共查询到20条相似文献，搜索用时 62 毫秒
1.
AIM: To detect the expression level of wip1 in lung cancer tissue and three lung cancer cell lines, and to explore the relations between the expression level of Wip1 in lung cancer and various clinical and pathological features. METHODS: Real-time PCR was employed to detect the expression of Wip1 mRNA in 44 specimens of non small cell lung cancer tissues and normal tissues. The relations between the expression of Wip1 mRNA and various clinical and pathological features were analyzed. Real-time PCR was also employed to detect the expression of Wip1 mRNA in A549, NCI-1299, NCI-H460 and HBE for relative quantitative analysis.RESULTS: In the 44 specimens, the expressions of Wip1 mRNA in both cancer tissues and normal lung tissues were positive. Wip1 gene was over-expressed in 17 specimens in 44 non small cell lung cancer specimens. The rate was 38.6%. The relative level of Wip1 mRNA in NSCLC tissues was significantly higher than that in normal lung tissues (ratio=2.1644±1.3940, P<0.01). The expression of Wip1 mRNA was also correlated with pathological grading (P<0.05). The relative level of Wip1 mRNA in three kinds of lung cancer cells was significantly higher than that in HBE cells. The difference was statistically significant (P<0.05).CONCLUSION: The Wip1 mRNA is over-expressed in non small cell lung cancer, indicating that Wip1 is related to the tumorigenesis and may become the new target of non small cell lung cancer gene therapy. The expression of Wip1 mRNA is related to tumor cell differentiation and may use for the molecular biological reference index to estimate the malignant degree of cancer. 相似文献
2.
AIM: To investigate the roles of KLF6 gene on nucleotide excision repair capacity of human hepatocellular carcinoma cell line HepG2. METHODS: Expression of KLF6 was detected by RT-PCR and Western blotting, followed by HepG2 cells treated with cisplatin (5 mg/L). Host cell reactivation assay was used to assess nucleotide excision capacity of cisplatin-damaged HepG2 cells.RESULTS: Upregulation of KLF6 mRNA or protein in HepG2 cells treated with 5 mg/L concentration of cisplatin was in a time-dependent manner, but KLF6 protein was degraded when exposed to cisplatin at same dose (5 mg/L) for 36 h. HCR assay showed that NER capacity of KLF6 overexpressing HepG2 cells was significantly enhanced, compared to that in control cells. CONCLUSION: DNA damage induced by cisplatin induces the expression of KLF6 gene. KLF6 gene may play an important role in mechanism of nucleotide excision repair in HepG2 cells. 相似文献
3.
AIM: To investigate the change of chemosensitivity of esophageal carcinoma cells before and after induction by radiation,and to detect the excision repair cross complementation group 1 (ERCC1) gene before and after induction,and further to analyze the relationship between ERCC1 expression and chemosensitivity.METHODS: The esophageal carcinoma cell EC9706 was radiated repeatedly by a long-term,intermittent ［60Co］-γ radiation to induce the radioresistance esophageal carcinoma cell EC9706-R.The IC50 and resistant index (RI) of EC9706 and EC9706-R were detected by MTT assay.The expression of ERCC1 was examined by immunocytochemistry and RT-PCR.RESULTS: The IC50 of EC9706 and EC9706-R cells to cisplatin were (1.480±0.012) mg/L and (1.836±0.008) mg/L,respectively (P<0.05),and the RI was 1.240±0.015.The tinctorial scores of ERCC1 protein in EC9706 and EC9706-R were 2.838±0.055 and 2.898±0.039 (P>0.05),and the relatively quantities (IDV) of ERCC1 mRNA in EC9706 and EC9706-R cells were 1.168±0.068 and 1.143±0.089 (P>0.05).SP and RT-PCR did not display visible difference in protein level and mRNA level.CONCLUSION: The chemosensitivity of EC9706-R cells to cisplatin is decreased compared with EC9706 cells,but ERCC1 expression does not change with the radioresistance and chemoresistance. 相似文献
4.
5.
6.
AIM: To determine the aberrant methylation status in the gene promoter regions of CDH13, RASSF1A, DLEC1, SEPT9and RUNX3by detecting the plasma specimens and the value of their combined detection for diagnosis of lung cancers. METHODS: Nest methylation specific PCR (nMSP) was used to detect the promoter methylation status of the 5 genes in the plasma from 106 normal controls， lung cancer tissues, lung benign tissues and the plasma from 106 patients with lung cancers. Multiple displacement amplification (MDA) was used to amplify modified genomic DNA to solve the problem of insufficient of plasma DNA template. RESULTS: The positive rates of promoter methylation of CDH13, RASSF1A, DLEC1, SEPT9and RUNX3in the lung cancer tissues were 51.9%, 44.3%, 54.7%, 36.8%, 24.5%, respectively, and those in the plasma were 46.2%, 41.5%, 50.9%, 31.1%, 19.8%, respectively. The results of the Kappa consistency check showed that the lung cancer tissues and the plasma had obviously coherence in the methylation status of the 5 gene promoter regions. Combination of DLEC1, CDH13, RASSF1A, and SEPT9 had a higher diagnostic efficiency than the others, as their ACC value was 0.8208 and youden index was 0.6415 (with the sensitivity of 81.13% and the specificity of 83.02%). CONCLUSION: Combination detection of promoter methylation of lung cancer-related genes in the plasma is expected to apply to the early diagnosis of lung cancer. 相似文献
7.
8.
AIM: To investigate the clinicopathological significance of the protein expression of phosphorylated ezrin at threonine 567 (pEZRThr567) in lung squamous cell carcinoma, adjacent tissues and normal tissues. METHODS: pEZRThr567 protein was detected in lung squamous carcinoma, adjacent and normal tissues by the method of immunohistochemistry. The correlation of pEZRThr567 expression with clinicopathological parameters of lung squamous carcinomas was also analyzed. The localization of pEZRThr567 was detected by immunofluorescence staining in lung squamous cell line EBC-1. RESULTS: The protein expression of pEZRThr567 in lung squamous carcinoma was significantly higher than that in the adjacent and normal lung tissues (P<0.01). pEZRThr567 mainly localized on the cell membrane, and its over-expression signi-ficantly correlated with the differentiation, clinical stage and lymph node metastasis in lung squamous carcinoma. CONCLUSION: pEZRThr567 may be an effective biomarker for prediction of malignant potential and poor prognosis of lung cancer. 相似文献
9.
AIM To investigate the activation of related repair pathways after bupivacaine-induced neuronal DNA damage by cDNA gene screening. METHODS The bupivacaine-induced SH-SY5Y neuronal damage and DNA damage model was established. The technique of cDNA microplate array was used to screen the 21 important regulatory factors in the DNA damage repair pathway. Post-analysis of these differentially expressed repair genes for the repair pathway enrichment and distribution was performed. The data were analyzed by GraphPad Prism 6 statistical software to compare differences between groups. RESULTS The viability of SH-SY5Y cells treated with bupivacaine at different concentrations （detected by CCK-8 assay） showed that the IC50 value of bupivacaine was 1.5 mmol/L. The comet assay related index （the comet tail） was increased （P <0.05）, the phosphorylation level of γH2AX protein was increased （P <0.05）, indicating that DNA damage in the SH-SY5Y cells was significantly aggravated after bupivacaine treatment. The results of cDNA microplate assay showed that compared withcontrol group, the differentially expressed genes after bupivacaine treatment were DNA-PKcs , PTEN , NTH1 , RAD9 , CSB , GADD45 , XPD, XPC-HR23B and P53 . The analysis showed that these repair genes were mainly concentrated in the following 3 repair mechanisms： base excision repair, nucleotide excision repair, and non-homologous reconstitution. CONCLUSION The repair genes differentially expressed after neuronal DNA damage caused by local anesthetics are mainly concentrated in the pathways of non-homologous end-joining, base excision repair and nucleotide excision repair. 相似文献
10.
AIM: To investigate the effects of simvastatin on the expression of Toll-like receptor 2 (TLR-2), interferon-γ (IFN-γ) and monocyte chemoattractant protein-1 (MCP-1) in lung tissues of mice with mouse cytomegalovirus (MCMV) pneumonia and to explore the possible mechanism. METHODS: Male BALB/c mice (6~8 weeks old, n=40) were randomly divided into 5 groups: normal control (NC) group, MCMV infection group, simvastatin group 1 (SMV1 group), simvastatin group 2 (SMV2 group), and simvastatin group 3 (SMV3 group). The mice in SMV1, SMV2 and SMV3 groups were gavaged with simvastatin (50 mg·kg-1·d-1 for 7 d) 7 d before, on the same day of and 3 d after intraperitoneal injection of MCMV, while the mice in normal control group and MCMV infection group were gavaged with the same volume of normal saline. HE staining was used to observe the pathological changes of lung tissues in mice. Total tissue protein was extracted from the lung homogenates to detect the expression of TLR-2 by Western blot and immunohistochemical staining. Real-time PCR was used to analyse the content of MCMV DNA. The levels of IFN-γ and MCP-1 were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: Compared with NC group, the pathological changes of the lung tissues of the mice in MCMV group showed alveolar interstitial edema, alveolar wall widening and a large number of inflammatory cells. The expression of TLR-2 in the lung tissues of the mice in model group was increased significantly. The content of MCMV DNA was increased, and the expression of IFN-γ and MCP-1 was also increased significantly. Compared with the mice in MCMV group, the pathological changes of the lung tissues of simvastatin groups showed that the inflammatory cells were decreased. The expression of TLR-2 was down-regulated. The content of MCMV DNA was decreased, and the levels of IFN-γ and MCP-1 were also decreased significantly. At the same time, the expression of TLR-2 and the content of MCMV DNA in SMV1 group were less than those in SMV2 and SMV3 groups (P<0.05), and no statistically significant difference between SMV2 and SMV3 groups was observed. CONCLUSION: Simvastatin down-regulates the TLR-2 signaling pathway, and reduces the expression of TLR-2 and replication of MCMV DNA, thus attenuating the pathological damage of the lung tissue. Early intervention with simvastatin plays an important role in preventing the infection of MCMV and reducing the inflammation. 相似文献
11.
QIN Ling GE Meng-xi ZHOU Xin-li HUNAG Ruo-fan ZHAN Qiong JI Xiao-yu ZHAO Yue-hua LIANG Xiao-hua 《园艺学报》2016,32(10):1892-1895
AIM: To explore the relationship between FRAS1 protein and brain metastases of non-small cell lung cancer (NSCLC).METHODS: The mRNA expression of FRAS1 in the brain metastatic tumor tissues and primary tumor tissues of NSCLC was detected by qPCR. The protein expression of FRAS1 in the tumor tissues and normal tissues adjacent to tumor tissues of NSCLC was measured by SP method of immunohistochemistry. The protein expression of FRAS1 in NSCLC primary tumor tissues with or without brain metastases was also determined.RESULTS: The mRNA expression of FRAS1 in the brain metastatic zone was nearly 10 times higher than that in the primary tumor tissues, and there was significant difference between the 2 groups (P<0.05). FRAS1 protein was expressed in the NSCLC primary tumor tissues, but was not found in the normal tissues adjacent to primary tumor tissues. The protein expression of FRAS1 in the NSCLC with brain metastases was significantly higher than that without brain metastases (P<0.01).CONCLUSION: FRAS1 protein may be associated with the occurrence of NSCLC. The over-expression of FRAS1 protein may be related to brain metastases with NSCLC. 相似文献
12.
AIM: To investigate the role of Bcl-2-associated athanogene 2 (BAG2) in the proliferation of human lung adenocarcinoma A549 cells and its clinical implications. METHODS: The abundance of BAG2 protein in A549 and lung bronchial epithelium (HBE) cells were measured by Western blot. After down-regulation of BAG2 by transfection of siRNA in A549 cells, the expression of cell proliferation and cell cycle related proteins were detected by CFSE assay, WST-1 assay and Western blot, respectively. Moreover, the expression of BAG2 in cDNA array which contained 10 pairs of lung cancer and adjacent tissue was verified. Meanwhile, BAG2 expression in GEO database, which included the human lung cancer and adjacent tissue microarray data was analyzed. The prognosis power of BAG2 was evaluated by the Kaplan-Meier survival curve analysis. RESULTS: BAG2 had remarkably higher expression level in A549 cells than that in HBE cells. Knockdown of BAG2 resulted in significantly inhibition of proliferation in A549 cells, accompany with the significantly down-regulation of cyclin B1 and cyclin E1. BAG2 was over-expressed in the lung cancer tissues, as compared with the adjacent normal tissues. Kaplan-Meier plotter and cDNA microarray results showed that patients with higher BAG2 expression were significantly associated with poorer survival. CONCLUSION: The BAG2 gene tends to regulate A549 cells proliferation via cyclin B1 and cyclin E1. BAG2 has significantly prognostic power on the survival of lung cancer patients. 相似文献
13.
14.
HONG Lei ZHOU Ji-hong LI Wei CHEN Yu-qing JIANG Peng YUAN Na-na WANG Xiao-jing ZHU Mao-xiang YANG Zhi-hua 《园艺学报》2017,33(7):1153-1162
15.
16.
GUO Jun-qi YANG Yun ZHANG Ying-quan LI Chun-qiao WANG Han-rui KONG Li-jun HU Jin-xia 《园艺学报》2019,35(10):1798-1803
AIM: To explore the role of neural precursor cell expression developmentally down-regulated protein 1 (NEDD1) in the development and progression of lung cancer. METHODS: The differences of NEDD1 expression levels between lung cancer tissues and tumor-adjacent tissues were analyzed by the method of immunohistochemistry and TCGA database. Kaplan-Meier curve was used to analyze the correlation between lung cancer prognosis and the expression level of NEDD1. The proliferation of A549 cells was tested by plate colony formation experiment after knock-down of NEDD1 expression. The apoptosis rate and cell cycle distribution were examined by flow cytometry. The migration ability of the A549 cells was detected by Transwell assay. The protein levels of cell cycle-related molecules were determined by Western blot. Database analysis was performed to evaluate the relationship between the expression of NEDD1 and cyclin-dependent kinases 2 (CDK2). RESULTS: Compared with the tumor-adjacent tissues, the expression level of NEDD1 in the lung cancer tissues was increased, so as the database analysis, and the higher expression of NEDD1 showed a poorer prognosis. Under light microscope, the A549 cells showed a low proliferation rate after silencing the NEDD1 expression, and the colony formation ability of the cells was also reduced; knock-down of NEDD1 expression induced the apoptosis and inhibited the cell migration; knock-down of NEDD1 expression blocked the cells in G1/S phase, and the protein levels of p-Rb and cyclinD1 were decreased, while the protein levels of p-Chk1, p-Chk2 and p-p53 were increased (P<0.05). A positive correlation between the expression of NEDD1 and CDK2 was noted by database analysis. CONCLUSION: NEDD1 plays an crucial role in promoting cell proliferation via inhibiting apoptosis and accelerating cell cycle, high expression of NEDD1 in lung adenocarcinoma tissue is related to poor prognosis, thus NEDD1 may be used as a candidate marker molecule for the diagnosis and prognosis of lung cancer. 相似文献
17.
AIM: To investigate the expression profile of myosin VI in various human carcinomas and adjacent normal tissues. METHODS: A piece of cancer profiling array containing 154 matched cDNA pairs from 19 tumors and the adjacent normal tissues and 10 diverse tumor cell lines were separately hybridized with radiolabeled probes for myosin VI and housekeeping gene ubiquitin. Immunohistochemistry (IHC) was used to confirm the expression profile of myosin VI in 40 cases of ovarian adjacent normal tissues, 8 cases of cystadenoma, 16 cases of borderline tumors and 52 cases of endometrioid carcinoma by tissue microarray. RESULTS: Myosin VI was expressed in all the tissues and cell lines. The expression of myosin VI was significantly higher in ovarian and colon cancer tissues than that in matched normal tissues. The results of IHC confirmed that myosin VI expression rates were 100% (52/52), 81.3% (13/16) and 10.4% (5/48) in the ovarain carcinoma, boderline tumor and nomal ovarian epithelium or cystadenoma, respectively. The expression of myosin VI protein was significantly higher and stronger in ovarain carcinoma than that in the borderline tumor, benign tumor or normal ovary tissues. A significant correlation was also found between the expression of myosin VI and the tumor grade of ovarain carcinoma. CONCLUSION: Differentiated expression of myosin VI is found in diverse malignant tumor tissues and cell lines, suggesting myosin VI plays an important role in the tumor development and progression. 相似文献
18.
AIM: To study the mRNA and protein expression of Kang ai1 (KAI1) tumor suppressor gene and to determine the relationship between KAI1 and invasiveness and metastasis of cervical cancer. METHODS: The expression of KAI1 metastasis suppressor was detected by immunohistochemistry in paraffin slides and by real-time quantitative polymerase chain reaction (RT-PCR) in fresh tissue. The samples included 20 cases of normal cervical tissues, 20 cases of cervical intraepithelial neoplasia (CIN) and 40 cases of cervical carcinoma. The results of the gene expression combined with the pathological and clinical data were also analyzed. RESULTS: The expression of KAI1 protein and mRNA was related to the tissue differentiation of cervix. The positive rates of KAI1 expression were the highest in the normal cervical tissue, the middle in CIN and the lowest in cervical carcinoma with significant difference among three groups (P<0.01). The expression of KAI1 protein was not related with the grade of CIN (P>0.05). However, both mRNA and protein expression of KAI1 were related to the differentiation and the clinical stages of cervical cancer (P<0.01) and also related to the metastasis of the cancer. The positive rates between the non-lymphatic metastasis and lymphatic metastasis (P<0.05) were significant different. Cox regression and logistic regression showed that the tissue differentiation, clinical stages, lymphatic metastasis and expression of KAI1 were all related factors with recurrence and prognosis of cervical cancer. CONCLUSION: The down-regulation of KAI1 tumor suppressor gene at both mRNA and protein levels is related to the differentiation, clinical stages and metastasis of cervical cancer, indicating that the expression of KAI1 is a prognostic factor for cervical cancer. 相似文献
19.
AIM: To know the variations of the cytochrome b gene in cancer tissue, paracarinoma tissue and normal tissue and to inquire into the relationship between mutations of mitochondrial genome and carcinogenesis. METHODS: Cellular total DNA was extracted.The cytochrome b genes of three tissues were amplifyed with polymerase chain reaction(PCR). PCR products were analysed by DNA auto-sequencing method. RESULTS: The cytochrome b gene of cancer tissue had the C to G mutation at nt 14931, the C to G mutation at nt 15004 and the T to C mutation at nt15435,respectively. The cytochrome b gene of paracarinoma tissue had the A to C mutation at nt 15436. The cytochrome b gene of normal tissue had not mutation. CONCLUSION:Mitochondrial DNA mutations could be the endogenous factors that induce nuclear genome mutation. It could promoto carcinogenesis. The paracarinoma tissue was abnormal in DNA molecular level. 相似文献
20.
YAN Cheng-quan CAI Sheng-yong MENG Bin WANG Peng-fei LI Lin ZHAO Chao-fei LIU Yi-fei MENG Xin 《园艺学报》2018,34(7):1256-1263
AIM:To investigate the biological functions of microRNA-29a (miR-29a) in prostate cancer and the molecular mechanism of miR-29a over-expression inhibiting malignant phenotypes of prostate cancer cells. METHODS:The levels of miR-29a expression in the prostate cancer tissues and cells were detected and analyzed using gene microarray and bioinformatics. The expression levels of miR-29a and lysine (K)-specific demethylase 4B (KDM4B) mRNA in prostate cancer tissues, paracarcinomatous tissues, 4 prostate cancer cell lines (PC3, DU145, LNCaP and ArCaP) and normal prostate epithelial cell line (RWPE-1) were measured by real-time PCR. PC3, DU145, LNCaP and ArCaP cells were transfected with pGenesil-1-miR-29a plasmid using transient transfection. The cell viability, colony formation rate and apoptotic rate were analyzed by MTT assay, colony formation assay and flow cytometry with Annexin V-FITC/PI staining, respectively. The protein expression of KDM4B was determined by Western blot. RESULTS:The results of gene microarray and bioinformatic analysis indicated that differential expression of miR-29a was found in the prostate cancer tissues and the paracarcinomatous tissues. The levels of miR-29a in the prostate cancer tissues and prostate cancer cells were significantly decreased, while the mRNA levels of KDM4B were notably increased compared with the paracarcinomatous tissues and RWPE-1 cells, respectively (P<0.05). Compared with negative control (pGenesil-1) group, the cell viability and colony formation rate were significantly decreased, the apoptotic rate was significantly increased, and the protein expression of KDM4B was notably inhibited in the prostate cancer cells with miR-29a over-expression (P<0.05). The cell viability was significantly enhanced, and the apoptosis was significantly inhibited in the prostate cancer cells with KDM4B over-expression (P<0.05). CONCLUSION:Low expression of miR-29a was found in the prostate cancer tissues and cells. miR-29a over-expression inhibits the growth of prostate cancer cells and induces apoptosis. The mechanism may be associated with inhibiting the protein expression of KDM4B. 相似文献