Change in expression of cyclin G2 in kidney cancer cell and its significance

This study aims to analyze the expression and clinical significance of cyclin G2 (CCNG2) in kidney carcinoma, and the biological effect in its cell line by CCNG2 overexpression. Immunohistochemistry and western blot were used to analyze CCNG2 protein expression in 63 cases of kidney cancer and normal tissues to study the relationship between CCNG2 expression and clinical factors. CCNG2 lentiviral vector and empty vector were respectively transfected into kidney ACHN cell line. During immunohistochemistry, the level of CCNG2 protein expression was found to be significantly lower in kidney cancer tissue than normal tissues (P?<?0.05). After Western blot, the relative amount of CCNG2 protein in kidney cancer tissue was respectively found to be significantly lower than in normal tissues (P?<?0.05). The level of CCNG2 protein expression was not correlated with gender, age, tumor size, and pathological types (P?>?0.05), but it was correlated with lymph node metastasis, clinic stage, and histological grade (P?<?0.05). Loss of CCNG2 expression correlated significantly with poor overall survival time by Kaplan–Meier analysis (P?<?0.05). The result of biological function show that ACHN cell-transfected CCNG2 had a lower survival fraction, higher percentage of the G0/G1 phases, and lower CDK2 protein expression compared with ACHN cell-untransfected CCNG2 (P?<?0.05). CCNG2 expression decreased in kidney cancer and correlated significantly with lymph node metastasis, clinical stage, histological grade, and poor overall survival, suggesting that CCNG2 may play important roles as a negative regulator to kidney cancer ACHN cell by promoting degradation of CDK2.     

Decreased expression of CCNG2 is significantly linked to the malignant transformation of gastric carcinoma

This study aimed to analyze the expression, clinical significance of cyclin G2 (CCNG2) in gastric carcinoma, and the biological effect in its cell line by CCNG2 overexpression. Immunohistochemistry and western blot were used to analyze CCNG2 protein expression in 87 cases of gastric cancer and normal tissues to study on the relationship between CCNG2 expression and clinical factors. CCNG2 lentiviral vector was transfected into gastric SGC-7901 cell line. RT-PCR and western blot were used to detect the mRNA level and protein of CCNG2. MTT assay and cell cycle were also conducted as to the influence of the upregulated expression of CCNG2 that might be found on SGC-7901 cell biological effect. Immunohistochemically, the level of CCNG2 protein expression was found to be significantly lower in gastric cancer tissue than in normal tissues (P?<?0.05). Western blot shows that the relative amount of CCNG2 protein in gastric cancer tissue was found to be significantly lower than in normal tissues (P?<?0.05). The level of CCNG2 protein expression was correlated with T stages, lymph node metastasis, clinical stage, and histological grade (P?<?0.05). Loss of CCNG2 expression correlated significantly with poor overall survival time by Kaplan–Meier analysis (P?<?0.05). The result of biological function showed that SGC-7901 cell-transfected CCNG2 had a lower survival fraction, higher percentage of the G0/G1 phases, and lower CDK2 protein expression compared with SGC-7901 cell untransfected CCNG2 (P?<?0.05). CCNG2 expression decreased in gastric cancer and correlated significantly T stages, lymph node metastasis, clinical stage, histological grade, and poor overall survival, suggesting that CCNG2 may play important roles as a negative regulator to gastric cancer cell by promoting degradation of CDK2.     

Filamin A regulates MMP-9 expression and suppresses prostate cancer cell migration and invasion

This study aims to analyze the expression and clinical significance of Filamin A (FLNA) in prostate carcinoma and the biological effect in its cell line by FLNA overexpression. Immunohistochemistry and Western blot were used to analyze FLNA protein expression in 68 cases of prostate cancer and 37 cases of normal tissues to study the influence of the upregulated expression of FLNA that might be found on PC-3 cell biological effect. In the immunohistochemical analysis, the level of FLNA protein expression was found to be significantly lower in prostate cancer tissue than in normal tissues (P?<?0.05). In the Western blot analysis, the relative amount of FLNA protein in prostate cancer tissue was found to be significantly lower than in normal tissues (P?<?0.05). The level of FLNA protein expression was not correlated with age and PSA concentration (P?>?0.05), but it was correlated with T stages, lymph node metastasis, clinic stage, and Gleason score (P?<?0.05). The result of biological function showed that PC-3 cell transfected FLNA had a lower survival fraction, a significant decrease in migration and invasion, and a lower matrix metallopeptidase 9 (MMP-9) protein expression compared with PC-3 cell untransfected FLNA (P?<?0.05). FLNA expression decreased in prostate cancer and correlated significantly with T stages, lymph node metastasis, clinic stage, and Gleason score, suggesting that FLNA may play important roles as a negative regulator to prostate cancer PC-3 cell by promoting the degradation of MMP-9.     

CCNG2 expression is downregulated in colorectal carcinoma and its clinical significance

This study aimed to analyze the expression, clinical significance of cyclin G2 (CCNG2) in colorectal carcinoma, and the biological effect in its cell line by CCNG2 overexpression. Immunohistochemistry and Western blot were used to analyze CCNG2 protein expression in colorectal cancer and to study the influence of the upregulated expression of CCNG2 that might be found on SW480 cell biological effect. We found that the level of CCNG2 protein expression was significantly lower in colorectal cancer tissue than normal tissues (P?<?0.05). The level of CCNG2 was correlated with T stages, lymph node metastasis, clinic stage, and histological grade (P?<?0.05). Loss of CCNG2 expression correlated significantly with poor overall survival time by Kaplan–Meier analysis (P?<?0.05). The result of biological function has shown that SW480 cell-transfected CCNG2 had a lower survival fraction, higher percentage of the G0/G1 phases, and lower CDK2 protein expression compared with SW480 cell-untransfected CCNG2 (P?<?0.05).     

BTG1 expression correlates with the pathogenesis and progression of breast carcinomas

This study aimed to analyze the expression, clinical significance of B cell translocation gene 1 (BTG1) in breast carcinoma and the biological effect in its cell line by BTG1 overexpression. Immunohistochemistry and western blot were used to analyze BTG1 protein expression in 72 cases of breast cancer and 36 cases of normal tissues to study the relationship between BTG1 expression and clinical factors. Recombinant lentiviral vector was constructed to over-express EMP-1 and then infect breast cancer MCF-7 cell line. Quantitative real-time RT-PCR (qRT-PCR) and western blot were used to detect the mRNA level and protein of BTG1. MTT assay, cell apoptosis, cell cycles, migration and invasion assays were also conducted as to the influence of the upregulated expression of BTG1 that might be found on MCF-7 cells biological effect. The level of BTG1 protein expression was found to be significantly lower in breast cancer tissue than normal tissues (P?<?0.05). Decreased expression of BTG1 was significantly correlated with tumor invasion, lymph node metastasis, clinic stage and histological grade of patients with breast cancer (P?<?0.05). Meanwhile, loss of BTG1 expression correlated significantly with poor overall survival time by Kaplan–Meier analysis (P?<?0.05). The result of biological function shown that MCF-7 cell transfected BTG1 had a lower survival fraction, higher percentage of the G0/G1 phases, higher cell apoptosis, significant decrease in migration and invasion, and lower CyclinD1, Bcl-2, and MMP-9 protein expression compared with MCF-7 cell untransfected BTG1 (P?<?0.05). BTG1 expression decreased in breast cancer and correlated significantly lymph node metastasis, clinic stage, histological grade, poor overall survival, proliferation, and metastasis in breast cancer cell by regulating CyclinD1, Bcl-2, and MMP-9 protein expression, suggesting that BTG1 may play important roles as a negative regulator to breast cancer cell.     

CCNG2在前列腺癌中的表达及其临床意义

[目的]探讨细胞周期蛋白G2（CCNG2）在前列腺癌中的表达及意义。[方法]采用免疫组织化学方法、Western blot检测85例前列腺癌组织及距其癌组织边缘2cm以上镜下未见癌浸润的正常组织中CCNG2蛋白的表达情况。[结果]免疫组织化学结果表明,CCNG2蛋白在前列腺癌组织及正常前列腺组织中的表达阳性率分别为31.8%、96.5%,差异有统计学意义（P〈0.05）。Western blot结果表明,CCNG2蛋白在前列腺癌组织的相对表达量较正常前列腺组织的相对表达量明显降低,差异具有统计学意义（P〈0.05）。CCNG2蛋白表达与前列腺癌患者年龄、肿瘤大小、PSA水平无关（P〉0.05）;而与Gleason score、淋巴结转移以及肿瘤临床分期有关（P〈0.05）。[结论]前列腺癌组织中CCNG2蛋白表达明显降低,且与前列腺癌Gleason score、淋巴结转移、临床分期有关。     

EMP1 inhibits nasopharyngeal cancer cell growth and metastasis through induction apoptosis and angiogenesis

This study aimed to analyze the expression, clinical significance of epithelial membrane protein-1 (EMP1) in nasopharyngeal carcinoma, and the biological effect in its cell line by EMP1 overexpression. Immunohistochemistry and Western blot were used to analyze the EMP1 protein expression in 75 cases of nasopharyngeal cancer and 31 cases of normal tissues to study the relationship between EMP1 expression and clinical factors. Recombinant lentiviral vector was constructed to overexpress EMP1 and then infect nasopharyngeal cancer CNE2 cell line. Quantitative real-time RT-PCR and Western blot were used to detect the mRNA level and protein of EMP1. MTT assay, cell apoptosis, migration, and invasion assays were also conducted to determine the influence of the upregulated expression of EMP1 that might be found on CNE2 cells’ biological effect. Immunohistochemistry and Western blot: The level of EMP1 protein expression was found to be significantly lower in nasopharyngeal cancer tissue than in the normal tissues (P?<?0.05). Decreased expression of EMP1 was significantly correlated with T stages, lymph node metastasis, clinic stage, and histological grade of patients with nasopharyngeal cancer (P?<?0.05). Meanwhile, the loss of EMP1 expression correlated significantly with poor overall survival time by Kaplan–Meier analysis (P?<?0.05). The result of biological function has shown that CNE2 cell-transfected EMP1 had a lower survival fraction, higher cell apoptosis, significant decrease in migration and invasion, higher caspase-9, and lower vascular endothelial growth factor C protein expression compared with CNE2 cell-untransfected EMP1 (P?<?0.05). EMP1 expression decreased in nasopharyngeal cancer and correlated significantly T stages, lymph node metastasis, clinic stage, histological grade, and poor overall survival, suggesting that EMP1 may play important roles as a negative regulator to nasopharyngeal cancer cell.     

EMP1, a member of a new family of antiproliferative genes in breast carcinoma

This study aimed to analyze the expression, clinical significance of epithelial membrane protein 1 (EMP1) in breast carcinoma and the biological effect in its cell line by EMP1 overexpression. Immunohistochemistry and western blot were used to analyze EMP1 protein expression in 67 cases of breast cancer and 35 cases of normal tissues to study the relationship between EMP1 expression and clinical factors. Quantitative real-time RT-PCR and western blot were used to detect the mRNA level and protein of EMP1. MTT assay, migration and invasion assays were also conducted as to the influence of the upregulated expression of EMP1 that might be found on MCF-7 cell biological effect. The relative amount of EMP1 protein in breast cancer tissue was found to be significantly lower than in normal tissues (P?<?0.05). The level of EMP1 protein expression was correlated with T stages, lymph node metastasis, clinic stage, and histological grade (P?<?0.05). Meanwhile, loss of EMP1 expression correlated significantly with poor overall survival time by Kaplan–Meier analysis (P?<?0.05). The result shown that MCF-7 cell transfected EMP1 had a lower survival fraction, higher cell apoptosis, significant decrease in migration and invasion, higher caspase-9, and lower VEGFC protein expression compared with MCF-7 cell untransfected EMP1 (P?<?0.05). EMP1 expression decreased in breast cancer and correlated significantly with lymph node metastasis, clinic stage, histological grade, and poor overall survival, T stages, suggesting that EMP1 may play important roles as a negative regulator to breast cancer MCF-7 cell by regulating the expression of caspase 9 and VEGFC protein.     

The expression of BTG1 is downregulated in NSCLC and possibly associated with tumor metastasis

This study aimed to analyze the expression, clinical significance of B cell translocation gene 1 (BTG1) in nonsmall cell lung cancer (NSCLC) and the biological effect in its cell line by BTG1 overexpression. Immunohistochemistry and western blot were used to analyze BTG1 protein expression in 82 cases of NSCLC and 38 cases of normal tissues to study the relationship between BTG1 expression and clinical factors. Recombinant lentiviral vector was constructed to overexpress EMP-1 and then infect NSCLC H1299 cell line. Quantitative real-time RT-PCR and western blot were used to detect the mRNA level and protein of BTG1. 3-[4,5-dimethylthiazol -2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay, cell apoptosis, cell cycles, and migration and invasion assays were also conducted as to the influence of the upregulated expression of BTG1 that might be found on H1299 cells biological effect. The level of BTG1 protein expression was found to be significantly lower in NSCLC tissue than normal tissues (P?<?0.05). Decreased expression of BTG1 was significantly correlated with lymph node metastasis, clinic stage, and histological grade of patients with NSCLC (P?<?0.05). Meanwhile, loss of BTG1 expression correlated significantly with poor overall survival time by Kaplan–Meier analysis (P?<?0.05). The result of biological function show that H1299 cell transfected BTG1 had a lower survival fraction; higher percentage of the G0/G1 phases; higher cell apoptosis; significant decrease in migration and invasion; and lower CyclinD1, Bcl-2, and MMP-9 protein expression compared with H1299 cell untransfected BTG1 (P?<?0.05). BTG1 expression decreased in NSCLC and correlated significantly with lymph node metastasis; clinical stage; histological grade; poor overall survival; cell proliferation; cell cycles; cell apoptosis; and migration and invasion in NSCLC cell by regulating CyclinD1, Bcl-2, and MMP-9 protein expression, suggesting that BTG1 may play important roles as a negative regulator to NSCLC cell.     

Clinical Significance of Mannose-Binding Lectin Expression in Thyroid Carcinoma Tissues

Mannose-binding lectin (MBL) plays an important role in the host defence against pathogens and carcinogenesis. This study aimed to analyze differential expression of MBL protein in thyroid cancer tissues and then to investigate the effects of rhMBL in thyroid cancer cells. Tissue specimens from 45 thyroid carcinoma patients and 45 adenoma patients were recruited for immunohistochemical analysis of MBL expression. Cell viability, apoptosis, RT-PCR and Western blot assays were used to detect changes in tumor cell viability, apoptosis, and gene expression, respectively, after treatment of thyroid cancer cells with rhMBL. MBL was differentially expressed in papillary thyroid carcinoma, adenoma, and the distant normal tissues (0.322?±?0.008, 0.227?±?0.003, and 0.113?±?0.003, respectively, P?<?0.05). MBL expression was associated with the advanced disease stage, histological grade, or lymph node metastasis in cancer patients (P?<?0.05). Moreover, rhMBL treatment of thyroid cancer cells reduced tumor cell viability but induced apoptosis in a dose- and time-dependent manner. rhMBL treatment also downregulated Bcl2 protein expression in thyroid cancer cells (P?<?0.05). In addition, expression p53 protein was increased in thyroid cancer cells after rhMBL treatment (P?<?0.05). The data from the current study demonstrate that MBL overexpression is associated with advanced thyroid carcinomas, and rhMBL treatment significantly reduced viability but induced apoptosis of thyroid cancer cell lines. Further studies will clarify whether overexpressed MBL in thyroid cancer tissues is functional.     

Effects of ARHI on cell cycle progression and apoptosis levels of breast cancer cells

The purposes of this study were to investigate the role of Aplysia Ras Homolog I (ARHI) on cell growth, proliferation, apoptosis, and other biological characteristics of HER2-positive breast cancer cells. Our goal was to provide experimental evidence for the development of future effective treatments of HER2-positive breast cancer. A pcDNA3.1-ARHI eukaryotic expression vector was constructed and transfected into the human HER2-positive breast cancer cell lines SK-BR-3 and JIMT-1. Then, various experimental methods were utilized to analyze the biological characteristics of ARHI-expressing breast cancer cells and to examine the impact of expression of the ARHI gene on cyclin D1, p27^Kip1, and calpain1 expression. We further analyzed the cells in each group after treatment with trastuzumab to examine the effects of this drug on various cellular characteristics. When we compared pcDNA3.1-ARHI-expressing SK-BR-3 and JIMT-1 cells to their respective empty vector and control groups, we found that cell viability was significantly lower (p?<?0.05) in the ARHI-expressing cells, and the proportions of G1 phase cells and apoptotic cells were significantly higher in the ARHI-expressing cells (p?<?0.05). In all groups of SK-BR-3 cells, trastuzumab treatment significantly decreased cell growth (p?<?0.05). The proportion of cells in G1 phase and the number of apoptotic cells in the pcDNA3.1-ARHI-expressing group were significantly higher than that in the empty vector group and the control group (p?<?0.05). The growth of pcDNA3.1-ARHI-transfected JIMT-1 cells was significantly decreased (p?<?0.05), while the proportion of apoptotic cells was significantly increased (p?<?0.05). Cell growth, viability, and the percentage of apoptotic cells were similar between the JIMT-1 empty vector and control groups. ARHI expression inhibited cyclin D1 expression in SK-BR-3 cells and JIMT-1 cells, while it promoted p27^Kip1 and calpain1 expression in these cells. ARHI expression inhibits the growth and proliferation of HER2-positive breast cancer cells, while it also promotes apoptosis in these cells. ARHI expression also improves the sensitivity of JIMT-1 cells to trastuzumab by inducing apoptosis.     

Implications of Bit1 and AIF overexpressions in esophageal squamous cell carcinoma

Overwhelming evidence has demonstrated that Bit1 and AIF as mitochondrial proteins are implicated in the development and progression of a variety of tumors. However, their expressions and biological functions in esophageal squamous cell carcinoma (ESCC) remain to be delineated. In the present study, we found that Bit1, AIF, and Bcl-2 levels in ESCC tissues were significantly higher than those in normal esophageal epithelial tissues and dysplasia tissues (P?<?0.05). Stepwise investigation demonstrated that Bit1 and Bcl-2 levels were both tightly associated with lymphatic metastasis and TNM staging (P?<?0.05), and the levels of Bit1 mRNA as well as AIF and Bcl-2 proteins were both closely related to tumor differentiation (P?<?0.05), but not related to the patients' age and gender (P?>?0.05). Importantly, Bit1 mRNA and protein levels in ESCC with lymphatic metastasis and TNM staging in III and IV were markedly higher than that without lymphatic metastasis and TMN staging in I and II. Further analysis showed that expression of Bit1 protein was both positively correlated with expressions of AIF and Bcl-2 proteins (r?=?0.408 and 0.405, respectively; P?<?0.05). Correctively, our data cited earlier suggest that Bit1 plays pivotal roles in the development and progression of ESCC, and its biological functions in ESCC may be closely associated with AIF and Bcl-2 levels.