＜0.01), and then decreased. Conclusion Toosendanin may affect intracellular cytoophidium assembling by regulating the expression of MYC.Objective Human gastric cancer SGC-7901 cells were treated with betulinic acid(BA)at the concentrations of 0, 10, 20, and 30 μg/ml, and treated with conventional chemotherapeutic drug 5-Fu as a positive control to explore its effect on cell proliferation. Trypan blue and GIEMSA staining method were used to investigate the effect of BA on cell growth inhibition and clone formation. EdU method and flow cytometry were used to explore the proliferation and cell cycle of SGC-7901 cells after treated with BA, respectively. qRT-PCR and Western blot were also applied to determine the mRNA and protein levels of cyclin D1 and cyclin B1. Results The cell growth inhibition rate was increased after treated with different concentrations of BA in SGC-7901 cells(P＜0.05). After treated for 48 h, BA decreased the clone information and cell proliferation of SGC-7901 cells markedly in dose-and time-dependent manners (P＜0.01). Flow cytometry analysis showed that BA obviously increased the proportion of SGC-7901 cells in G1 phase but decreased the proportion of those in S phase. qRT-PCR and Western blot analysis showed that the mRNA and protein levels of cyclin D1 and cyclin B1 were significantly downregulated by BA at different concentrations(P＜0.01). Compared with the 5-Fu control group, when the concentration of BA was 20 μg/ml and 30 μg/ml, the cell proliferation ability was significantly decreased, the cell cycle was inhibited, and the expression of cyclin was reduced (all P＜0.05). Conclusion The betulinic acid regulates the proliferation of SGC-7901 cells by inhibiting the expressions of cyclin D1 and cyclin B1, which leads to cell cycle arrest and proliferative inhibition.Objective To investigate the effects of long-chain non-coding RNA (lncRNA) UNC5B-AS1 on the adhesion, invasion and migration of lung cancer cells by regulating the expression of miR-218-5p. Methods Twenty specimens of lung cancer patients and corresponding paracancerous tissues were surgically removed and collected from the oncology department of Chongqing Three Gorges Central Hospital from June 2017 to June 2019. Real-time quantitative PCR (qRT-PCR) was used to detect the expressions of UNC5B-AS1 in human bronchial epithelial cells HBE and different lung cancer cells of A549, H1437, H1975, H1299 and H460. UNC5B-AS1 siRNA was transfected into lung cancer A549 cells. Adhesion assay, transwell invasion assay and scratch assay were used to detect the effect of UNC5B-AS1 on adhesion, invasion and migration of A549 cells. qRT-PCR and dual luciferase reporter gene were used for the detection and identification of UNC5B-AS1 targeting miR-218-5p. The expression of epithelial-mesenchymal transition (EMT)-related protein was detected by Western blot. Results The expression of UNC5B-AS1 in lung cancer tissues and cells was significantly higher than that in adjacent tissues and bronchial epithelial cells (P＜0.05). The expression of UNC5B-AS1 in lung cancer A549 cells was the highest (P＜0.05). Down-regulation of UNC5B-AS1 expression inhibited adhesion, invasion and migration of A549 cells (P＜0.05). qRT-PCR and dual luciferase reporter assay experiments showed that UNC5B-AS1 targeted the regulation of miR-218-5p expression. Down-regulation of UNC5B-AS1 inhibited E-cadherin protein expression and promoted Vimentin and Twist protein expression. Conclusion lncRNA UNC5B-AS1 promotes adhesion, invasion and migration of lung cancer cells through targeted regulation of miR-218-5p expression, and its mechanism may be related to the promotion of EMT.Objective To investigate the toxic effects of vitamin C (VC) combined with temozolomide (TMZ) on gliomas and its mechanism. Methods Human glioma cells BMG-1 and SHG44 cells were cultured in vitro, specifically divided into control group (without VC and TMZ), TMZ group (0.2 mmol/L), VC (0.5 mmol/L)+TMZ(0.2 mmol/L) group and TMZ(0.2 mmol/L TMZ)+U0126(10 μmol/L)group, each experiment was repeated three times. Cell survival rate was detected by MTT assay; Cell apoptosis was detected by flow cytometry and Annexin V-FITC/PI staining; Reactive oxygen species (ROS) levels were detected by ROS detection kit, and Western blot was used to detect the expression levels of proteins related to apoptosis, autophagy and ERK pathway. Results Compared with the control group, the survival rate of glioma cells in the TMZ group was decreased significantly(P＜0.05). Compared with the TMZ group, the survival rate of glioma cells in the VC+TMZ group was decreased significantly(P＜0.01), the cell apoptosis rate was increased, and the expressions of Bax, Cleaved caspase-3 and Cleaved PARP protein were increased, while the expression of Bcl-2 was decreased. The ROS level and autophagy rate were decreased, while the expression of LC3-II/LC3-1 was decreased, and the expression of p62 was increased in the VC+TMZ group (all P＜0.05). Anlotinib inhibitor At the same time, VC combined with TMZ decreased the expression level of p-ERK1/2-related protein in BMG-1 and SHG44 cells, and increased the apoptosis rate (P＜0.05). Conclusion VC combined with temozolomide can enhance the toxicity of glioma cells. This effect is to promote apoptosis and inhibit temozolomide-mediated autophagy through the regulation of the ERK signaling pathway.Objective To explore the role and mechanism of polysaccharide-1 (syndecan-1) in the transformation of lung epithelial stroma (EMT) in rats with chronic obstructive pulmonary disease (COPD). Methods Thirty male SD rats of clean grade were randomly divided into sham operation group (normal saline injection after tracheal exposure, n=10), COPD group (fumigation after injection of 1 mg/ml lipopolysaccharide, transfection of 100 μl empty virus, n=10) and syndecan-1 overexpression group (fumigation after injection of 1 mg/ml lipopolysaccharide, and transfection of 100 μl carrying rat syndecan-1 gene Ad-CMV-GFP-SDC1, n=10), once a day for two weeks. After the treatment, the lung function was detected and lung tissues were collected. HE staining was used to observe lung injury. The expression levels of syndecan-1, vimentin and E-cadherin in lung tissue of rats in each group were detected by immunohistochemistry. Western blot was used to detect the expressions of TGF-β1, Smad2/3 and p-Smad2/3. The mRNA levels of vimenrotein were significantly decreased (P＜0.05). Conclusion In COPD rats, TGF-β/Smad signal pathway activation induced the production of EMT; overexpression of syndecan-1 could inhibit the EMT mediated by TGF-β/Smad signal pathway, and improve the lung tissue injury of COPD rats.Objective To investigate the effects of Bushen Zhuanggu granule on the expressions of serum growth hormone (GH) and insulin-like growth factor-1(IGF-1) and their receptors in bone tissues of ovariectomized rats. Methods Forty-eight SD female rats (weight 273±21.3 g) were divided into 4 four groups the dosage of Bushen Zhuanggu granule group (BSZG) was 2.5 g/(kg·d),the do -sage of estradiol group(E2) was 0.071mg/(kg·d),sham group (SHAM) and ovariectomized model group (OVX group) were given the same amount of saline by oral administration.Each group included 12 rats,the treatments were conducted once a day. After 3 and 6 months of treatment,bone mineral density (B -MD) was measured by bone density instrument;the serum levels of GH and IGF-1 were detected by EL-ISA;the expressions of GHR and IGF-1R of bone tissue were detected by qPCR;the optical density(OD)value and positive cell count of pituitary GH immunohistochemical tablets were analyzed by Image J software,respectively. Results ①After 3 months interventioGF-1 in serum and its receptors in bone tissues of ovariectomized osteoporosis rats to prevent further loss of bone mass and increase bone mineral density.Objective To study the expression and correlation of mir-203a and its target gene ATM in breast cancer tissues, so as to provide theoretical basis for the pathogenesis of breast cancer, especially lymph node metastasis. Methods Thirty paired breast cancer and paracancer normal tissues were collected, and RT-qPCR was used to detect the relative expression levels of mir-203a and ATM in the samples of the two groups. Correlation analysis was conducted for mir-203a and ATM, and correlation analysis was conducted for the pathological characteristics, so as to compare whether there were statistical differences between mir-203a and ATM in lymph node metastasis and non-metastasis. Results Compared with normal paracancer tissues, the expression level of mir-203a in breast cancer tissues was significantly increased (P＜0.01), and the expression level of ATM was significantly decreased (P＜0.01), showing a significant negative correlation between the two tissues (r=-0.847,P＜0.01).The expression level of mir-203a and ATM was significantly correlated with lymph node metastasis and different clinical stages (P＜0.
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