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.     

miR-34a regulates cisplatin-induce gastric cancer cell death by modulating PI3K/AKT/survivin pathway

The purposes of this study were to determine the expression profiles of microRNA-34a (miR-34a) in human gastric cancer cell line (SGC-7901) and cisplatin-resistant cell lines (SGC-7901/DDP), and to establish the correlation between miR-34a expression profile and the sensitivity of human gastric cancer cell to cisplatin-based pattern, thereby providing new methods and strategies for treating gastric cancer. Gastric cancer cell line (SGC-7901) and cisplatin-resistant cell line (SGC-7901/DDP) were cultivated in vitro, respectively. Quantitative real-time PCR (qRT-PCR) and Western blot were utilized to determine the expression profiles of miR-34a and survivin in both gastric cancer cell lines. With miR-34a mimic and miR-34a inhibitor transfected into SGC-7901 and SGC-7901/DDP for 48 h, post-transfection changes of miR-34a expression was determined; the effects of miR-34a ectopic expression on the viability of cisplatin-induce gastric cancer cell were assayed by the MTT method. The effects of miR-34a ectopic expression on apoptosis of cisplatin-induce gastric cancer cell were determined by Annexin V/propidium iodide (PI) double staining method and flow cytometry. The effects of miR-34a ectopic expression on the AKT and p-AKT expression of cisplatin-induce gastric cancer cells were determined by Western blot and flow cytometry with the PI3K pathway inhibitor Wortmannin. As shown by qRT-PCR and Western blot analyses, the expression of miR-34a in cisplatin-resistant cell lines decreased significantly in comparison to that of SGC-7901 cell line (p?<?0.05), while significant up-regulation of survivin expression was also observed (p?<?0.05). Compared with the control group, the expression of miR-34a increased significantly in SGC-7901 cells transfected with miR-34a mimic for 48 h (p?<?0.01). After miR-34a inhibitor transfection, the expression of miR-34a decreased significantly (p?<?0.05). The viability of cisplatin-induce gastric cancer cells increased significantly (p?<?0.05) with significant decrease of apoptosis after miR-34a expression inhibition, as demonstrated by MTT and flow cytometry with miR-34a over-expression, the viability of cisplatin-induce gastric cancer cells decreased significantly (p?<?0.05), with significant apoptosis increase (p?<?0.05). As shown by Western blot and flow cytometry, in comparison to the control group, Wortmannin could inhibit miR-34a inhibitor and DDP induced up-regulation of p-AKT significantly (p?<?0.05) and stimulated apoptosis. In conclusion, miR-34a expression was down-regulated in cisplatin-resistant cell lines. miR-34a over-expression could improve the sensitivity of gastric cancer cells against cisplatin-based chemotherapies, with PI3K/AKT/survivin signaling pathway possibly involved in the mechanism.     

蒿甲醚对胃癌细胞增殖、侵袭和迁移的抑制作用研究

目的:研究蒿甲醚对胃癌细胞（AGS和SGC-7901）的增殖、侵袭以及迁移的影响并探讨其分子机制。方法:分别利用MTT、集落形成试验检测胃癌细胞的活力和生长;流式细胞技术检测胃癌细胞的凋亡率;利用细胞侵袭和划痕愈合试验检测胃癌细胞的侵袭和迁移;Western blot检测相关蛋白的表达水平。结果:蒿甲醚（0~800 μmol/L）能够浓度和时间依赖性的抑制 AGS和SGC-7901细胞的增殖（P＜0.05）。集落形成试验以及流式细胞术结果显示蒿甲醚（400 和 600 μmol/L）能够抑制AGS和SGC-7901细胞的生长以及促进细胞凋亡（P＜0.05）。细胞侵袭和划痕愈合试验发现蒿甲醚（400 和 600 μmol/L）能够抑制AGS和SGC-7901细胞的侵袭和迁移（P＜0.05）。Western blot结果显示蒿甲醚(400 和 600 μmol/L)能够增加AGS和SGC-7901细胞的cleaved caspase-3,cleaved caspase-9以及Bax的蛋白水平（P＜0.05）;同时能够抑制N-cadherin 和vimentin的蛋白表达并促进E-cadherin蛋白的表达。结论:蒿甲醚可以显著抑制胃癌细胞的增殖、侵袭以及迁移,其机制可能是与促进细胞凋亡以及抑制上皮间质转化有关。     

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.     

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.     

Beclin 1 expression is an independent prognostic factor for gastric carcinomas

Beclin 1, an important autophagy-related protein in human cells, is involved in autophagy, differentiation, anti-apoptosis, and cancer progression, which is increased during periods of cell stress and extinguished during the cell cycle. In order to clarify the role of Beclin 1 in gastric carcinogenesis and subsequent progression, its expression was examined by immunohistochemistry and in situ hybridization (ISH) on tissue microarrays containing gastric carcinomas, adjacent non-neoplastic mucosa, and metastatic lymph node. Gastric carcinoma tissue and cell lines were studied for Beclin 1 expression by Western blot or RT-PCR, respectively. The results demonstrated that Beclin 1 was distinctively expressed in GES-1, AGS, BGC-823, GT-3 TKB, HGC-27, KATO-III, MGC-803, MKN28, MKN45, SCH, SGC-7901, or STKM-2 at both mRNA and protein levels. However, Beclin 1 mRNA was highly expressed in gastric carcinoma than matched mucosa by real-time PCR and ISH (P?<?0.05). Beclin 1 expression was negatively related to distant metastasis and poor prognosis of gastric carcinoma (P?<?0.05). Beclin 1 was highly expressed in male than female patients with gastric carcinoma (P?<?0.05). The 65-year-elder patients with gastric carcinoma had higher Beclin 1 expression than the younger ones (P?<?0.05). The diffuse-type carcinomas showed less Beclin 1 expression than intestinal- and mixed-type ones (P?<?0.05). In intestinal-type gastric carcinoma, Beclin 1 expression was inversely associated with venous invasion, lymph node metastasis, and tumor–node–metastasis (TNM) staging (P?<?0.05). Kaplan–Meier analysis indicated that Beclin 1 expression was positively linked to favorable prognosis of the patients with overall and intestinal-type carcinoma (P?<?0.05). Cox’s proportional hazard model indicated that venous invasion, lymph node metastasis, distant metastasis, TNM staging, and Beclin 1 expression were independent prognostic factors for gastric carcinomas (P?<?0.05). It was suggested that aberrant Beclin 1 expression is closely linked to pathogenesis, metastasis, and differentiation of gastric carcinoma. Beclin 1 expression might be employed to indicate the favorable prognosis of gastric carcinomas as an independent factor.     

Tumor-associated mesothelial cells are negative prognostic factors in gastric cancer and promote peritoneal dissemination of adherent gastric cancer cells by chemotaxis

Peritoneal dissemination is highly frequent in gastric cancer. Damage to human peritoneal mesothelial cell (HPMC) barriers provokes gastric cancer peritoneal dissemination (GCPD), the key events during GCPD, is characterized by fibroblastic development. In this study, we have studied the association between fibroblast activation protein (FAP) expression in peritoneum and the pathological features of the primary tumor. The clinical prognosis of gastric cancer patients was evaluated according to FAP expression. In a gastric cancer cell-HPMC co-culture system, expression of E-cadherin, α-smooth muscle actin, and FAP were evaluated by Western blotting. Gastric cancer cell migration and adhesion to HPMC were also assayed. Our results showed positive peritoneal staining of FAP in 36/86 cases (41.9 %), which was associated with a higher TNM stage in primary gastric cancer and higher incidence of GCPD (both p?<?0.05). Survival analysis showed FAP expression was an independent prognostic factor of poor survival (p?=?0.02). Peritoneum of FAP-positive expression exhibited a distinct fibrotic development and expressed higher level of the mesenchymal marker α-SMA, which was confirmed by the in vitro Western blot assay. In HPMC and gastric cancer cell adherence assay, SGC-7901 cells preferentially adhered to TA-HPMC at different cell densities (both p?<?0.05). Additionally, SGC-7901 cells were more prone to chemotaxis by FAP-expressed tumor-associated–human peritoneal mesothelial cells (TA-HPMC) compared with HPMC co-cultured with normal gastric glandular epithelial cells in a time-dependent manner (both p?<?0.05). Our study indicated a positive correlation between peritoneum FAP expression and GCPD. FAP-expressed TA-HPMC might be an important cellular component and instigator of GCPD.     

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.     

EYA1 通过调控PTEN/PI3K/AKT信号通路抑制胃癌SGC-7901 细胞的恶性生物学行为

[摘要] 目的:探讨EYA1(eyes absent 1)通过调控PTEN/PI3K/AKT信号通路抑制胃癌SGC-7901细胞的恶性进展及其相关机制。方法:收集2016年6月至2018年6月陆军军医大学附属西南医院全军普通外科中心29例胃癌组织及其癌旁组织标本,采用Wb和qPCR实验检测胃癌组织和癌旁组织中EYA1 mRNA和蛋白的表达水平。人胃癌细胞株SGC-7901培养完成后,采用过表达EYA1质粒或siRNA干扰质粒转染胃癌SGC-7901细胞;分别采用MTT、流式细胞术、划痕愈合和Transwell实验检测胃癌SGC-7901细胞的增殖、凋亡、迁移和侵袭能力。结果:胃癌组织中EYA1 mRNA 和蛋白表达水平较癌旁组织均明显降低（P<0.01）;过表达EYA1可明显提高SGC-7901 细胞的增殖、迁移和侵袭能力（均P<0.05）、抑制细胞凋亡（P<0.05）。过表达EYA1 可明显促进PTEN的表达、抑制PI3K/AKT通路的激活（均P<0.05或P<0.01）;但在PTEN干扰后以上作用均受到了明显抑制（均P<0.05或P<0.01）。结论:EYA1可通过促进PTEN的表达抑制PI3K/AKT信号通路,从而抑制胃癌SGC-7901细胞的恶性生物学行为。     

PRMT5在胃癌中的表达及其对胃癌细胞增殖、凋亡、迁移能力的影响

背景与目的:蛋白精氨酸甲基转移酶5(protein arginine methyltransferase 5,PRMT5)是一种能调控细胞周期的酶,对细胞分裂周期有影响,可以通过调控细胞分裂周期影响细胞的增殖与凋亡。探讨PRMT5在胃癌中的表达及对胃癌细胞增殖、凋亡、迁移能力的影响。方法:采用蛋白质印迹法(Western blot)检测2016年5月-2019年1月在海南省肿瘤医院确诊为胃癌并进行手术治疗的患者的胃癌组织及其癌旁组织(距离癌组织>5 cm)标本(共88例)中的PRMT5的表达,分析PRMT5相对表达量与胃癌临床特征的关系;用PRMT5小干扰RNA(PRMT5-siRNA)和阴性对照(siRNA-NC)转染人胃癌细胞系SGC-7901,以未转染的SGC-7901细胞作为对照组。采用实时荧光定量聚合酶链反应(real-time fluorescence quantitative polymerase chain reaction,RTFQ-PCR)和Western blot检测转染后细胞中PRMT5 mRNA表达和蛋白水平;采用细胞计数试剂盒-8(cell counting kit-8,CCK-8)检测细胞增殖;采用流式细胞术(flow cytometry,FCM)检测细胞凋亡;采用划痕实验检测细胞迁移能力;采用Transwell细胞侵袭实验检测细胞侵袭能力;采用Western blot检测cleaved caspase 3、磷脂酰肌醇3激酶(phosphoinositide 3-kinase,PI3K)、蛋白激酶B(protein kinase B,AKT)和磷酸化AKT(phosphorylated-AKT,p-AKT)蛋白表达。结果:PRMT5在胃癌组织中的表达高于癌旁组织(P<0.01);PRMT5表达水平与胃癌的病理学分级、分期、淋巴结转移有关(P均<0.05);转染后siRNA-NC组和对照组PRMT5 mRNA和蛋白表达量、胃癌细胞的增殖率、凋亡率、cleaved caspase 3、PI3K、AKT、p-AKT蛋白表达量、划痕愈合率、细胞侵袭数差异均无统计学意义(P>0.05),转染后siRNA-NC组和对照组PRMT5 mRNA和蛋白表达量、胃癌细胞增殖率、PI3K、p-AKT、AKT蛋白表达量、划痕愈合率、细胞侵袭数均高于PRMT5-siRNA组,而凋亡率、cleaved caspase 3低于PRMT5-siRNA组(P均<0.05)。结论:PRMT5在胃癌组织中表达明显升高,其表达水平与胃癌的发生、发展、转移恶化密切相关,下调PRMT5的表达可明显减弱胃癌细胞的增殖、迁移能力,同时促进胃癌细胞的凋亡。     

RNAi-mediated gene silencing of vascular endothelial growth factor-C inhibits tumor lymphangiogenesis and growth of gastric cancer in vivo in mice

Overexpression of vascular endothelial growth factor-C (VEGF-C) has been implicated as a critical molecular signal in tumor development by promoting intratumoral lymphangiogenesis. The aim of this study was to explore whether small hairpin RNA (shRNA) targeting VEGF-C could inhibit gastric cancer lymphangiogenesis and tumor growth. Plasmid-mediated expression of VEGF-C–shRNA was employed to silence VEGF-C gene expression in human SGC-7901 cell lines. The inhibition of the target gene expression was quantified by real-time quantitative polymerase chain reaction, Western blotting, and enzyme-linked immunosorbent assay. In vitro, the cell viability was determined by MTT assay, flow cytometry analysis, and migration assay. After VEGF-C knockdown was confirmed, the stable cells were inoculated into nude mice. Tumor growth, lymph vessel density (LVD), and microvascular density were compared for mice administered either VEGF-C–shRNA or control. VEGF-C–shRNA causes effective and specific downregulation of VEGF-C expression (P?<?0.05). The migration activity of SGC-7901 cells was attenuated in vitro (P?<?0.05). Tumor growth rate and LVD was suppressed in vivo (P?<?0.05). VEGF-C–shRNA effectively suppressed gastric cancer cell migration in vivo, retards tumorigenicity, and lymphangiogenesis in nude mice.     

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.     

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).