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ObjectiveTo explore the effects of the main component of Realgar arsenic disulfide （As2S2） on DNA methylation of SKM-1 cells with myelodysplastic syndrome. MethodCell Counting Kit-8 （CCK-8） was used to detect the inhibitory effect of As2S2（0， 1， 2， 4， 8， 16 μmol·L-1）on SKM-1 cells. Propidium iodide （PI） staining was applied to detect the effect of As2S2（0， 1， 2， 4 μmol·L-1）on the SKM-1 cell cycle. The effect of As2S2 （0， 4 μmol·L-1） on the methylation of SKM-1 cells on a genome-wide scale was observed by using Human Methylation 850K BeadChip， followed by Kyoto Encyclopedia of Genes and Genomes （KEGG） and gene ontology （GO） analyses. According to the microarray data， the antioncogene TUSC3 was selected， and real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot were adopted to investigate the effect of As2S2 （0， 1， 2， 4 μmol·L-1） on the mRNA and protein expression of TUSC3， respectively. ResultCompared with the conditions in the blank group， As2S2 inhibited SKM-1 cells， increased the proportion of cells in the G0/G1 phase， and decreased the proportion of cells in the S phase（P<0.05）. The 850K microarray showed that 4 μmol·L-1 As2S2 could significantly induce DNA methylation in SKM-1 cells， with 12 710 differentially methylated genes involved （50% hypermethylated and 50% hypomethylated genes）. KEGG and GO analyses showed that differentially methylated genes were involved in many important biological functions and signaling pathways， including purine metabolism， natural killer cell-mediated cytotoxicity， endocytosis， chemokine signaling pathway， and nuclear ubiquitin ligase complex. In terms of downstream gene expression， Real-time PCR and Western blot showed that As2S2 increased the expression of TUSC3， as compared with the conditions in the blank group （P<0.05）. ConclusionAs2S2， the main component of Realgar， has a significant regulatory effect on the methylation of SKM-1 cells， which is presumedly achieved by increasing the expression of TUSC3.
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@#Oral lichen planus (OLP) is a common chronic inflammatory disease with unclear etiology, in which disorder of the cell-mediated local immune response plays an important role. MicroRNAs (miRNAs) have been found to play an important role in the occurrence and development of inflammatory responses and autoimmune diseases. In recent years, many studies have reported that miRNAs may be related to OLP. According to a literature review, high expression of miRNA-19a and low expression of miRNA-122, miRNA-199, miRNA-138, miRNA-635 and miRNA-578 may be related to the occurrence of OLP by regulating cytokines such as interleukin, interferon and tumor necrosis factor. The low expression of miRNA-125a and the high expression of miRNA-132, miRNA-146a and miRNA-155 may be related to the severity of OLP by influencing the differentiation of CD4+ T cells in the Th1/Th2 subgroup. High expression of miRNA-26a, miRNA-29a and miRNA-31 and low expression of miRNA-27b, miRNA-200a and miRNA-137 may be associated with malignant risk of OLP through functionally related genomes, transcription factors and miRNA coregulatory networks. Some deficiencies remain in current studies. For example, many studies using microarrays to screen differentially expressed miRNAs have not been further grouped according to the type of OLP or cancer risk.
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@#[Abstract] Objective: To quantify the expression of growth arrest and DNA damage inducible protein 45g (GADD45g) gene in the bone marrow samples of patients withAML (acute myeloid leukemia) and inAML cell lines, as well as to study the correlation between the GADD45g expression and prognostic outcome in patients withAML and investigate the role of GADD45g over-expression in proliferation, apoptosis, senescence, differentiation, cell cycle arrest, and drug sensitivity in AML cell lines. Methods: In the study, a total of 27 cases of bone marrow specimens were selected from patients initially diagnosed as AML in Hospital of Blood Diseases affiliated to Chinese Academy of Medical Sciences from January 2013 to December 2016. mRNA and protein expression levels of GADD45g in BMMNCs (Bone marrow mononuclear cells) from patients with AML and healthy donors and in AML cell lines were quantified by quantitative real-time PCR and Western blotting. The correlation between GADD45g expression and overall survival (OS), coupled with event-free survival (EFS) in patients with AML was analyzed in two gene expression datasets (GSE10358, GSE425-GPL317). Lentiviral vectors over-expressing GADD45g were constructed and transfected into AML cell lines (U937, THP-1 and Molm-13 cell lines). The role of GADD45g over-expression in cell proliferation, colony formation, senescence, apoptosis, cell cycle arrest, differentiation and drug sensitivity of U937, THP-1 and Molm-13 cells were detected by cell counting, colony-forming assay, β-galactosidase staining and flow cytometric analysis of Annexin V/7AAD staining, PI staining and so on, respectively. Results: Expression of GADD45g was dramatically down-regulated in BMMNCs in AML patients and AML cell lines compared to that from healthy donors (all P<0.01). The OS (P<0.05) and EFS (P<0.05) of AML patients with low GADD45g expression were significantly shorter that those of AML patients with higher GADD45g level. Enforced expression of GADD45g could inhibit cell growth and colony formation, promote senescence and apoptosis, induce cell cycle arrest and differentiation and enhance drug sensitivity in AML cell lines (P<0.05 or P<0.01). Conclusion: GADD45g expression was remarkably silenced in marrow tissues of patients withAML andAML cell lines; it showed remarkable and all-around inhibiting effect onAMLcell lines, indicating that GADD45g expression has prognostic value inAML.
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Prostate cancer is the most prevalent male urogenital malignancy.Androgen deprivation therapy is the principal method for initial treatment for the patients,but the majority of them will eventually develop progressive disease,a status called castration-resistant prostate carcinoma.Lots of susceptibility genes,tumor suppressor genes and oncogenes,and their variations rdevant to the occurrence and development of prostate cancer have been revealed by the studies of molecular oncology.These findings on the molecular basis of prostate carcinogenesis will further improve the strategies on prevention,diagnosis and clinical management for prostate carcinoma.
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Cervical carcinoma is a serious threat to the health of women around the world ,and its inci-dence ranks at the second position after breast cancer in female reproductive system .In addition to oncogene acti-vation and inactivation of tumor suppressor gene ,endogenous and exogenous factors also affect the development of cervical cancer .
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Objective To explore the effects of miR-218 on biological functions of renal cell carcinoma cell line through regulating the expression levels of miR-218.Methods The pcDNA3.1-miR-218 was transfected into renal carcinoma cell line A498 and 769-P and the expression of miR-218 was detected.The cell activity,invasion,apoptosis and proliferation of transfected renal carcinoma cell line were analyzed in vitro.Results After plasmid transfected A498/769-P renal carcinoma cell line,the expression level of miR-218 (1.99,1.64) was significantly higher than that of the control group (1.00) (t =60.82,10.89,P ＜ 0.000 1) The cell viability (0.90±0.10,0.68±0.06) was lower than that of the control group (1.39±0.14,1.24±0.08) by CCK8 experiment (t =15.02,31.69,P ＜ 0.000 1).The cell invasion was lower than that of control group by Transwell experiment (t =15.78,18.80,P ＜ 0.000 1).The apoptosis ratio was higher by AnnxinV-FITC experiment,the apoptosis ration of control group and transfected group were respectively 0.25 ％,45.77 ％ in A498 cell line and 0.11％,45.57 ％ in 769-P cell line.The proliferation was lower than that of the control group (P ＜ 0.000 1).Conclusion Up-regulation of miR-218 expression can inhibit the growth of renal cell carcinoma cell line in vitro.
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Fox family transcription factors have crucial biology functions,including the regulation of proliferation,differentiation and tumorigenesis.Deregulation of Fox proteins expression may act as both oncogenes and tumor suppressors,the relevant researches have been paid more and more attentions.Here,this review focuses on the roles of Fox family genes in oncogenesis from the articles published recently.
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ObjectiveTo investigate the effect of PTEN on cell proliferation in human breast cancer cell BT549.MethodsThe plasmid pcDNA3-PTEN was used to transfect the PTEN - null breast cancer cell BT549 by lipo - transfection.After G418 selection,BT549 cells which stably expressed PTEN were obtained and amplified.Western blot were used to determine the target protein expression,the cell viability was tested by MTT assay.Results(1)Compared with the control,PTEN-BT549 cells demonstrated high expression of PTEN protein ;(2)The proliferation speed of PTEN-BT549 was obviously slower than BT549 and pcDNA3-BT549 cells( P ＜ 0.05 ).ConclusionAnti-oncogene PTEN suppresses the growth of breast cancer cell BT549.
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Objective To investigate the expression of SHP-1 and JAK1 mRNA in acute leukemia patients and their impact on disease development,and outcome of the primary chemotherapy.Methods Semi-quantitative reverse transcription polymerase chain reaction was used to measure the expression of SHP-1 and Janus kinase 1(JAK1)mRNA in 93 patients with acute leukemia(AL)and 20 healthy adults as normal 、controls(NC).Results The expression of SHP-1 mRNA in de novo AL patients was significantly lower than that in NC group(P=0.000),which was elevated when complete remission(CR)was achieved(P=0.032)and decreased after the disease relapsed (P=0.015).The expression of JAK1 mRNA in NC group was a lower than that in de novo AL group, but with no statistical significance(P=o.051).While there was statistical significance between NC group and relapsed AL group(P=0.047).The complete remission(CR)rate of the primary chemotherapy in SHP-1 positive group Was 88.9%,but 60.38%in negative group,and there was a statistical significance between them(P=0.018).There Was a negative correlation between the expression level of SHP-1 and JAKI mRNA (P=0.048).Conclusion The expression of SHP-1 mRNA Was significantly decreased or absent in the specimens of acute leukemia patients,and the positive expression of SHP-1 mRNA may be proposed as a factor of preferable therapeutic efficacy in de novo AL and a marker for the progress of the disease.The abundance of JAK1 mRNA was possibly elevated in patients with acute leukemia.
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Objective To investigate the effect of the exogenous fragile hisdidine triad(FHIT) gene on the proliferation and the apoptosis of cutaneous carcinoma cell line A431,and to explore the mechanism of tumor suppression by the FHIT gene.Methods The plasmids pcDNA3-FHIT and pcDNA3-vector were transfected into the cutaneous carcinoma cell line A431 without FHIT gene expression,and then the transfected cells were screened by G418 and the expression of FHIT was determined by the immunocytochemical staining technique.The effect of FHIT on the growth characteristics of cutaneous carcinoma cell line A431 was observed by MTT,colony forming test and flow cytometry.Results Stable FHIT gene expressing A431 cells were produced,the proliferation activity and colony forming capability of A431FHIT were suppressed,whereas the apoptosis was increased.All these differences between A431-FHIT cells and the two control groups of cutaneous carcinoma cells had statistical significance.Conclusion Transfecting the exogenous FHIT gene into cutaneous carcinoma cells line A431can suppress the proliferation of tumor cells,and can also induce apoptosis and cell cycle arrest.
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Objective To investigate the correlation between the expressions of tumour suppressor gene PTEN and oncogene C-myc in colorectal carcinoma.Methods The expressions of PTEN and C-myc protein in normal colorectal mucosa(n=8), adjacent non-cancerous tissues(n=10) and primary colorectal carcinoma tissues(n=60) were observed by S-P immunohistochemical assay.Results Of 60 colorectal carcinoma tissues,C-myc protein was detected in 46 cases.The expression rate of C-myc in the primary colorectal carcinoma tissues(76.70%) was significantly higher than that in the normal(0) and adjacent non-cancerous tissues(10%)(P0.05).The positive expression rate of PTEN protein in the primary colorectal carcinoma tissues(25.00%,15/60) was significantly lower than that in the normal(100%) and adjacent non-cancerous tissues(90%)(P
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Objective: To study the influence of the Ewi-anticarcinogen Prescription on associated gene protein in process of rat hepatocarcinoma induced by diethylnitrosamine (DEN). Methods: Rats hepatocarcinoma model was induced by DEN, while the Eqi-anticarcinogen Prescription was used during the stage. At the end of 12th week and 16th week, the influence of the Eqi-anticarcinogen Prescription on positive expression of PCNA and p53 protein were examined by immuneohistochemical method. Results: The positive expression of p53 protein was occurred in precancerous hyperp lastic nodules; The Eqi-anticarcinogen Prescription can significantly inhibit the overexpression of p53 (P
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Background and purpose:Lung cancer is thought to be caused by multiple-step carcinogenesis. Identification of the genetic alterations that occur in tumors is an important approach to understanding carcinogenesis. We identified chromosomal abnormality in lung cancer by the molecular cytogenetic techniques of comparative genomic hybridisation(CGH),the technology could help to comprehend the relationship between chromosome abnormality, different patho-types,and clinical features of lung cancer.Methods:CGH was used to detect the global genomic aberration in the fresh cancer tissue cells from 30 patients with lung cancer.Results:Chromosomal abnormality were detected in all of 30 cases with lung cancer,the altofrequent gains in 1p11-p22,5p11-p14,16p 11-P12,19q13, 19p 13,20p12,21q21 and the altofrequent losses in 5q,6p24-pter,9p31-qter,13q21-qter,14q21-qter were found in all three types of lung cancer,the marked differences of chromosomal abnormalities in three types of lung cancer were also found.Conclusions:The cytogenetic aberration exists generally in lung cancer cells,the cytogenetic aberration is the base of the initiation and progression of the lung cancer.There are some different chromosomal abnormalities between different types of lung cancer,which may serve as a marker to differential diagnosos of the three types of lung cancer.As to the progression of malignant neoplastic disease,the complexity of chromosomal abnormality is obviously elevated.Different carcinogenic agents(smoking for example)may induce different chromosomal abnormalities.
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In order to evaluate the factor. which affect the five year survival rate and prognosti c factors of the early carcinoma of the esophagus and the gastric cardia treated with endoscopic Nd : YAG laser therapy , thirty-three patients were followed. Of the 33 patients , 32 ( 97% ) cases were cured , resul- ting in the disappearance of the cancer cells. They were followed up for 3 3- 78 months , with a mean of 55. 3 months. The survival rate of the 32 patients treated with endoscopic laser was computed with the Product limit estimate method ,and was compared with the natural history of early superficial carcinoma . of the esophagus and the gastric cardia. The five year survival rate was in 97% of the 32 patients treated with laser therapy ,in contrast to 67% (P
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Objective To observe the effect of Herba Hedyotis Diffusae(HHD) on expression of heat shock protein 70(HSP70) and P16 anti-oncogene protein in mice with H22 cell transplanted tumor. Methods The mice were immunized with hepatoma-lines-H22 cells which were treated by Chinese herbs firstly. According to the pretreatment of the Chinese herbs and whether the H22 cells being blocked by HSP70 monoclonal antibody,the mice were divided into 5 groups:HHD non-blocking group,HHD-blocking group,Radix Codonopsis(RC)-blocking group,RC non-blocking group,and RPMI-1640 control group. Then the treated H22 Cells were translated into the mice. The expression of HSP70 and P16 anti-oncogene protein in mice with transplanted H22 liver carcinoma was detected by immunohistochemical marking method. Results The expressions of HSP70 was up-regulated in HDD non-blocking group and RC non-blocking group,in particular in RC non-blocking group,and the difference was significant as compared with HHD-blocking group,RC-blocking group and control blank group.The expression of P16 anti-oncogene protein was up-regulated in the treatment groups,and the difference was significant in comparison with the control group. The effect on P16 anti-oncogene protein expression was stronger in HDD groups than that in RC groups,but the difference was insignificant between the blocking group and the non-blocking group of each herb. Conclusion The anti-tumor effect of HDD may be achieved by inducing HSP70 expression in transplanted H22 neoplasia and by enhancing the immunogenicity. The up-regulation of P16 anti-oncogene expression by HHD and RC has no direct relationship with the induction of HSP70,and the related mechanism needs further research.