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Background and purpose: MORC2 (microrchidia family CW-type zinc finger 2, MORC2) is a newly identified chromatin remodeling protein that plays key roles in DNA-based biological processes including gene transcription and DNA damage repair. However, its functional role in breast cancer development and progression re-mains unknown. ALDH1A3 (aldehyde dehydrogenase 1 family member A3), a member of the aldehyde dehydrogenases (ALDH) superfamily, is a putative breast cancer stem cell marker, but its regulatory mechanism in breast cancer is poor-ly characterized. This study aimed to investigate the effects of knockdown of endogenous MORC2 on the expression levels of ALDH1A3 and the breast cancer stem-like phenotype in MCF-7 cells. Methods: Human breast cancer MCF-7 cells were infected with negative control short hairpin RNAs (shNC) and specific shRNAs targeting human MORC2 (shMORC2), followed by selection with puromycin to generate stable MORC2 gene knockdown cell lines. Western blot and real-time fluorescent quantitative polymerase chain reaction (RTFQ-PCR) were used to examine the protein and mRNA levels of ALDH1A3 in MCF-7 cells stably expressing shNC and shMORC2. Microsphere formation and fluo-rescence-activated cell sorting (FACS) assays were used to analyze the effects of knockdown of MORC2 on the breast cancer stem-like phenotype. Results: Western blot and RTFQ-PCR analyses revealed that the protein and mRNA levels of ALDH1A3 were significantly down-regulated in shMORC2 expressing cells as compared with shNC -transfected control cells. Moreover, mammosphere formation assay showed that knockdown of endogenous MORC2 in MCF-7 cells significantly reduced the ability of cells to form microspheres. Consistently, FACS assays demonstrated that shMORC2-transfected cells had a lower proportion of ALDH-positive stem cells as compared with shNC expressing cells. In contrast, knockdown of MORC2 did not significantly affect the CD44+CD24- stem cell population. Conclusion:MORC2 promotes a breast cancer stem-like phenotype through, at least in part, regulating ALDH1A3 expression.
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Objective To investigate the effect of super-selective intracoronary administration on acute myocardial in farction patients.Methods A total of 240 patients with ST-segment elevation myocardial infarction who received emergency percutaneous coronary intervention in our department from March 2012 to January 2014 were selected and divided into the intravenous drug administration group (n=77),the conventional intracoronary drug administration group (n=81) and the super-selective intracoronary drug administration group (n=82).Parameters,including the Thrombolysis in Myocardial Infarction (TIMI) classification,ST segment resolution after operation,peak values of creatine kinase MB (CK-MB) and troponin-I (cTn-I),left ventricular ejection fraction,left ventricular end-diastolic diameter (LVEDD),major adverse cardiovascular events and bleeding events,were compared between the groups.Results There were no significant differences in TIMI flow grade between the three groups (x2 =0.14,P=0.529).The percentage of patients with complete ST segment resolution after operation was higher in the super-selective intracoronary drug administration group than in the intravenous drug administration and conventional intracoronary drug administration groups (74.4％ vs.62.3％,61.7％,x2 =8.24,P＜0.05).Peak values of CK-MB and cTn-I were lower in the super-selective intracoronary drug administration group than in the other groups (P＜0.05).There were no significant differences in left ventricular ejection fraction and LVEDD between the three groups after operation,but left ventricular ejection fraction and the incidence of angina pectoris significantly improved in the super-selective intracoronary drug administration group than in the other groups after a three month follow-up (P＜0.05).There were no significant differences in target lesion revascularization,nonfatal myocardial infarction and druginduced thrombocytopenia between the three groups (P ＞ 0.05).Conclusions Super-selective intracoronary drug administration can significantly enhance cardiac function and alleviate angina pectoris in patients with acute myocardial infarction,and should be a recommended method.
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Objective To investigate the ultrasonic imaging features of thyroid follicular adenoma for conducting the correct diagnosis and differentiation diagnosis.Methods The clinical and imaging data in 64 cases of pathologically proven thyroid follicular adenoma were analyzed on the maximal diameter of tumor,nodularity number,high and low echogenicity,peripheral halo,echo hom-ogeneity,calcifications,and so on.The misdiagnosis causes were investigated.Results The mass was mainly solid or cystic-solid mixed echo.The ultrasonic imaging features of thyroid follicular adenoma were non-peripheral halo or thin wall halo,hyperecho or isoecho,internal macrocalcifications and peripheral calcifications,homogeneous echo structure.Conclusion The ultrasonographic examination can provide the better diagnosis and differentiation diagnosis on thyroid follicular carcinoma.
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Experimental research of injury on tumor tissue in vitro is conducted with homemade energy-controllable steep pulse device. With the comparison of histological assay results between treatment group and non-treatment group, basic phenomenon of electrochemical reaction and pathology reaction of tumor tissue during the experiment is observed. The results showed the irreversible breakdown penetrating effect of energy-controllable steep pulse on tumor cells and the feasibility of this therapy are also demonstrated. These results provide a consolidate theoretic and applicable basis for further study on mechanism and animal experiment in vivo.
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Female , Humans , Male , Middle Aged , Electric Stimulation Therapy , Methods , Electromagnetic Fields , In Vitro Techniques , Neoplasms , Pathology , TherapeuticsABSTRACT
Background and purpose:Rabs are members of Ras-related small GTPase superfamily. Rab27A is a unique member in the Rab family and has specific implications in human genetic diseases. We studied the potential role of Rab27A in proliferation, distribution of cell cycle, apoptosis and invasion of breast cancer cells and its mechanism(s). Methods:The eukaryotic expression vector containing Rab27A open reading frame (ORF) pcDNA3.1(+) - Rab27A was constructed and transfected into MDA-MB-231 breast cancer cells. Then we detected the changes in terms of cell growth, cell cycle distribution, apoptosis and in vitro invasion capability before and after transfection. We also applied RT-PCR to investigate the molecular basis.Results:① The expression of Rab27A was increased as invasive and metastatic ability increased in four human breast cancer cell lines. ② Overexpression of Rab27A can promote breast cancer cells to grow faster, increase the proportion of S phase cells, avoid apoptosis and invade in vitro. ③ Rab27A transfectants constitutively enhanced the expression of Cyclin D1, MMP-7 and MMP-9 in MDA-MB-231 cell lines, on the contrary, that of p16 were down-regulated constitutively. Reduced Rab27A expression by RNAi down-regulated the expression of Cyclin D1, MMP-7 and MMP-9, and up-regulated p16 expression.Conclusions:Rab27A can stimulate breast cancer cells to proliferate, increase the proportion of cells in S phase,avoid apoptosis and invade in vitro by regulating the expression of Cyclin D1, MMP-7, MMP-9 and p16.
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More and more studies indicate that there are many similarities such as pathophysiological process,gene expression,immune escape,angiogenesis and invasion characteristic between embryo implantation and neoplasm invasion and metastasis, which are taken for two "blackboxes" in medical field at present. Not only will cross studies between both sides promote respective subject development, but also become the breach to reveal life origin,developmental biology of neoplasm and embryo and intrinsic mechanisms of embryo implantation and neoplasm invasion and metastasis.
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AIM: To explore interaction and biological behaviou r changes of two kinds of cells-blastocysts and hepatocarcinoma cells in the same microenvi ronment. METHODS:The models of mouse blastocysts co-cultured wit h human hepatoca rcinoma cell lines were established, then biological behaviours and mutual effe c ts of the two kinds of cells in co-culture system were observed. RESULTS: Co mpared with control group, hepatocarcinoma cells with differently invasive and met astatic potential significantly enhanced the rates of blastocyst hatchment , at t achment and outgrowth(P0 05). The blastocyst ha tched and attached to hepatocarcinoma cells with differently invasive and metast atic p otential. Then, differential trophoblasts invaded hepatocarcinoma cells. The clear-cut interfaces were gradually formed between both sides. Hepatocarcinoma cells o n interface showed changes of growth direction and cell shapes and did not inv ade blastocysts. CONCLUSIONS: Hepatocarcinoma cells promoted bla stocyst develo pment. Blastocysts implanted and invaded hepatocarcinoma cells with differentl y i nvasive and metastatic potential in vitro, which indicate that blastocyst i mplan tation in vitro does not relate with the kinds and differential level of int erac tional cells and the low selectivity maybe relate with high adaptability of earl y life.