ABSTRACT
Os exossomos são vesículas extracelulares originadas por brotamento interno da membrana de endossomos tardios que representam uma eficiente forma de comunicação intercelular. Devido às suas múltiplas funções biológicas, o foco de alguns estudos atuais tem se concentrado na análise do seu papel no desenvolvimento do câncer, progressão da doença, invasão, angiogênese e formação de metástases tumorais. Nesta perspectiva, o presente estudo objetivou caracterizar os exossomos secretados por duas linhagens celulares de carcinomas epidermoide oral (CEO) (SCC-15 e HSC-3) e avaliar seus efeitos sobre uma linhagem de células endoteliais (HUVEC), em relação à sua capacidade de formação de estruturas vasculares, taxas de migração, proliferação e índices de apoptose/necrose. Médias significativamente maiores de células com potencial invasivo (p<0,0001) e migratório (p<0,0001) foram observadas para a linhagem HSC-3. Ultraestruturalmente, verificou-se que as partículas derivadas da linhagem SCC-15 exibiram morfologia arredondada e diâmetro inferior a 150 nm. Nenhuma diferença estatisticamente significativa foi revelada entre as linhagens celulares estudadas, considerando a quantificação de nanovesículas (p=0,2252) e tamanho exossomal (p=0,1765). Por imunofluorescência indireta, identificou-se que 22,15% dos exossomos secretados pelas células SCC-15 e 18,37% dos exossomos derivados da linhagem HSC-3 expressaram o anticorpo anti-Anexina. No que se refere aos ensaios funcionais com as HUVECs, o tratamento com exossomos derivados da linhagem SCC-15 induziu um aumento significativo da capacidade de formação de estruturas vasculares (p<0,0001), potencial migratório (p=0,0016) e taxa de apoptose (p<0,0001), enquanto que uma redução da proliferação celular foi apontada (p=0,0030). Por outro lado, o tratamento com exossomos secretados pela linhagem HSC-3 promoveu uma redução significativa da formação tubular (p<0,0001), motilidade (p=0,0042) e proliferação celular (p=0,0010), ao passo que nenhuma diferença estatisticamente significativa foi observada no índice apoptótico (p=0,3004). Os resultados do presente estudo indicaram a participação dos exossomos derivados de linhagens de CEO no processo de angiogênese tumoral, onde as células SCC-15 exibiram forte resposta proangiogênica e a linhagem HSC-3 demonstrou efeito antiangiogênico (AU).
Exosome are extracellular microvesicles originated by inward budding of late endosomal membrane that represent an efficient form of intercellular communication. Because of its multiple biological functions, the focus of some recent studies has concentrated on the analysis of its role in cancer development, disease progression, invasion, angiogenesis and tumor metastasis formation. In this perspective, the present study aimed to characterize the secreted exosomes by two cell lines of oral squamous cell carcinomas (OSCC) (SCC-15 and HSC-3) and to evaluate its effects on a cell line of endothelial cells (HUVEC), in relation to their ability to form vascular structures, rates of migration, proliferation, and apoptosis / necrosis indices. Significantly higher means of cells with invasive (p<0.0001) and migratory potential (p = <0.0001) were observed for the HSC-3 cell line. Ultrastructurally, it was found that particles derived from the SCC-15 cell line exhibited a rounded morphology and diameter of less than 150 nm. No statistically significant difference was revealed between the studied cell lines, considering the nanovesicles quantization (p=0.2252) and exossomal size (p=0.1765). By indirect immunofluorescence, it was found that 22.15% of exosomes secreted by SCC-15 cells and 18.37% of exosomes derived from HSC-3 cells expressed anti-annexin antibody. With regard to the functional tests with HUVECs, treatment with exosomes derived from SCC-15 cell line induced a significant increase in their capacity of formation of vascular structures (p = <0.0001), migratory potential (p=0.0016) and rate of apoptosis (p<0.0001), while a decrease in cell proliferation was noted (p = 0.0030). On the other hand, the treatment with exosomes secreted by HSC-3 cell line produced a significant reduction in tubule formation (p<0.0001), motility (p = 0.0042) and cell proliferation (p=0.0010), whereas no statistically significant difference was observed in the apoptotic index (p=0.3004). The results of this study indicated the involvement of exosomes derived from OSCC cell lines in tumor angiogenesis process, in which the SCC-15 cells exhibited strong proangiogenic response and HSC-3 cell line showed antiangiogenic effect (AU).
Subject(s)
Tumor Cells, Cultured , Endothelial Cells , Exosomes , Extracellular Vesicles , Squamous Cell Carcinoma of Head and Neck/pathology , Neovascularization, Pathologic/pathology , In Vitro Techniques , Immunohistochemistry/methods , Microscopy, Electron/methods , Statistics, Nonparametric , Disease Progression , Ki-67 Antigen , Angiogenesis InhibitorsABSTRACT
Background and purpose:As the second general platinum antineoplastic agent, carboplatin has been applied in treating more and more malignant tumors clinically. But it has severe bone marrow suppression when applied in large doses. The purpose of this research was to explore the influence of carboplatin of fractional dose, combined with X ray,on the immunity of Lewis lung cancer in mice. Methods:The model of tumor-bearing mice was induced by injecting Lewis lung cancer cells into the right infra-axillary dermis. In cases given the same total dose, the tumor growth and the immune suppression effect of carboplatin of single dose or of fractional dose , combined with X ray radiation, on the mouse with Lewis lung cancer were observed. Results:The concentration of IL-10 and TNF-? in serum,the spleen exponent were respectively(144.9?48.4)ng/ml,(194.63?64.4)ng/ml,(12.07?2.2)mg/ g in the control group;(279.0?46.9)ng/ml,(71.5?8.4)ng/ml,(5.52?1.31)mg/g in carboplatin of single dose with X ray radiation group, which ,compared with the control group, can dramatically increase the concentration of IL-10,decrease the concentration of TNF-? in the serum ,and dramatically decrease the spleen exponent(P
ABSTRACT
Background and purpose:The theory of cancer stem cell offers us a new thought about tumors, more and more kinds of cancer stem cell were isolated and indentif ied from corresponding cancer tissue. Our aim was to investigate the content of side population cells in SW480 human colorectal cancer ce11 line and to enrich cancer stem- like cells in SW480 through serum-free medium (SFM) culture. Methods:The percentage of side population cells in human colorectal cancer cell line SW480 was detected with ? ow cytometry. SW480 cell line was cultivated in serum- free medium(SFM) supplemented with growth factors and the cancer stem-like cells reforming into ? oating spheres were isolated. The isolated cancer stem-like cells were identifi ed by limited-dilution assay, differentiation assay, self- renewal assay, and alternative cultivation assay. Results:The percentage of SP cells was 1.2% in SW480,In the absence of serum, a minority (0.54%-0.62%) of cancer stem-like cells in SW480 cells survived, proliferated and formed into the suspended tumor cell spheres. SW480 cancer stem-like cells possessed proliferative, self-renewal and differentiation potential, which were responsible for the ? oating tumor clone. Serum addition into SFM resulted in the proliferation of cancer stem-like cells; after several generations and alternated cultivation in SSM and SFM, cancer stem-like cells maintained their characteristics. Conclusions:SW480 cell line contains a tiny minority of SP cells with stem cell properties.The cancer stem-like cells in SW480 line can be maintained in SFM using a floating culture method.
ABSTRACT
Background and purpose:Arsenic trioxide,verified as a breakthrough in the management of acute promyelocytic leukemia,has been applied to a variety of solid tumors.Gall bladder carcinoma,lacking specific clinical manifestations,is usually diagnosed at advanced stages of the diseases and few cases can be resected by operation.Chemotherapy has not shown significant activity in gall bladder carcinoma.This study was to investigate the biological effect of As2O3 on the growth of human gall bladder carcinoma cell and its mechanism.Methods:GBC cells were cultured with different concentrations of As2O3,the proliferative activity of the cells was detected by MTT methods,and the cell cycle status was carried out by flow cytometry(FCM).Western blot and RT-PCR were performed to analyse the expression of cyclin D1,D2,D3,CDK4 and CDK6.GBC cells were transient transfected with cyclin D1 promoter construct pGL3 and then treated by different doses of As2O3.The luciferase activity was measured.Results:The treatment of As2O3 in gall bladder carcinoma cells could inhibit the growth of cells in a time and dose dependent manner,make cells arrest in G1 phase and down regulate the expression of cyclin D1.In addition,the activity of cyclin D1 promoter was down-regulated by As2O3 in a dose-dependent manner and decreased about 70 percent when treated with 4 ?mol/L As2O3.Conclusions:As2O3 can significantly inhibit the growth of human gall bladder carcinoma cells as well as down-regulate the expression of cyclin D1 in vitro.
ABSTRACT
Background and purpose:Overexpression of human telomerase reverse transcriptase(hTERT)plays a critical role in the process of immortalization of tumor cells.This study aims to investigate siRNA's effects on endogenous hTERT mRNA level and growth of breast cancer cells by targeting hTERT with its specific siRNA.The ultimate goal was to further elaborate the possible mechanism of immortalization in breast cancer cells.Methods:Real-Time RT-PCR was used to determine the hTERT transcripts in various breast cancer cells.hTERT siRNA was transfected into MCF7 cells with lipofectamine 2000.Cell growth was illustrated by growth curve,and cells apoptosis percentage was measured with Flow Cytometry(FACS).The relative expression levels of immortalization-related genes were evaluated with Real-Time RT-PCR.Results:Overexpressions of hTERT were demonstrated in all tested breast cancer cell lines.The inhibitory effects of hTERT siRNA were shown on both hTERT mRNA levels and cell growth from day 4 post transfection.Apoptosis was induced by hTERT siRNA as well.Certain immortalization-related genes were reduced by more than 50%,such as RAC1,PCYT2,FDFT1 and ATP5G2.Conclusions:hTERT siRNA specifically inhibited hTERT at mRNA level as well as cell growth.The apoptosis and downregulation of immortalization-related genes due to hTERT siRNA was demonstrated.
ABSTRACT
Background and purpose:Micro-environmental hypoxia is a common phenomenon in most human solid tumors,and this investigation is done to observe the expression of HIF-1? and chemo-resistance-associated genes in human colon cancer cell line under hypoxic micro-environment in vitro,and study the influence of micro-environmental hypoxia on chemo-resistance and the possible mechanisms in human colon cancer.Methods:Human colon cancer cell line SW620 was cultured under hypoxia for 12,24,48 hr,with normoxia as control.Then the expression of HIF-1? and chemo-resistance-associated genes mdr1/P-Gp、LRP were investigated by RT-PCR and western-blot.Results:With prolongation of the hypoxic time,the mRNA expressions of HIF-1? and LRP remained at the same level,but the mRNA expressions of mdr1 showed a time-dependent increase(P
ABSTRACT
Background and purpose:The incidence of hepatoma is high. The outcome of treatment on hepatoma is poor.So we investigated the effect and mechanism of a selective cyclooxygenase-2 inhibitor celecoxib on the proliferation and apoptosis of SMMC-7721 hepatoma cell line. Methods:MTT assay was used to study the inhibitive effect of celecoxib on the growth of SMMC-7721 hepatoma cell. The effect of celecoxib on cell cycle and apoptosis on cells was studied by flow cytometry(FCM).Transmission electron microscopy (TEM) was used to display the morphological change of the SMMC-7721 hepatoma cell . The biochemical character of apoptosis was viewed on the agarose gel electrophoresis.The expression of bax gene and bcl-2 gene were measured by immunohistochemistry.Results:The SMMC-7721 cells were cultured in media that contained 25,50,75,100 ?mol/L celecoxib,by means of MTT, the inhibition rate was(15?3)%,(34.6?2.4)%,56.8?1.0)%,(86.2?0.4)% respectively after 24 hours; but the inhibition rate was (33.4?0.7)%,(66.7?1.8)%,(76.1?2.4)%,(97.3?0.8)% respectively after 48 hours(P
ABSTRACT
Background and purpose:HIF-1? (Hypoxia-inducible factor-1?) is an important transcription factor under hypoxia condition. It plays the role of dominating the expressions of correlative genes. It also promotes tumor deterioration, tumor metastasis and tumor invasion. The molecular role of HIF-1? has been intensively studied in cancer basic research. This article is to investigate the expression of HIF-1? under hypoxic and reoxygenation induced by CoCl_ 2 and the impact of hypoxia-inducible transcription factor-1? on human ovarian carcinoma cell line HO-8910PM. Methods:Semi quantitative reverse transcription-polymerase chain reaction (RT-PCR) is performed to detect the expression of HIF-1? mRNA in human ovarian carcinoma cell HO-8910PM exposed during the phase of hypoxia and reoxygenation. The relations of the quantity-efficiency and the time-efficiency were analyzed. The effects of HIF-1? gene on the proliferation, invasion and adhesion of HO-8910PM cell were estimated by either MTT, Boyden cell or cell adhesion tests.Results:There was endogenous expression of HIF-1? in human ovarian carcinoma cell line HO-8910PM. RT-PCR show that over-expression of HIF-1? mRNA could be measured under hypoxia induced by CoCl_ 2 (P
ABSTRACT
Background and purpose:To investigate the induction of apoptosis by epigallocatechin-3-gallate(EGCG) in xenograft nude mice with human gastric cancer cells and its molecular mechanism. Methods:Human gastric cancer cells were planted into nude mice in order to establish the cancer model, the different dosages of EGCG were injected intraperitoneally in the nude mice. After treatment, flow cytometry (FCM) was used to detect the apoptosis of implanted tumor cells. Immunohistochemical staining was used to detect the expression of apoptosis-related genes like Bal-2 and Bax in implanted tumor.Results:EGCG significantly inhibited tumor growth after being injecting intraperitoneally in the nude mice. The apoptotic cells in implanted tumor could be detected by flow cytometry with PI staining. The expressions of Bax、Caspase-3 were upregulated and Bcl-2 expression was downregulated in implanted tumor.Conclusions:EGCG could significantly inhibit tumor growth in xenograft nude mice with human gastric cancer cells through inducing apoptosis. The down-regulation of Bcl-2 expression and up-regulation of Bax expression observed could result in the activation of Caspase-3, the pathway might account for the induction of apoptosis.
ABSTRACT
BACKGROUND: Ginsenosides, the extract of Panax ginseng, exert various pharmacological effects such as anticancer activity by the mechanism that is not yet defined. In this study, we proposed that the anticancer effect of ginsenoside Rb1 is related to tumor cell apoptosis and ginsenoside Rb1 induces the tumor cell apoptosis via the nitric oxide (NO) production. METHODS: Rat C6 glioma cells were activated by treating with lipopolysaccharide (LPS), interferon (IFN)-gamma , and tumor necrosis factor (TNF)-alpha on the culture medium to investigate the effects of ginsenoside Rb1. RESULTS: Compared with C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha, C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha/ginsenoside Rb1 showed marked increase in the NO production and apoptosis. Ginsenoside Rb1 induces the NO production in C6 glioma cells in dose-dependent manner. When C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha/ginsenoside Rb1 were incubated with the specific inhibitor of iNOS, S-Methyl-2-thiopseudoureasulfate (SMT), both NO production and apoptosis in C6 glioma cells was significantly decreased. Ginsenoside Rb1 induced the expression of iNOS mRNA and iNOS protein in C6 glioma cells. CONCLUSIONS: These results suggest that the induction of iNOS expression and subsequent
Subject(s)
Animals , Rats , Apoptosis , Ginsenosides , Glioma , Interferons , Nitric Oxide Synthase , Nitric Oxide , Panax , RNA, Messenger , Tumor Cells, Cultured , Tumor Necrosis Factor-alphaABSTRACT
Purpose:To study the difference in gene expression profile between HCC cell strains with high and low metastatic potential.Methods:The gene expression profile of high and low metastatic HCC cell strains were analyzed by cDNA microarray, and genes with differential expression were further verified by RT PCR.Results:384 differentially expressed genes were detected between high and low metastatic HCC strains, making up 32% of the total genes studied. RT PCR analysis on 4 genes chosen demonstrated the same results as those revealed by the array technique.Conclusions:Obvious difference in gene expression patterns was observed between high and low metastatic HCC cell strains, chromosome 8p may contain metastasis promote and inhibitory genes.
ABSTRACT
Purpose:To explore effects of dexamethasone and vincristine on apoptosis and activation of NF ?B of HL60 n cells induced by cytosine arabinoside (Ara C). Methods:Apoptosis induced by Ara C in HL60 n cells was analysed by Tunel and DNA electrophoresis. The DNA binding activation of NF ?B of HL60 n cells was determined by electrophoretic mobility shift assay(EMSA).Results:The apoptosis and activation of NF ?B of HL60 n cells could be induced by Ara C. Dexamethasone 1?mol/L and vincristine 0.1?mol/L increased significantly the apoptosis induced by Ara C (increased by 39.1% and 59.2%, P
ABSTRACT
Purpose:The objective of the study is to investigate the pattern of apoptosis and to explore the effect of Fas/FasL on the process of apoptosis induced by daunorubicin (DNR) on human myeloid leukemia cell line HL 60.Methods:The effect on apoptosis and the expression of Fas and FasL antigen induced by DNR on cell line HL 60 were measured by fluorescence microscope ,DNA electrophoresis and flow cytometry analysis.Results:DNR could induce typical apoptosis of HL 60 cells with the DNR plating concentration at 0.1,1 ?g/ml after 6 hours. Morphological changes such as apoptosis bodies, chromatic condensation and cytoplasm budding were observed by fluorescence microscope. Sub G 1 peaks was found by flow cytometry. HL 60 cell apoptosis rate reached a peak at 24 hours. Sub G 1 peaks were not found by flow cytometry with the DNR plating concentration at 10 ?g/ml after 6 hours. DNR could upregulate the expression of Fas and FasL of HL 60 cells.Conclusions:Apoptosis induced by DNR is one of the primary mechanisms in chemotherapy. Fas/FasL system participate in the apoptosis induced by DNR .
ABSTRACT
Background and purpose:Wuxing soup is popular for it's anti-cancer effect in folk medicine and deserved to be further studied by modern scientific methods.This research aimed to explore its anti-cancer effect and to study the influence on the immunity of melanoma in mice. Methods :Inhibition of different ingredients and concentrations of Wuxing soup on the growth of the mouse melanoma B16 cells was detected by MTT in vitro.Animal experiment was performed to determine its anti-cancer effect in vivo.C57/BL6 mice were randomly divided into three groups after vaccination of B16 cell,and then given intragastrically with different soups for 25 days.All mice were killed on day 26 after inoculation.The weight of tumors were recorded.The anti-tumor immune function was measured by T lymphocyte transforming assay and NK killing assay.The different effect of different ingredients was also observed. Results :Our result showed that different ingredients soup exerted different inhibition on B16 cell growth and Wuxing soup was the strongest one of all and in dose-dependent manner in vitro.The animal experiment indicated that different ingredients soup has different inhibition on melanoma,the soup-treated mouse display improved T lymphocyte transforming assay and NK killing ability.Among the different soups,Wuxing soup showed the strongest anti-cancer effect and immune enhancement. Conclusions :Wuxing soup is an effective anti-cancer agent in melanoma mice and can enhance the immunity of the mice with melanoma.
ABSTRACT
Background and purpose:Epithelial-mesenchymal transitions(EMTs) occur as key steps during embryonic morphogenesis,and are now implicated in the progression of primary tumors towards metastases.We have found that the transcription factor Twist,a master regulator of EMT,was expressed markedly in human lung carcinoma cell line(A549).This study is to investigate the effects of short hairpin RNA(shRNA) targeting Twist on EMT and invasion ability of A549 cells in vitro.Methods:RNA interference plasmid that can express short hairpin RNA(shRNA) targeting Twist(positive RNAi plasmid) or express shRNA that does not match any known human coding mRNA(negative RNAi plasmid)was designed,constructed,and transfected into A549 cells line.Positive RNAi A549 cells(Pi group) expressing Twist suppressed or negative RNAi A549 cells(Ni group) expressing Twist uninfluenced was selected by neomycin resistance.In normal(control,C),Pi and Ni group A549 cells,Twist,alpha-smooth muscle actin(?-SMA) and E-cadherin expression were examined by reverse transcription-polymerase chain reaction(RT-PCR) and Western blot,invasion ability were examined by Boyden chamber model.Results:1,In C group,both Twist and ?-SMA expressions were strongly positive,but E-cadherin was poorly expressed.The number of A549 cells permeating septum of Boyden chamber(NCS) was equal to 57.4?3.4.2,In Pi group,compared with that in C group,Twist and?-SMA expression,and NCS were all decreased,but E-cadherin expression was significantly increased(P
ABSTRACT
Background and Purpose:Cyclooxygenase-2(COX-2) plays an important part in tumor genesis,growth,and angiogenesis.Many inhibitors of COX-2 could inhibit proliferation and induce apoptosis of cancer cells. This study investigated the impact of NS398 on anti-proliferation and the induction of apoptosis in human osteosarcoma cell line MG-63.Methods:Cell proliferation is measured by MTT method.Characteristic changes of apoptosis in morphology are observed by fluorescence microscopy、transmission electron microscopy(TEM) and quantitatively by TDT-mediated dUTP-biotin nick end-labeling(TUNEL) assay.The apoptotic rates are calculated by flow cytometry(FCM).Results:The growth inhibition rates of MG-63 cells treated with 1,10,50,100 and 200 ?mol/L NS398 are 14.7%,23.5%,33.6%,52.5% and 81.4%,respectively(P
ABSTRACT
Purpose:To invastigate the changes of the related signaling pathways and it's mechanism of reguation of mitogen activated protein kinase cascade(MAPK) by SUM149 cells induced plasmid of dominant-negative E-cadherin mutant H-2k~d-E-cadherin.Methods:Using western blot method,we examined the signal pathway of mitogen activated protein kinase(MAPK) between the dominant-negative mutant E-cadherin transfected SUM149 cells and controls.Results:Compared with the controls,the phosphorylated extracellular signal regulated kinase P44/42 expresion of the SUM149 cells which expressed higher dominant-negative mutant E-cadherin was significantly down-regulated.Conclusions:In this cell line model,the down-regulation of P44/42 may involve the regulation of MMPs.
ABSTRACT
Purpose:To investigate the effect of CD40 ligandization on breast cancer cell line and endothelial vein cell line.Methods:The expression of CD40 and its ligand on breast cancer cell line(M231),EVC cell line,fresh clinic breast cancer cell were determined by indirect immunofluorescence assay with flow cytometry(FCM) analysis.Then M231 cells cultured with CD40 agonsitic monoclone antibody,adriamycin alone or in combinations for 72 hours and proliferation of M231cells was determined by MTT assay.FCM was employed to study the cells' death or apopotosis with Annexin V PI assay.Results:M231 and ECV cell line and fresh clinic breast cancer cell are highly expressed CD40 but no CD40L.CD40 ligandization can not only inhibit the proliferation of M231 cell line but also inhibit ECV cell line by promoting the death or apoptosis of these cells.Combined CD40 agonsitic monoclone antibody with adriamycin may obviously inhibit proliferation of M231 and ECV cell line.Conclusions:CD40 ligandization may have double therapeutic effect to breast cancer: inhibit the proliferation of breast cancer cell and inhibit tumor angiogenesis by inhibiting vascular endothelial cell.
ABSTRACT
Purpose:To detect the abnormalities of WWOX(WW domain containing oxidoreductase) gene in human lung adenocarcinoma cell line A549. Methods:Deletion of WWOX exons 6-8 transcript was analyzed by reverse transcriptase-PCR technology; loss of heterozygosity (LOH) of WWOX gene was analyzed by PCR-based assays for dinucleotide repeat polymorphisms technology. Aberrant expression of WWOX protein was analyzed by western blot. Results:A549 cells samples showed loss of WWOX exons 6-8 transcript.This deletion was not detected in normal primary cultured human bronchial epithelial cells samples.Three microsatellites(D16S3029、D16S3096、D16S504)did not have LOH in the normal primary cultured human bronchial epithelial cells samples, but D16S2029 and D16S3096 were all found to have LOH in A549 Cells samples. We further observed that expression of WWOX protein was significantly lower in A549 cell samples compared to the normal primary cultured human bronchial epithelial cells samples. Conclusions:WWOX gene may be important during tumorigenesis in lung adenocarcinoma cancer.Deletion of exons 6-8,LOH and aberrant expression of protein are all modes of WWOX gene inactivity in lung adenocarcinoma cancer.
ABSTRACT
Purpose:To investigate the effects of octreotide on TGF-? autocrine in human hepatocellular carcinoma cells SMMC-7721 and TGF-?-induced cells proliferation. Methods:The expression of TGF-?in SMMC-7721 was determined by radioimmunoassay and reverse-transcriptase polymerase chain reaction(RT-PCR). The expression of epidermal growth factor receptor (EGFR) in the cells was determined by immunohistochemistry method and RT-PCR. The proliferative activity of the cells was evaluated by flow cytometry and colony-forming assay. Results:The content of TGF-?was significantly attenuated by octreotide and the inhibitor rate was 15.0%~26.7%. TGF-?mRNA index was decreased by octreotide.TGF-?increased the expression of EGFR both in mRNA and protein level,while octreotide inhibited the expression induced by TGF-?. Proliferative index (PI) and colony-forming rates were obviously lower in octreotide and TGF-?-treated cells than those in TGF-?-treated cells. Conclusions:There exists a TGF-? autocrine loop in human hepatocellular carcinoma cells SMMC-7721. octreotide could inhibit TGF-? autocrine in the cells, and consequently exerts an inhibitory effect on cell proliferation.