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@#Objective: To explore the genes that may be regulated by cell division cycle 25A (CDC25A) with gene chip technology, and to elucidate and verify that CDC25A has a regulatory effect on the expression of liver cancer related genes. Methods: CDC25A expression in human liver cancer HepG2 cells was silenced by siRNA interference technology and a nude mouse xenograft model of liver cancer was successfully constructed in our previous research. Affymetrix human gene expression profiling microarray was used to further screen differentially expressed genes (DEGs) after silencing CDC25A in liver cancer xenografts, and GO analysis and KEGG analysis were performed. Some of the DEGs were verified by qPCR. Results: The chip screened 188 DEGs in liver cancer xenograft tissues after CDC25A silence, including 78 up-regulated genes and 110 down-regulated genes. These DEGs mainly involved in cell proliferation, apoptosis, protein complex binding, extracellular space, etc., and associated with the changes in pathways such as focal adhesions and extracellular matrix (ECM) receptor interactions. qPCR showed that the expression of HIPK2 mRNA was up-regulated and the mRNA expressions of (microfibrillar-associated protein 5(MFAP5) and cyclin D1 (CCND1) were down-regulated, which were consistent with the results of microarray detection. Conclusion: Using human gene expression profiling chip, the DEGs in liver cancer xenograft tissues in nude mice after silencing CDC25Awere successfully screened, providing effective clues for exploring the effect of CDC25Aon the growth of liver cancer.
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AIM:To investigate the role of Krüppel-like factor 17(KLF17)in nude mouse xenograft model, and to explore the target genes regulated by KLF 17, the target gene functions and the signaling pathways involved.ME-THODS:The KLF17 was stably up-regulated in human lung adenocarcinoma A 549 cells and down-regulated in human lung adenocarcinoma H322 cells by lentiviral infection.BLAB/c nu/nu nude mice(n=11)were divided into KLF17 up-regual-tion group(n=5)and KLF17 down-regulation group(n=6).The right and left bodies of the nude mice were subcutane-ously injected with KLF17-up-/down-regulating cells and the counterpart empty vectors were used as control cells,respec-tively.The effects of KLF17 on the growth of the cell-derived xenografts in nude mice were analyzed.The mRNA and pro-tein expression levels of KLF17 in xenograft tumor tissues were analyzed by real-time PCR and immunohistochemical stai-ning,respectively.Transcriptome sequencing was used to explore the differentially expressed genes in the xenograft tumors derived from KLF17-up-regulating A549 cells,and the functions of the potential target genes were analyzed using the lung adenocarcinoma data from The Cancer Genome Atlas(TCGA)database.Gene Ontology and KEGG PATHWAY enrichment analyses were performed to analyze the functions of the differentially expressed genes and the involved signal pathways.RE-SULTS:The growth rate of KLF17-up-regulating A549 cell-derived xenograft tumors in the nude mice was significantly lower than that in empty control group(P<0.05),while the growth rate and the weight of KLF 17-down-regulating H322 cell-derived xenograft tumors in nude mice were significantly higher than those in empty control group(P<0.01 and P<0.05,respectively).In the A549 cell-derived xenograft tumor model,the KLF17 mRNA and protein were significantly in-creased in KLF17 up-regualtion group.The transcriptome sequencing showed the potential target genes regulated by KLF 17 were ras homolog family member V(RHOV)and coronin 1C(CORO1C).Ten-year cumulative survival time of the patients with lung adenocarcinoma from TCGA database was significantly different between high and low expression of RHOV and CORO1C at mRNA level.Increased expression levels of RHOV and CORO1C were correlated with short survival time in the patients with lung adnocarcinoma.The results of Gene Ontology and KEGG PATHWAY enrichment analyses indicated that the target genes(differentially expressed genes)regulated by KLF17 were related to the stimulation response,growth and adhesion of tumor cells,and participated in chemotaxis-,adhesion-and extracellular matrix receptor-related signaling path-ways.CONCLUSION:KLF17 inhibits the xenograft tumor growth in nude mice,and inhibits the oncogenes such as RHOV and CORO1C.The target genes regulated by KLF17 participate in the regulation of tumor adhesion-and growth-related sig-naling pathways.
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Objective To investigate up-regulation of lncRNA-AK058003 expression in SK-Hep1 hepatocellular carcinoma cells and its effect on the growth of human hepatocellular carcinoma xenograft tumor in nude mice.Methods The recombinant plasmid of lncRNA-AK058003 and empty plasmid were transferred into SK-Hep1 human hepatocellular carcinoma cell line by the method of slow virus transfection.The overexpression of lncRNA-AK058003 cell line was screened by neomycin.Overexpression of lncRNA-AK058003 in SK-Hep1 hepatocarcinoma cells was detected by quantitative PCR.SK-Hep1 hepatocellular carcinoma cells stably overexpressing lncRNA-AK058003 and SK-Hep1 hepatocellular carcinoma cells containing empty plasmids were injected subcutaneously into armpit of nude mice.The long and short diameters of the transplanted tumor were measured regularly to calculate the volume of the xenograft tumor.After 35 days of feeding we measure the weight of the xenograft tumor.Results The recombinant plasmid of lncRNA-AK058003 was successfully constructed and stably over expressed in hepatocellular carcinoma cells.The experimental results of subcutaneous tumor bearing nude mice showed that the volume(308.4 ± 439.4mm3),weight (0.464 ± 0.518g)and growth rate of the xenograft tumor in the over expression group were lower than that of the empty plasmid group(1410.0 ± 973.0mm3,1.363 ± 0.856g,P ＜ 0.05).Conclusion LncRNA-AK058003 has inhibitory effect on the proliferation of human hepatocellular carcinoma xenograft tumor in nude miee.
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Objective To investigate up-regulation of lncRNA-AK058003 expression in SK-Hep1 hepatocellular carcinoma cells and its effect on the growth of human hepatocellular carcinoma xenograft tumor in nude mice.Methods The recombinant plasmid of lncRNA-AK058003 and empty plasmid were transferred into SK-Hep1 human hepatocellular carcinoma cell line by the method of slow virus transfection.The overexpression of lncRNA-AK058003 cell line was screened by neomycin.Overexpression of lncRNA-AK058003 in SK-Hep1 hepatocarcinoma cells was detected by quantitative PCR.SK-Hep1 hepatocellular carcinoma cells stably overexpressing lncRNA-AK058003 and SK-Hep1 hepatocellular carcinoma cells containing empty plasmids were injected subcutaneously into armpit of nude mice.The long and short diameters of the transplanted tumor were measured regularly to calculate the volume of the xenograft tumor.After 35 days of feeding we measure the weight of the xenograft tumor.Results The recombinant plasmid of lncRNA-AK058003 was successfully constructed and stably over expressed in hepatocellular carcinoma cells.The experimental results of subcutaneous tumor bearing nude mice showed that the volume(308.4 ± 439.4mm3),weight (0.464 ± 0.518g)and growth rate of the xenograft tumor in the over expression group were lower than that of the empty plasmid group(1410.0 ± 973.0mm3,1.363 ± 0.856g,P ＜ 0.05).Conclusion LncRNA-AK058003 has inhibitory effect on the proliferation of human hepatocellular carcinoma xenograft tumor in nude miee.
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Objective To obtain a thyroid cancer cell line integrated with luciferase and fluorescence,and to establish a metastatic nude mouse model of papillary thyroid cancer monitored with in vivo imaging system. Methods Lentivirus carrying recombinant plasmid containing luciferase gene and mCherry gene infected high malignant papillary thyroid cancer cell line (BHP10-3SCmice). The stable thyroid cancer cell line (BHP10-3mluc) labeled with luciferase and mCherry selected by hygromycin, analyzed for fluorescence with fluorescence microscopy and bioluminescence with in vitro analysis and in vivo imaging. 0.25 ml(5×106/ml)BHP10-3mluc cell suspension were injected into the left thigh intramuscular tissue of 5-week-old nude mice to establish BALB/C nude mice metastatic tumor model. The growth and metastasis of the tumors were monitored weekly with in vivo imaging system. The nude mice were sacrificed on the 42th day and the tissues with metastatic tumors were analyzed by fluorescent imaging ex vivo. The ectopic implanted tumors and metastatic lesions were verified by tissue sections with Hematoxylin and Eosin staining. Results BHP10-3mluc cells showed similar growth characteristics to the original BHP10-3SCmice cells and stably expressed luciferase and mCherry. At the end of the first week after ectopic implantation,the xenograft tumors were found and in the 6th week,the tumors were found to metastasized to adjacent lymph nodes and lungs,which was consistent with the results of pathology.The growth and metastasis of tumors can be accurately monitored with in vivo imaging system. Conclusions A PTC cell line stably expressing bioluciferase and fluorescence was successfully established.The nude mouse model of PTC metastatic tumor generated by intramuscular inoculation of those cells can be well monitored with in vivo imaging system, which provides ideal models for researches on tumor growth, metastasis,and drug treatment.
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Objective To study the effect of PIM-1 gene silence by RNA interference (RNAi) on the growth of human prostate cancer xenograft tumor in nude mice. Methods The xenograft tumor model of human prostate cancer was established by injecting PC-3 cells in armpits of 12 nude mice. After modeling, the nude mice were randomly divided into three groups: interference plasmid group (injecting with RNAi recombinant plasmid), empty plasmid group and negative control group (liposome every), 4 mice in each group. Mice were injected every 2 days for 5 times. The tumor volumes of xenografts were measured during experiment, and the curve of tumor growth was drawn accordingly. The quality of tumor was measured, and the inhibitory rate of tumor was calculated at the end of the experiments. The expression levels of PIM-1, c-MYC mRNA and protein in xenograft tumors were detected by real-time PCR and Western blot assay, respectively. Furthermore, immunohistochemistry staining was used to verify the expression of PIM-1. Results The xenograft tumor model of human prostate cancer was established successfully. The volume of tumor was significantly decreased 6 days after the injection treatment in interference plasmid group than that of empty plasmid group and negative control group. The effect of suppressing tumor growth was remarkable. The expression levels of PIM-1 mRNA and protein were down-regulated significantly in interference plasmid group than those of other two groups. The immunohistochemical staining of PIM-1 showed the same changes. There was no significant difference in c-MYC protein level between the three groups. But interestingly, the c-MYC mRNA level was significantly decreased in interference plasmid group than that of other two groups. Conclusion The silence of PIM-1 gene by RNAi recombinant plasmid can result a significant growth suppression of the human prostate cancer xenograft tumors in nude mice. The expression of c-MYC gene is down-regulated at translation level in the therapeutic group concomitantly. PIM-1 may be a promising target of gene therapy for prostate cancer.
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Objective Renal cell carcinoma ( RCC) is a common renal malignancy, which is resistant to nearly all chemo-therapeutics and radiotherapy.Wnt signaling plays an important role in the tumorigenesis and cell proliferation and apoptosis of RCC. This study was to explore the inhibiting effect of 15-oxospiramilactone NC043, a new Wnt molecule inhibiter, on the xenograft growth of human renal carcinoma (ACHN) cells in nude mice. Methods ACHN cells (1 ×107) were suspended in 100μL PBS and injec-ted subcutaneously into the right side of the posterior flank of female BALB/c athymic nude mice to establish a xenograft model.The nude mice bearing ACHN cells were randomly divided into three groups, negative control, low-dose medication, and high-dose medica-tion, treated by daily intraperitoneal injection of 3%DMSO, NC043 at 45μg/kg, and NC043 at 90μg/kg, respectively, for 15 days. At 16 days, all the mice were killed, the body weight and tumor volume obtained, and the expressions of ki67, TCF4 and β-catenin determined by immunohistochemistry. Results NC043 significantly inhibited the growth of the xenograft tumor, with an inhibition rate of 36.4%in the 45 ug/kg group and 56.4% in 90 μg/kg group.The expressions of ki67, TCF4, andβ-catenin were markedly down-regu-lated in a dose-dependent manner ( P <0.01 ) . Conclusion NC043 can effectively suppress the growth of ACHN cells in the xeno-graft tumor and reduce the expression of Wnt-related proteins, andtherefore is a potential compound for the treatment of renal cell carcinoma.
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Patient-derived xenograft models (PDXs) of lung cancer are obtained by directly implanting lung cancer tissue fragments in-to immunocompromised mice. The implanted tumor fragments can be proliferated and passaged in these mice models. The PDXs maintain the tumor microenvironment, histological and pathological characteristics, and tumor biomarkers of the original tumor tis-sues. The PDX also offers an ideal mice model that mimics the human tumor microenvironment. These models have important roles in the pre-clinical evaluation of cancer, the assessment of anti-tumor drug responses, and the analysis of biomarkers. These models also present a new direction for the individualized therapy of lung cancer patients.
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Objective:To investigate the inhibitory effect and its possible molecular mechanisms of MicroRNA-34a(miR-34a) on the human nasopharyngeal carcinoma CNE-2 cell line subcutaneous xenograft tumor in nude mice.Methods: The human nasopharyngeal carcinoma CNE-2 cell line was cultured in vitro.miR-34a and Scrambled miRNA recombinant plasmids were successfully established and stably transfected into CNE-2 cells.Fifteen six-week-old male nude mice were divided randomly into three groups:miR-34a group(5 mice) ,Scrambled miRNA group(5 mice) ,Blank control group(5 mice).Different CNE-2 cells were subcuta-neously injected on the back near right lower limb.Tumor volumes were examined every 7 days.Mice were executed on the 35 days,and the eventual average tumor volumes and weights were examined.Total RNA and protein were isolated from tumors,and the expression of miR-34a,CDK6,and Bcl-2 mRNA and protein were determined by qRT-PCR and western blot,respectively.Results: The relative expressions of miR-34a was significantly up-regulated in miR-34a transfected group compared to Scrambled miRNA transfected group (P (849.62±101.32) mm3 ,respectively,and the eventual average tumor weights in miR-34a group,Scrambled miRNA group and blank control group were(0.81±0.13)g,(1.47±0.21)g and(1.58±0.37)g,respectively.Both the eventual average tumor volumes and weights in miR-34a group were lower compared to the other two groups(P<0.05).qRT-PCR results revealed that the expression of miR-34a in miR-34a transfected group was significantly higher than in the other two groups,while the mRNA and protein expression of CDK6 and Bcl-2 were lower than the other two groups ( P<0.05 ) .Conclusion: miR-34a may inhibit the growth of human nasopharyngeal carcinoma CNE-2 cell line subcutaneous xenograft tumor in nude mice by down-regulating CDK6 and Bcl-2.
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Objective To explore the effects of up-and down-regulation of Cox-2 expression on the growth and radiation sensitivity of human esophageal cancer EC9706 xenograft in nude mice.Methods Cox-2 specific siRNA and Cox-2 gene eukaryotic expression vector were constructed and transfected to esophageal cancer cells EC9706, and the stable transfected cell lines were obtained by the method of G418 screening.The expressions of Cox-2 mRNA and its protein were detected by RT-PCR and Western blot, respectively.The inhibitory effects of Cox-2 regulation combined with X-ray irradiation on cancer cell growth were detected by the nude mouse xenograft assay.Results Cox-2 gene expression was significantly decreased in the Cox-2 down-regulated group and increased in the Cox-2 up-regulated group.Compared with the control group without gene transfer, the average volumes of EC9706 xenograft tumor in the Cox-2 up-and down-regulated group significantly decreased (F =34.26, P ＜ 0.05) and increased (F =26.38, P ＜ 0.05) , respectively.After 20 Gy X-ray irradiation, the average volume of xenograft was significantly reduced in the Cox-2 down-regulated group (F =16.35, P ＜ 0.05) , but it had no significantly changes in the Cox-2 up-regulated group.Conclusions Down-regulation of Cox-2 expression inhibits the growth of human esophageal cancer EC9706 xenograft in a nude mice and increases cell radiation sensitivity, but upregulation of Cox-2 expression makes tumor cells to become radioresistant.
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Aim To examine the inhibitory effect of re-combinant cardiac troponin fusion protein composed of subunit I and artificial peptide which was called CIS on tumor growth. Methods The CIS ’ s effect on the growth of human umbilical vein endothelial cells ( HU-VEC) was examined using MTT assay in vitro. Chick chorioallantoic membrane model was applied to study the alteration of angiogenesis treated with purified re-combinant CIS protein. The effect of tumor growth trea-ted with CIS was observed using several in vivo mice xenograft models. Results There was a statistically significant reduction in HUVEC cell proliferative rate when the cells were treated with purified CIS fusion protein, which was also shown in a dose-dependent manner. A decreased amount of new blood vessel for-mation ( angiogenesis) on chick embryo chorioallantoic membranes was observed in recombinant CIS protein treated group compared to the untreated control group. A significant inhibition of tumor growth rate was a-chieved in CIS treated mice compared to CIS untreated control mice in 6 different mouse xenograft models. Conclusions The fusion protein CIS shows the inhibi-tory effect on the tumor growth in our in vivo mouse models, and such inhibition could be mediated by the mechanism of CIS’ s effect on the decrease of HUVEC cell proliferation and further the reduction of angiogen-esis in tumor tissues. This work could provide the foundation for the in-depth investigations on the phar-maceutical application of CIS targeting anti-tumor ther-apy.
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Objective Diallyl disulfide ( DADS) has achieved remarkable effects in treatment and research of diverserfied cancers.The article was to explore the effects and the mechanism of DADS on the xenograft growth of human small cell lung cancer ( SCLC) cells in nude mice . Methods A total of 25 nude mice were selected to establish xenograft model of NCI-H446 human SCLC cells.The nude mice bearing with SCLC H446 were divided into 5 groups by random selection:positive control group(DDP 66 mg/kg), negative control group(physiological saline), 20 mg/kg DADS group, 60 mg/kg DADS group and 180 mg/kg DADS group, which is 40.6%, 53.1%and 66.4%, respectively.The growth of xenograft tumor in mice was observed after being treated with differ-ent concentrations of DADS .The morphological changes of the tumors were examined under light microscopy .Phase distribution and apoptosis of xenograft cells were analyzed by flow cytometry ( FCM) . Results The growth of xenograft tumor were inhibited signifi-cantly by DADS, resulting in decreased cell density and cellular atypia .Moreover, xenograft cell cycle was blocked in G 2/M and cell apoptosis rate was enhanced . Conclusion DADS can significantly inhibit the growth of NCI-H446 cells and lead to apoptosis .
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Objective To investigate the method for effective establishment of nude rat tumor xenograft model of human lung cancer cells A549 in order to provide the experimental basis for tumor-related interventional research in vivo. Methods A549 cell lines were subcutaneously transplanted in nude rats, then single-cell suspension or tumor tissue block were prepared when the tumor lesion was established. The single-cell suspension and tumor tissue block were transplanted into subcutaneous tissue behind ear in rats. The tumor formation rate, growth situation and cell cycle of primary xenograft tumor group, the secondary single-cell suspension group and the secondary tumor block group were evaluated. The results were analyzed. Results The tumor formation rate of the secondary tumor block group was significantly higher than that of the other two groups. The tumor cells quickly proliferated with less tumor variation. Tumor cell cycle analysis indicated that G2/M ratio of the secondary tumor block group was remarkably higher than that of the other two groups. Conclusion Transplantation with tumor tissue block can significantly increase the tumor formation rate of human lung cancer cells A549 in experimental rats. This technique is an effective method for the establishment of nude rat tumor xenograft model.
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Background and purpose:Thalidomide can enhance the radiation sensitivity on tumor effectively, but the mechanism of radiosensitization is still unclear. The present study aimed to investigate whether thalidomide could enhance the radiation sensitivity on colon cancer transplanted tumor of mouse, and to investigate the underlying mechanism. Methods: We established the model of colon26 colonic carcinoma, and the mice were divided into 4 groups:Control group, the thalidomide group, the radiotherapy group and thalidomide+radiotherapy group. From the day of treatment, tumors were measured every other day. Then, the xenograft tumor growth curve was depicted. Tumor volumes were measured in different treatment groups, then, the inhibitory rates of tumor growth were calcutated. Using immunohistochemical method in to detect the expression of microvessel density (MVD) in tumor tissue. Results:The mean tumor volumes at day 22 were (4.97±1.20)cm3 (control group), (2.90±0.92)cm3 (T group), (2.66±0.88)cm3 (R group), and (1.89±0.76)cm3 (T+R group). The tumor inhibition rate in the combination group (61.9%) was signiifcantly higher than the other groups (41.7%, 46.5%, P<0.05). The radiotherapy sensitization enhancement ratio of the combined treatment group was 2.27 times than in the radiotherapy group. Thalidomide combined with radiation therapy can significantly inhibit microvessel density of tumor:The decreasing MVD of T+R group, T group and R group were respectively 46.8%, 40.7%and 37.7%, and there was statistical significance between T+R group and T group (P<0.05 ), so as between T+R group and R group. It could be found more necrotic cells in tumor of group, and there was statistical signiifcance between T+R group and control group (P<0.05). Conclusion:Thalidomide can enhance the radiosensitivity mice of colonic carcinoma, and its mechanism may be related to the inhibition of tumor angiogenesis related.
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Objective To study the impact of compound zhe-bei granule and adriamycin on p53 gene expression in the P388 xenograft tumor.Methods The tumor xenografts model was established by injecting the mouse lymphocytic leukemia cells(P388) in the subcutis of anterior axillary of Kunming mice,and then was treated with CZBG by intragastric administration and different doses of adriamycin by intraperitoneal injection(i.p.).After the end of the experiment,tumor was striped completely,and the expression of p53 gene in xenograft tumor of each group was detected by fluorescence quantitative polymerase chain reaction,and the relative quantification of p53 gene of each group was computed using 2-??Ct method.Results Comparing the 2-??Ct values of p53 gene relative expression of each group,no statistical significance was found(F=0.56,P=0.7557).And the relative expression value of p53 gene of CZBG joint high-dose ADM group was higher,while the relative expression value of CZBG joint low-dose ADM group was lower.Conclusion Combined use of CZBG and ADM is able to raise the expression of p53 tumor suppressor gene in the P388 xenograft tumor.
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Objective To study the inhibitory effect and its mechanism of sodium butyrate on human laryngeal carcinoma in nude mice. Methods Human laryngeal carcinoma cell line Hep-2 was seeded in the subcutaneous layer of 12 nude mice to built laryngeal carcinoma xenograft model. Then they were randomly and equally divided into 2 groups. Sodium butyrate was given in experimental group while phosphatic-buffered saline (PBS) was used in control group for 4 weeks. Tumor size and body weight of the mice were measured at regular time-intervals. The tumor,heart,liver,lungs,spleen and kidneys were removed at the end of treatment. Tumor sections were examined by electronic microscopy. TUNEL method and immunohistochemical S-P method were used for detecting the expression of Ki-67 nuclear antigen and survivin protein. The heart,liver,lung,spleen and kidney sections were examined after HE staining for assessment of toxicity. Results In experimental group,the volume of tumors was reduced,the area of necrosis in tumors was widened,the apoptotic rate was increased obviously and the expression level of Ki-67 nuclear antigen and survivin protein was decreased as compared with control group. During treatment,all the nude mice grew well and there were no toxic reactions. At the end of treatment,there were no abnormal changes in heart,liver,lung,spleen and kidney sections examined under light microscope. Conclusion Sodium butyrate can significantly inhibit the growth of human laryngeal carcinoma xenograft in nude mice. Its mechanism may be related to the apoptosis in tumor cells by inhibiting the expression of survivin protein and Ki-67 nuclear antigen. There is no toxicity to heart,liver,lungs,spleen and kidneys at a treatment dose of sodium butyrate.
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Objective To establish the animal model bearing BRCA1-overexpressing breast tumor in athymic mouse so as to investigate the effects of lovastatin (LOV) on the growth of the xenograft tumor and understand its mechanism. Methods After amplification and identification, pcDNA3-beta-HA-hsBRCA1 plasmid was transfected into MCF-7 cells by liposome transfection to deliver a high level of BRCA1 gene expression examined with RT-PCR and Western blotting (named MCF-7 BRCA1 ). Twenty athymic mouse models of BRCA1-overexpressing xenograft tumor were established by respectively inoculating 2?10 6 MCF-7 cells and MCF-7 BRCA1 cells to right anterior part of the back. Four weeks later, lovastatin at the dose of 50 mg/kg was injected around the tumor for 10 d. Then the tumor volume was measured, the histopathological changes of xenograft tumor were observed with electron microscope by HE staining, the expressions of cyclinD1, CDK4 mRNA and protein were detected by RT-PCR and Western blotting. Results The athymic mouse model of xenograft breast tumor was successfully established after MCF-7 cells were transfected with pcDNA3-beta-HA-hsBRCA1 plasmids. The incidence rate of xenografted breast tumor in athymic mouse was 100%. Routine HE staining of paraffin-embedded section proved that the tumor was a mammary carcinoma in nature. Treated with lovastatin for 10 d, the tumor volume of mouse implanted with MCF-7 cells was large (0.48 cm 3 ) and there was a slight change in expressions of cyclinD1, CDK4 mRNA and protein, while the tumor volume of mouse inoculating MCF-7 BRCA1 cells was small (0.21 cm 3 ) and the expressions of cyclinD1, CDK4 mRNA and protein obviously descended. The two groups showed diminution in cancer cells and increase of necrosis, more significant in those mice inoculating MCF-7 BRCA1 cells. Conclusion Lovastatin could resist the proliferation of BRCA1-overexpressing breast tumor, which may relate to the decrease of the cyclinD1, CDK4 mRNA and protein expressions.