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Study on the mediating role of tumor suppressor gene PRDM5 in cervical squamous cell carcinoma induced by HPV16 virus

Haiyan CHENG ; Jing MA ; Ziwei FENG ; Kejin HUANG ; Yuxia WANG ; Yunyan ZHANG

Practical Oncology Journal.2018;32(6):483-487. doi:10.11904/j.issn.1002-3070.2018.06.001

Objective The aim of this study was to explore whether the down-regulation of tumor suppressor gene PRDM5 is one of the mechanisms of HPV16 virus infection leading to cervical cancer. Methods The expressions of PRDM5 protein and HPV16 E6/HPV18 E6 protein in cervical cancer tissues and normal cervical tissues were detected by immunohistochemistry. After transfected with HPV16 E6 shRNA plasmid,the expression of PRDM5 gene was detected in SiHa cells by RT-PCR and Western blot. Results The positive expression rate of HPV 16/18 E6 in cervical cancer tissues was significantly higher than that in normal cervical tissues. The expression level of PRDM5 protein in cervical cancer tissues was lower than that in normal cervical tissues. After HPV16 E6 shRNA3 was transfected into SiHa cells to interfere with the expression of HPV16 E6 gene,the expression of PRDM5 at mRNA and protein levels was up-regulated in SiHa cells. Conclusion PRDM5 may mediate the development of cervical cancer caused by HPV16 virus infection.

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Inhibitory effect and mechanism of Nultin-3 combined with cisplatin on oral squamous cell carcinoma

Jun SHI ; Xiaobing NI ; Min MAO ; Xingchun PENG

Practical Oncology Journal.2018;32(6):488-492. doi:10.11904/j.issn.1002-3070.2018.06.002

Objective The objective of this study was to investigate the inhibitory effect of MDM2 inhibitor Nultin-3 com-bined with cisplatin on human oral squamous cell carcinoma(OSCC)Tca8113 cells and its mechanism. Methods Human OSCC Tca8113 cells were treated with Nultin-3,cisplatin,Nultin-3 combined with cisplatin,or vehicle control groups. The proliferation of Tca8113 cells was determined by thiazolyl blue(MTT)assay. The expression of MDM2,P53,Caspase-9 and Caspase-3 protein was determined by Western blot. Results The proliferative rate of OSCC ca8133 cells treated with Nultin-3 combined with cisplatin was significantly lower than that of other groups(P<0. 05). The relative expression of Caspase-9,Caspase-3 and P53 protein in the Nultin-3 combined with cisplatin was significantly higher than those of the Nultin-3 and cisplatin alone groups(P<0. 05). In addi-tion,the relative expression of MDM2 protein in the Nultin-3 combined with cisplatin group was significantly lower than that of the cisplatin and Nultin-3 alone groups(P<0. 05). Conclusion Nultin-3 combined with cisplatin has synergistic effect on oral squa-mous cell carcinoma Tca8113 cells. Nultin-3 regulates the MDM2-p53 signaling pathway and up-regulates the expression of pro-apoptotic proteins Caspase-9 and Casapase-3 to enhance the inhibition of cisplatin on oral squamous cell carcinoma,providing a solid theoretical basis for clinical research and treatment.

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Therapeutic effect of sequential local injection of heterogeneic lymphocytes and autologus lymphocytes on transplanted hepatocarcinoma in mice

Bing XU ; Suqin HUANG ; Linlan WU ; Jianwei WEI ; Xiaomei YANG ; Zhiping ZHAO ; Yi CHEN ; Xiaozhi JIANG

Practical Oncology Journal.2018;32(6):493-497. doi:10.11904/j.issn.1002-3070.2018.06.003

Objective The aim of this study was to investigate the anti-tumor effect on sequential injection of heterogeneic lymphocyte(HL)and autogeneic lymphocyte(AL). Methods The HL was prepared by using CC3HF1 mice as feeders. CB6F1 mice were used as recipients,and Hepa1-6 cells were inoculated into the recepients′groin subcutis. A cryoprecipitate was extracted from mouse plasma by freeze-thaw method to prepare fibrin Glue(FG);FG was combined with HL or AL to be FG-HL or FG-AL. The experimental treatment consisted of two stages. At first stage(15 d),FG-HL were injected on the surface of the tumor-bearing tissue of the recipients as the experimental group,and FG-phosphate buffer saline(FG-PBS)were injected on the surface of the tumor-bearing tissue of the rest recipients as the control group. The immunological factors such as tumor cell killing rate of the spleen lym-phocytes and numbers of lymphocytes,CD8 +T and NK in the two groups were detected,respectively. At later stage(10 d),a part of mice were randomly selected from the experimental and control groups,and the lymphocytes( AL) were used to form FG-AL,which were injected on the surface of tumor-bearing tissues in the rest of mice. Tumors in mice of the two groups were compared for tumor volume and tumor inhibition rate. Results The tumor cell killing rate of AL in the experimental group(26. 70 ± 7. 22) was signifi-cantly higher than that in the control group(5. 70 ± 2. 68)(P<0. 01). Numbers of mouse spleen lymphocytes,CD8 +T cells and NK cells were significantly higher than the corresponding values of the control group(P<0. 05). After the two-stage treatment,the aver-age tumor volume of the experimental group[(1.20 ±0.33)cm3]was significantly smaller than that of control group[(2.05 ±0.37) cm3](P<0. 01). The tumor inhibition rate in the experiment group was 41. 5% when compared to the control group. Conclusion Local injections of FG-HL followed by FG-AL can significantly inhibit the growth of transplanted tumor in mice;it is expected to become an anti-tumor biological therapy.

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Molecular mechanism of UHRF1 inhibiting proliferation of lung adenocarcinoma cells by regulating autophagy

Xiusen BIAN ; Guang LI ; Xinyu GUAN ; Yi ZHANG ; Chang DI ; Can MA

Practical Oncology Journal.2018;32(6):498-502. doi:10.11904/j.issn.1002-3070.2018.06.004

Objective The objective of this study was to investigate the proliferation,autophagy and the potential mechanism of Ubiquitin-like with PHD and ring finger domains 1(UHRF1)in lung adenocarcinoma cells. Methods The expression of UHRF1 in lung adenocarcinoma tissues was determined by the bioinformatics website(TCGA). The expression of UHRF1 in lung adenocarci-noma cell lines(PC-9,A549 and H1299)and human bronchial epithelial cells(16HBE)was detected by qRT-PCR and Western blot. After transfection of UHRF1-shRNA,CCK-8,clone formation and ki67 were performed to detect the changes in the prolifera-tive capacity of lung adenocarcinoma A549 cells. Western blot was used to detect the changes of autophagy-associated proteins(LC3-I/II and Beclin-1)and proliferation-related proteins(CDK6,Rb and PCNA). Transmission electron microscopy was used to ob-serve the effect of UHRF1 on autophagosomes in A549 cells. Results The expression of UHRF1 in lung adenocarcinoma tissues was significantly higher than that in adjacent tissues. Compared with normal bronchial epithelial 16HBE cells,the mRNA and protein levels of UHRF1 in lung adenocarcinoma A549 and H1299 cells were significantly increased. In addition,CCK-8 assay and colony forma-tion experiments showed that silencing UHRF1 reduced the growth of A549 cells. Ki-67 immunofluorescence staining showed that the proliferation ability of A549 cells after knocking out UHRF1 was significantly lower than that in the normal control group. Further-more,knockdown of UHRF1 resulted in an increased expression of CKD6 and PCNA proteins in comparison with the control-siRNA group. The expression of Rb protein was down-regulated in the UHRF1-siRNA group. Silencing UHRF1 increased the ratio of LC3-II/LC3-I, induced up -regulation of Beclin -1 expression and promoted the formation of autophagic bodies in A549 cells. Conclusion UHRF1 is highly expressed in lung adenocarcinoma,and silencing UHRF1 can inhibit proliferation. This effect may be regulated by promoting autophagy.

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Study of the effect of astragalin on proliferation of ovarian cancer cells by inhibiting the glycolytic pathway induced Via HIF-1α

Ling SONG ; Qiong FU

Practical Oncology Journal.2018;32(6):503-509. doi:10.11904/j.issn.1002-3070.2018.06.005

Objective The objective of this study was to explore the effect of astragalin on human ovarian cancer OVCAR-8 cells in 2 D and 3 D culture conditions and its possible mechanism. Methods CCK-8 assay was use to detect the effect of astra-galin on the proliferation of OVCAR-8 cells in 2 D culture conditions. The 3 D cell proliferation activity assay kit was used to detect the effect of astragalin on OVCAR-8 cells in 3 D culture conditions. Cell apoptosis kit was used to detect the cell apoptosis rate after astragaline treatment. In addition,Western blot was used to detect the levels of apoptosis related proteins such as Bcl2(B-cell lym-phoma 2),Bax(Bcl-2-associated X protein),cleaved-caspase-3 and glycolysis related proteins such as Glut-1(Glucose trans-porter-1),Glut3,HK2(Hexokinase 2),PDK-1(Pyruvate dehydrogenase lipoamide kinase-1),PDK3 and HIF-1α(hypoxia-in-ducible factor-1α)in OVCAR-8 cells after astragaline treatments in 2 D and 3 D culture conditions. HK2 activity was detected in OVCAR-8 cells by Elisa. Results Astragaline at doses of 4~100 μmol/L significantly inhibited the proliferation of OVCAR-8 cells in 2 D culture conditions,and showed a dose-and time-dependent manner(P<0. 05). Astragalin significantly inhibited the proliferation of OVCAR-8 cells in 3 D culture conditions(P<0. 05). Astragalin also significantly inhibited the migration ability of OVCAR-8 cells(P<0. 05). In addition,astragaline significantly increased apoptosis rate,decreased the levels of Bcl2,Glut1,Glut3, HK2,PDK1 and PDK3 proteins and increased the levels of Bax and cleaved-caspase-3 proteins in OVCAR-8 cells both in 2 D and 3 D culture conditions(P<0. 05). Astragaline significantly decreased the expression of HIF-1α in OVCAR-8 cells in 3 D cul-ture conditions(P<0. 05). In addition,astragalin decreased HK2 activity in OVCAR-8 cells under 2 D culture conditions in a dose-dependent manner(P<0. 05). Conclusion Astragalin has an inhibitory effect on the proliferation of OVCAR-8 cells both in 2 D and 3 D culture conditions. Its mechanism may be related to inhibiting glycolytic and the mitochondrial apoptotic pathways induced by HIF-1α.

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miR-219 regulates PRKCI expression in tongue squamous cell carcinoma

Lei WANG ; Huanyu JIANG ; Kaibin SONG

Practical Oncology Journal.2018;32(6):510-514. doi:10.11904/j.issn.1002-3070.2018.06.006

Objective The objective of this study were to investigate the effects of miR-219 on cell proliferation,invasion and metastasis and the correlation between PRKCI and miR-219 expression in tongue squamous cell carcinoma. Methods The lu-ciferase reporter gene assay was used to verify the predicted target gene. The expression of PRKCI in tongue squamous cell carcinoma cells overexpressed exogenous miR-219 was detected by qRT-PCR and Western blot. Finally,the reverse effects of PRKCI on the proliferation,clone formation,migration and invasion ability were examined in stable overexpressing miR-219 tongue squamous cell carcinoma(TSCC)cells by MTT assay,cell plate cloning assay,scratch assay and Transwell chamber assays. qRT-PCR assay was used to determine the expression of PRKCI gene and miR-219 in tongue squamous cell carcinoma tissues,and the relationship be-tween PRKCI and miR-219 was further analyzed. Results The bioinformatics analysis predicted that the downstream target gene of miR-219 was PRKCI. The double luciferase reporter gene assay showed that miR-219 was able to reduce the fluorescence activity of the wild type PRKCI reporter vector. In addition,qRT-PCR and Western blot also showed that miR-219 could down-regulate the expression of PRKCI in TSCC cells. MTT results showed that overexpression of PRKCI could reverse the inhibitory effect of miR-219 on the proliferation of TSCC cells,and further demonstrated that the overexpression of PRKCI could reverse the inhibitory effect of miR-219 on the proliferation, invasion and metastasis of TSCC cells by cell plate cloning, scratch and Transwell experiments. Conclusion MiR-219 plays a role in inhibiting tumor by directly targeting PRKCI and negatively regulating the expression of PRK-CI. miR-219 was negatively correlated with PRKCI expression in tongue squamous cell carcinoma.

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The role and mechanism of TRAP1 in the development of esophageal cancer

Fang YU ; Pei ZHAO

Practical Oncology Journal.2018;32(6):515-519. doi:10.11904/j.issn.1002-3070.2018.06.007

Objective The aim of this study was to investigate the role and mechanism of tumor necrosis factor receptor-re-lated protein 1(TRAP1)in the progression of human esophageal cancer. Methods Immunohistochemistry was used to detect the ex-pression of TRAP1 and S100A8 in human esophageal cancer tissues. A stably knocked-down TRAP1 cell line was established in the esophageal cancer KYSE150 cell line,the proliferation ability was detected by CCK-8,the transfer ability was detected by Transwell, and apoptosis was detected by flow cytometry. We conducted a gene profiling study to detect the expression of genes related to tumor progression. The expression of TRAP1 downstream genes-E-Cadherin,N-Cadherin and S100A8 was detected by Real-Time fluo-rescent quantitative PCR. Results The expression of TRAP1 in esophageal carcinoma was significantly higher than that in adjacent tissues and correlated with S100A8(χ2=4. 141,P<0. 001). The KYSE150 cell line with down-regulated of TRAP1(KYSE150-TRAP1)was established,and the expression of TRAP1 was down-regulated by 85% ,cell invaded ability was decreased by 46% ,no changes of cell proliferation and apoptosis were observed,when compared to the KYSE150 control cells. The expression level of E-cadherin was increased by 19% ,and the expression level of S100A8 was decreased by 39% in KYSE150-TRAP1 cells. Conclusion TRAP1 is overexpressed in esophageal carcinoma and promotes the metastasis of esophageal carcinoma by regulating S100A8 ex-pression.

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Relationship between human papillomavirus infection and prognosis of lung cancer:A meta-analysis

Yalong WANG ; Zhangyan LYU ; Fan ZHANG ; Xiaoshuang FENG ; Luopei WEI ; Xin LI ; Yan WEN ; Yushun GAO ; Qi XUE ; Shugeng GAO ; Fengwei TAN

Practical Oncology Journal.2018;32(6):520-526. doi:10.11904/j.issn.1002-3070.2018.06.008

Objective The objective of this study was to explore the association between human papillomavirus( HPV) and prognosis of lung cancer by meta-analysis. Methods The PubMed,Embase and Cochrane literature databases studies were searched using a combination of subject terms and free words. As of October 2018,a total of 123 related documents were obtained. After screen-ing the literature according to inclusion and exclusion criteria,the basic information of the study,HPV detection methods,lung cancer patients,hazard ratio(HR)values and 95% confidence interval(CI)were extracted from each study. The meta-analysis of random effects models was used to evaluate the correlation between HPV infection and prognosis in patients with lung cancer. Heterogeneity was assessed using the Q test and I2statistics,and publication bias was tested using Egger′s linear regression test and Begg′s rank cor-relation test. Results The study finally included 11 articles(9 in Asia,2 in Europe and US),and 1439 patients with lung cancer. Meta-analysis using a random-effects model showed no significant association between HPV infection and prognosis of lung cancer (HR=0. 90,95% CI:0. 71~1. 13). A stratified analysis of lung cancer pathological subtypes showed that the prognosis of patients with HPV-infected lung adenocarcinoma was significantly better than that in patients without HPV-infected lung adenocarcinoma (HR=0. 65,95% CI:0. 49~0. 85). Sensitivity analysis was performed by sequentially removing the included studies,and the results were not statistically significant. The results of Egger′s test(P=0. 708)and Begg′s test(P=0. 784)suggest that there is no publica-tion bias in this study. Conclusion HPV infection may be related to the prognostic of patients with lung adenocarcinoma. More basic and clinical studies are needed to further explore the association between HPV infection and lung adenocarcinoma as well as the corre-sponding mechanisms in the future.

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Expression of Pim-1 in primary hepatocellular carcinoma and its clinical significance

Xiaojun HU ; Xiao LI

Practical Oncology Journal.2018;32(6):527-532. doi:10.11904/j.issn.1002-3070.2018.06.009

Objective The aim of this study was to determine the expression of Pim-1 in primary hepatocellular carcinoma (PHC)and its clinical significance. Methods Immunohistochemical staining(IHC) was used to detect the expression of Pim-1 in 122 cases of PHC tissues,corresponding paracancer tissues,and 85 normal liver tissues. The relationship between the expression of Pim-1 protein and clinicopathological parameters was analyzed retrospectively. K-M method was used to analyze the effect of differ-ent Pim-1 expression on the survival time of PHC patients. Cox proportional hazard regression models were used to analyze risk fac-tors affecting survival time in patients with PHC. Results The total positive expression rate of Pim-1 protein in PHC tissues was 88. 5% ,which was significantly higher than that in adjacent tissues and normal liver tissues(P<0. 05). Univariate statistical analysis showed that patients with high expression of Pim-1 protein had poor preoperative liver function,more tumors,larger tumor diameter, high incidence of lymph node metastasis and high TNM stage(P<0. 05). Survival analysis suggested that the survival time of patients in the low expression group was significantly longer than that in the high expression of Pim-1 group(P<0. 05). Multivariate statisti-cal analysis showed that high expression of Pim-1 protein was an independent risk factor for survival time in patients with PHC(P<0. 001). Conclusion The expression level of Pim-1 in PHC tissues is significantly increased,which is related to the clinical pro-gress of PHC and the survival time of patients. Pim-1 overexpression indicates the poor prognosis of PHC patients.

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Study on predicting the cervical cancinogenesis by high-risk human papillomavirus load and the unbalanced expression of Th1/Th2

Yanli FU ; Yang YU ; Wei WEI ; Jingjing ZOU ; Xiang SUN

Practical Oncology Journal.2018;32(6):533-537. doi:10.11904/j.issn.1002-3070.2018.06.010

Objective The aims of this study were to compare the different expression between high-risk human papilloma-virus load(HR-HPV DNA)and Th1/Th2 type cytokines in local different microenvironments of cervix,and to explore the possibility and significance of predicting cervical cancer. Methods A total of 339 patients with persistent HR-HPV infection were divided into cervical intraepithelial neoplasia(CIN)and cervical cancer. Forty patients with HPV-negative and cytological examination of normal cervix were used as controls. PCR fluorescence assay and double antibody sandwich were used. ELISA assay were used to detect HPV-DNA and Th1 type cytokines including IL-2,IFN-γ,TNF-ɑ and Th2 type cytokines including IL-4,IL-6 and IL-10 from cervical secretion. The ratio of TNF-ɑ/IL-10 was used as an index to measure the immune balance of Th1/Th2. Univariate and multivariate logistic regression were performed to analyze the data and then to screen the predicting indicators of cervical cancer. Results Univariate analysis showed that HR-HPV DNA,IL-2,IL-4,IL-6,IL-10,IFN-γ,TNF-ɑ and TNF-ɑ/IL-10 were significantly different between CIN and cervical cancer groups(P<0. 05),which could be used as a risk factor for predicting cervical cancer. Multivariate logistic regression analysis showed that IL-10,IFN-γ,TNF-ɑ,TNF-ɑ/IL-10 were the influencing factors of cervical cancer. The regression model fitted goodness test was Nagelkerke(R2= 0. 982),the pre-judgment rate for CIN was 99. 5% ,the pre-judgment rate of cervical cancer was 100% ,and the total positive rate was 99. 7% ,suggesting good fitting effect was good and the prediction accuracy was high. Conclusion CINⅠand CINⅡhave abnormal expression of Th cytokine,but they do not affect Th1/Th2 balance. Th1/Th2 imbalance in CINⅢ stage and Th2 dominant expression promote the occurrence of cervical cancer. Based on the regression model for predicting cervical carcinogenesis,cervical immunity caused inhibitory microenvironment by local immune imbalance is the key link in HR-HPV persistent infection and cervical cancer,and has nothing to do with HR-HPV DNA.

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