Keratinocyte growth factor receptor expression in normal colorectal epithelial cells and differentiated type of colorectal cancer

The keratinocyte growth factor receptor, also known as KGFR/FGFR2 IIIb, is mainly localized in epithelial cells and participates in the proliferation of these cells. In the present study, we attempted to clarify the expression and role of KGFR in human colorectal cancer. The KGFR protein was detected in several colorectal cancer cell lines. Immuno-histochemically, KGFR was expressed on the luminal surface of epithelial cells in normal colorectal tissues. KGFR was expressed in 35 of 56 (62.5%) colorectal cancer patients and localized at the center of the cancer nests. Cytokeratin 20 (CK 20) colocalized with KGFR. In contrast, Ki-67 localized at the periphery of the cancer nests. Clinicopathologically, a high level of KGFR expression was associated with well-differentiated histological type (p<0.0001) and shallow wall invasion (p<0.0174). These findings indicate that KGFR may play important roles in the differentiation of normal colorectal epithelial cells and establishment of the well-differentiated histological type of colorectal cancer cells.     

Expression of keratinocyte growth factor receptor (KGFR/FGFR2 IIIb) in human uterine cervical cancer

Keratinocyte growth factor receptor (KGFR), also known as FGFR2 IIIb, is a splice variant of FGFR-2. KGFR is expressed in many types of epithelial cell and is activated with four known ligands [FGF-1, FGF-3, FGF-7 (also known as KGF) and FGF-10] that are predominantly synthesized by mesenchymal cells. KGFR is highly expressed in the late-proliferative phase of a normal endometrium and in endometrial adenocarcinoma. In the present study, we attempted to determine the expression and localization of KGFR in human cervical cancer cell lines and cervical cancer tissues. The KGFR protein was detected in CaSki and HeLa cells, but not in ME-180 cells of cervical cancer cell lines. In non-cancer cervical tissues, KGFR immunoreactivity was weakly expressed in the surface of squamous epithelial cells and vascular smooth muscle cells. Immunohistochemically, the KGFR protein was detected in squamous cell carcinoma in 36 of 42 (86%) cervical cancer patients. In cervical cancer tissues, KGFR was detected in 17 of 18 (94%) of patients with the keratinizing type and 19 of 24 (79%) of patients with the non-keratinizing type of cervical cancer. Furthermore, KGFR was prominently localized in proliferating reserve cells and squamous metaplastic reserve cells adjacent to cancer cells. In contrast, KGFR was not detected in cervical ductal cells in cancer or non-cancer cervical tissues. These findings may indicate that KGFR mediates the growth and differentiation of reserve cells and squamous cell carcinoma in the cervix.     

Expression and roles of keratinocyte growth factor and its receptor in esophageal cancer cells

The keratinocyte growth factor receptor (KGFR), also known as FGFR2 IIIb, is mainly localized in epithelial cells and is activated by the keratinocyte growth factor (KGF) that is predominantly synthesized by mesenchymal cells. In this study, we examined the roles of KGFR and KGF in human esophageal cancer (EC). In noncancerous esophageal tissues, KGFR was localized in epithelial cells from the basal region of the epithelium to the lower one-third of the epithelium, and KGF was weakly localized in the basal to parabasal epithelial cells. On the other hand, Ki-67 was localized in the parabasal cells. In EC tissues, KGFR and KGF were expressed in cancer cells in 22 and 37 of 54 patients, respectively. The coexpression of KGFR and KGF in cancer cells was detected in 14 of 54 (26%) patients. Clinicopathologically, KGFR expression correlated with the well-differentiated cell type of EC (p<0.001), and KGF expression correlated with lymphatic invasion and lymph node metastasis (p=0.004 and 0.021, respectively). The coexpression of KGFR and KGF in cancer cells correlated with the well-differentiated cell type of EC (p=0.001). KGFR-positive, KGF-positive and KGFR/KGF coexpression patients tended to have shorter survival rates, but the survival rates were not statistically significantly different (p=0.44, 0.059 and 0.112, respectively). In human EC cell lines (TE-1, TE-8 and TE-11), KGFR mRNA was expressed but no KGF mRNA was detected. The KGFR mRNA level was highest in TE-1 cells, derived from well-differentiated SCC and lowest in TE-8 cells. KGFR was detected in the cancer cell lines by Western blot analysis. Recombinant human KGF significantly stimulated the growth of TE-8 and -11 cells, derived from moderately differentiated SCC, but had no effect on TE-1 cell growth. These results suggest that KGFR expression correlates with the differentiation of a normal esophageal epithelium and the well-differentiated cell type of EC. On the other hand, KGF may induce the growth of some EC cells in a paracrine manner and closely correlates with lymphatic invasion and lymph node metastasis.     

沉默ERK5对胃癌SGC-7901、BGC-823细胞生物学功能的影响

目的 探讨沉默细胞外信号调节激酶5（extracellular signal regulated kinase 5,ERK5）对胃癌细胞SGC-7901、BGC-823生物学功能的影响。方法 实时荧光定量PCR法（qRT-PCR）检测人胃癌细胞株和人胃黏膜上皮细胞株ERK5 mRNA的表达水平。应用短发荚RNA（shRNA）干扰技术沉默胃癌细胞SGC-7901、BGC-823中ERK5的表达。CCK-8法检测ERK5沉默后胃癌细胞的生长能力,平板克隆实验检测细胞克隆形成能力,Transwell 实验检测细胞侵袭和迁移能力,流式细胞仪检测细胞凋亡和周期分布。结果 与胃黏膜上皮细胞GES-1相比,胃癌细胞SGC-7901、BGC-823、AGS、HGC-27中ERK5 mRNA均呈高表达,相对表达量分别为2.696±0.501、1.865±0.185、1.793±0.137和1.530±0.093（P<0.05）。ERK5-shRNA有效沉默胃癌细胞SGC-7901、BGC-823中ERK5的表达水平,沉默效率分别为（74.4±1.5）%和（69.1±3.9）%,差异有统计学意义（P<0.05）。沉默 ERK5的表达能有效抑制胃癌细胞增殖、克隆形成、迁移和侵袭能力（P<0.05）,而促进胃癌细胞凋亡（P<0.05）,并诱导细胞周期阻滞于G0/G1期。结论 沉默ERK5可显著抑制胃癌细胞SGC-7901、BGC-823的生长侵袭,促进细胞凋亡,ERK5可能是胃癌治疗的潜在靶点。     

piR-9994对胃癌细胞增殖、迁移及侵袭的影响及其机制

目的 探讨piR-9994对胃癌细胞生物学行为的影响及可能机制。方法 qRT-PCR检测piR-9994在胃癌细胞系（MGC803和AGS）和正常胃上皮细胞（GES-1）中的表达情况;构建过表达和敲低piR-9994的MGC803胃癌细胞株,MTT、克隆形成实验检测piR-9994表达变化对细胞增殖能力的影响,划痕愈合实验和Transwell侵袭实验检测细胞迁移和侵袭能力。qRT-PCR和Western blot检测细胞增殖和EMT相关基因表达。结果 piR-9994在胃癌细胞MGC803中表达水平显著高于正常人胃黏膜上皮细胞GES-1（P<0.05）。piR-9994过表达促进胃癌细胞增殖、侵袭和转移,敲低则作用相反。piR-9994表达与细胞周期密切相关,特别是S期。piR-9994过表达促进增殖相关基因PCNA、CCND1、Bcl-2表达,抑制凋亡基因c-PARP表达,促进EMT相关基因N-cadherin、MMP7、Twist和Vimentin表达及抑制E-cadherin表达;敲低则作用相反。结论 piR-9994异常表达影响胃癌细胞增殖、侵袭、转移及EMT进程。piR-9994可能是胃癌新的标志物和治疗靶点。     

干扰FBXO2表达对胃癌细胞增殖、侵袭、迁移及EMT的影响

目的：探讨F框蛋白2（F-box only protein 2,FBXO2）基因在人胃癌细胞系中表达及其对胃癌细胞增殖、迁移、侵袭和EMT 的影响。方法：选择胃癌细胞系 MGC-803、AGS、SGC-7901、MKN-28以及正常胃黏膜上皮细胞株 GES-1,qPCR 法检测细胞中FBXO2 mRNA表达水平。设计靶向抑制FBXO2表达的特异siRNA,并瞬时转染MGC-803细胞,转染siRNA无义序列的为阴性对照。qPCR法检测转染48 h后MGC-803细胞中FBXO2 mRNA表达水平;用MTT法、细胞划痕愈合法、Transwell小室法检测降低 FBXO2表达对细胞增殖、迁移和侵袭的影响,WB 法检测细胞中 EMT 相关蛋白 E-cadherin、N-cadherin、vimentin的表达。结果：4种胃癌细胞中FBXO2 mRNA表达水平显著高于胃黏膜上皮细胞GES-1（P<0.05或P<0.01）。与阴性对照组相比,siRNA[1]FBXO2组MGC-803细胞中FBXO2 mRNA表达下调（P<0.01）,该细胞的增殖、迁移和侵袭能力受到显著抑制（P<0.05或P<0.01）,E-cadherin蛋白表达明显升高（P<0.01）,N-cadherin、vimentin蛋白表达显著降低（均 P<0.01）。结论：低表达的 FBXO2可抑制胃癌细胞的增殖、迁移和侵袭能力,该抑制作用可能与EMT过程有关。     

长链非编码RNA H19促进人胃癌MGC-803细胞增殖的实验研究

目的 探讨长链非编码RNA H19在胃癌组织及细胞株中的表达情况及其对人胃癌细胞增殖的影响。方法 采用实时定量PCR检测30例胃癌组织及其对应癌旁组织,以及胃癌细胞株MGC-803、SGC-7901和胃黏膜上皮正常GES-1细胞中H19的表达情况;分析胃癌组织H19表达与临床病理特征（年龄、性别、分化程度、肿瘤浸润深度、淋巴结转移及TNM分期）的关系。将胃癌MGC-803细胞分别转染H19特异性小干扰RNA（si-H19组）和阴性对照序列（si-NC组）,分别采用四甲基偶氮唑蓝法和克隆形成实验检测两组细胞的增殖情况。结果 与癌旁组织和黏膜上皮正常细胞相比较,胃癌组织和细胞株中H19的表达水平升高。胃癌组织中H19表达与年龄、性别、分化程度均无关（P＞0.05）,但与肿瘤浸润深度、淋巴结转移及TNM分期有关（P＜0.05）。si-H19组中H19表达水平低于si-NC组,且细胞活力和细胞克隆数均低于si-NC组,以上差异均有统计学意义（P＜0.05）。结论 胃癌组织及细胞株中H19呈高表达,下调H19表达能显著抑制胃癌细胞的增殖能力,H19可能参与了胃癌的发生、发展。     

Inhibition of gastric cancer cell growth and invasion through siRNA-mediated knockdown of guanine nucleotide exchange factor Vav3

Vav3, a Rho GTPase guanine nucleotide exchange factor, is associated with tumor growth, apoptosis, invasion and metastasis, and angiogenesis. However, the role of Vav3 in gastric cancer remains unclear. In this study, Vav3 expression was blocked by specific siRNA in gastric cancer cell line MGC803. MTT was used to assay cell proliferation activity; wound healing assay and transwell assay were applied to detect cell migration and invasion ability; and qRT-PCR and Western blot were employed to detect expression levels of Vav3 as well as proliferation, migration, and invasion-related genes. The results showed that Vav3 expression in gastric cancer tissues and cell lines was significantly upregulated and was higher than that in adjacent tissues of cancer and normal gastric mucosal cell lines. Vav3 knockdown inhibited proliferation, migration, and invasion of MGC803 gastric cancer cells. The expression of P21, P27, TIMP-1, and TIMP-2 was upregulated, while proliferating cell nuclear antigen, cyclin E1, matrix metalloproteinase (MMP)-2, and MMP-7 were downregulated by Vav3 knockdown in MGC803 gastric cells. In conclusion, Vav3 is involved in the proliferation, migration, and invasion of gastric cancer cell as a tumor oncogene.     

干扰LASP1基因表达对胃癌细胞BGC823增殖、迁移及侵袭能力的影响

背景与目的：LASP1是一种新的肌动蛋白结合蛋白,参与细胞骨架的重组调控及细胞迁移,在多种恶性肿瘤中高表达,并与肿瘤的增殖、侵袭和转移密切相关。但目前LASP1在胃癌发生、发展中的作用少见报道。该研究旨在探讨LASP1在胃癌增殖和侵袭中的作用及分子机制。方法：利用实时荧光定量聚合酶链反应(real-time fluorescent quantitative polymerase chain reaction,RTFQ-PCR)和蛋白［质］印迹法(Western blot)检测LASP1在不同胃癌细胞系中的表达,应用RNA干扰技术抑制BGC823细胞中LASP1的表达,采用RTFQ-PCR和Western blot检测转染后LASP1的表达,应用体外增殖、迁移和侵袭实验检测转染后细胞的增殖、迁移和侵袭能力,通过F-actin聚合实验检测细胞的F-actin的聚合能力,采用Western blot检测转染前后BGC823细胞中Akt的磷酸化情况。结果：LASP1在胃癌BGC823细胞中高表达。RNA干扰技术沉默LASP1基因后,干扰组与对照组相比,LASP1的mRNA和蛋白表达水平均明显下降。细胞增殖实验显示,干扰组细胞的增殖率低于对照组(P<0.05);Transwell迁移和侵袭实验发现,与对照组相比,干扰组细胞的迁移和侵袭能力均明显降低(P<0.05);在干扰组细胞内的F-actin聚合量比对照组减少(P<0.05);在干扰组细胞内Akt磷酸化受到抑制。结论：LASP1的表达降低可以抑制胃癌BGC823细胞的体外增殖、迁移和侵袭能力,LASP1通过调节F-actin的聚合和Akt磷酸化从而影响胃癌细胞的侵袭、转移。     

Significance of the association between heparin-binding epidermal growth factor-like growth factor and CD9 in human gastric cancer

Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a member of the EGF family. Juxtacrine activity of proHB-EGF (the membrane-anchored form of HB-EGF) has been shown to be significantly potentiated when it is coexpressed with CD9 in vitro. The purpose of our study was to investigate the issue of whether proHB-EGF and CD9 are coexpressed in gastric cancer. HB-EGF gene expression and protein production in human gastric cancers was investigated, and EGF receptor and CD9 expressions were also evaluated. HB-EGF mRNA levels in gastric cancers were elevated, compared with normal gastric tissues, especially in the intestinal type. ProHB-EGF immunoreactivity was detected primarily in the cytoplasm and plasma membrane of gastric cancer cells. Of 66 patients, 40 (60.6%) exhibited proHB-EGF immunoreactivity and the level of its expression was significantly associated with tumor status (p < 0.01) and histological differentiation (p < 0.001). In addition, proHB-EGF mRNA was detected at high levels in the intestinal type by in situ hybridization. CD9 immunoreactivity was found to be preserved in 26 of 36 patients (72.2%) and CD9 protein expression was inversely associated with lymph node status (p < 0.05). A significant correlation between its expression and histological differentiation (p < 0.01) was found, and the association of CD9 with proHB-EGF was increased in the intestinal type, as evidenced by an immunoprecipitation method. These results indicate that the coexpression of proHB-EGF and CD9 may be involved in the tumorigenesis and/or proliferation of gastric cancers in a juxtacrine manner.     

Caspase-8在胃腺癌组织中的表达及与临床病理特征和预后的关系

目的:探讨胃腺癌组织中Caspase-8的表达及其与患者临床病理特征、预后的关系,并进一步研究Caspase-8表达对胃癌细胞增殖的影响。方法:采用qPCR法及免疫组化法检测胃腺癌组织中Caspase-8 mRNA和蛋白的表达,并在胃腺癌细胞株中进行进一步研究。结果:胃腺癌组织中Caspase-8 mRNA和蛋白的表达均低于癌旁胃黏膜组织,Caspase-8蛋白的表达与患者的年龄、性别、脉管癌栓、淋巴结转移和浸润深度无关（P＞0.05）,而与肿瘤分化程度、临床分期有关（P＜0.05）;生存分析显示Caspase-8蛋白低表达患者生存时间短,预后不良;进一步细胞研究结果表明,抑制Caspase-8的表达可以促进胃癌细胞的增殖。结论:Caspase-8在胃腺癌中表达下调,与胃腺癌细胞的增殖相关,对预后判断可能有一定参考价值。     

剪接因子SF3b6通过MAPK信号通路促进胃癌细胞的增殖和迁移

目的:探讨剪接因子3b亚基6(splicing factor 3b subunit6,SF3b6)对胃癌细胞增殖、凋亡、侵袭和迁移等的影响及其作用机制.方法:通过组织芯片检测SF3b6在胃癌和癌旁组织中的表达,采用WB和qPCR检测SF3b6在正常永生化胃上皮细胞(GES-1)和胃癌细胞系(HGC27、AGS、BGC8...     

miR-1271-5p在胃癌组织的表达及对胃癌AGS细胞生物学行为的影响

目的 探讨miR-1271-5p在胃癌组织和细胞中的表达及其对胃癌细胞增殖、侵袭和迁移的影响。方法 收集2011年6月至2014年6月广西医科大学附属肿瘤医院90例手术切除胃癌组织及相应癌旁组织。采用qRT-PCR法检测胃癌组织及相应癌旁组织,人胃癌细胞系（SGC-7901、MGC-803、AGS）和人正常胃黏膜上皮细胞系GES1中miR-1271-5p的表达情况。利用瞬时转染法将miR-1271-5p mimics（过表达miR-1271-5p组）和miR-NC（阴性对照组）分别转染胃癌AGS细胞,建立过表达miR-1271-5p的胃癌AGS细胞系,然后采用CCK-8法检测转染后的胃癌AGS细胞增殖能力,平板克隆形成实验检测细胞克隆形成能力,Transwell实验检测细胞迁移和侵袭能力。结果 miR-1271-5p在胃癌组织和胃癌细胞（SGC-7901、MGC-803、AGS）中的表达均低于相应癌旁组织及人正常胃黏膜上皮GES1细胞（均P<0.01）。与阴性对照组相比,过表达miR-1271-5p组胃癌AGS细胞增殖活力降低（P<0.01）,细胞集落形成数减少（P<0.01）,迁移和侵袭细胞数量亦减少（P<0.01）。结论 miR-1271-5p在胃癌组织和细胞中低表达,上调miR-1271-5p可抑制胃癌AGS细胞的增殖、迁移和侵袭。     

Effects of bone sialoprotein on pancreatic cancer cell growth, invasion and metastasis

Bone sialoprotein (BSP) is an acidic glycoprotein that plays an important role in cancer cell growth, migration and invasion. The expression, localization and possible function of BSP in chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) were analyzed by QRT-PCR, laser capture microdissection, DNA microarray analysis, immunoblotting, radioimmunoassays and immunohistochemistry as well as cell growth, invasion, scattering, and adhesion assays. BSP mRNA was detected in 40.7% of normal, in 80% of CP and in 86.4% of PDAC samples. The median BSP mRNA levels were 6.1 and 0.9copies/microl cDNA in PDAC and CP tissues, respectively, and zero copies/microl cDNA in normal pancreatic tissues. BSP was weakly present in the cytoplasm of islet cells and ductal cells in 20% of normal pancreatic tissues. BSP was localized in the tubular complexes of both CP and PDAC, as well as in pancreatic cancer cells. Five out of 8 pancreatic cancer cell lines expressed BSP mRNA. Recombinant BSP (rBSP) inhibited Capan-1 and SU8686 pancreatic cancer cell growth, with a maximal effect of -46.4+/-12.0% in Capan-1 cells and -45.7+/-14.5% in SU8686 cells. rBSP decreased the invasion of SU8686 cells by -59.1+/-11.2% and of Capan-1 cells by -13.3+/-3.8% (P<0.05), whereas it did not affect scattering or adhesion of both cell lines. In conclusion, endogenous BSP expression levels in pancreatic cancer cells and low to absent BSP expression in the surrounding stromal tissue elements may indirectly act to enhance the proliferation and invasion of pancreatic cancer cells.     

CPNE7通过上皮间质转化影响胃癌细胞增殖、迁移和侵袭

目的:探讨CPNE7在胃癌组织和细胞中的表达及影响胃癌细胞增殖、迁移和侵袭的机制。方法:基于生物信息学数据库GEPIA 从转录水平分析CPNE7在胃癌及癌旁正常组织中的表达差异。qRT-PCR法检测CPNE7在3种胃癌细胞系(AGS、MKN-45、HGC-27)和胃黏膜正常上皮细胞(GES-1)中的表达,选择表达量相对较高的AGS细胞作为后续实验细胞。通过慢病毒转染AGS细胞敲减CPNE7的表达,根据不同处理分为RNAi-vector组、RNAi-1组、RNAi-2组、RNAi-3组,qRT-PCR、Western blot验证细胞转染效率,选择敲减效率最有效的RNAi-1(实验组)和RNAi-vector(对照组)进行后续实验。采用CCK-8法检测细胞活力,EdU和克隆形成实验检测细胞增殖和克隆形成能力,划痕愈合实验和Transwell实验检测细胞迁移与侵袭能力,Western blot检测细胞凋亡相关蛋白(Caspase3、Caspase7、Caspase9、Bax、Bcl-2)及上皮间质转化（epithelial-mesenchymal transition,EMT)相关蛋白（E-cadherin、N-cadherin、Vimentin)的表达水平。结果:CPNE7在胃癌组织中的表达明显高于正常组织(P＜0.05)。与正常胃黏膜上皮细胞(GES-1)相比较,CPNE7在胃癌细胞中明显高表达(P＜0.05),在AGS胃癌细胞中CPNE7相对表达量最高（P＜0.001)。与RNAi-vector组相比较,敲减CPNE7可抑制胃癌细胞的增殖、迁移和侵袭（P＜0.05)。与RNAi-vector组相比较,敲减CPNE7可上调细胞凋亡相关蛋白Caspase3、Caspase7、Caspase9、Bax的表达,下调Bcl-2的表达（P＜0.05)。与RNAi-vector组相比较,敲减CPNE7可增加上皮标志物蛋白(E-cadherin)的表达水平(P＜0.01),降低间质标志物蛋白(N-cadherin、Vimentin)的表达水平（P＜0.01)。结论:CPNE7在胃癌组织和细胞中表达上调,敲减CPNE7可通过影响EMT进程抑制胃癌细胞增殖、迁移与侵袭,其可能成为胃癌的潜在分子标志物。     

In vitro and in vivo effects of repifermin (keratinocyte growth factor-2, KGF-2) on human carcinoma cells

PURPOSE: Repifermin (keratinocyte growth factor-2, KGF-2) is a growth factor that selectively induces epithelial cell proliferation, differentiation and migration. The objective of this study was to assess the effect of repifermin on in vitro tumor cell proliferation and in vivo tumor growth using a variety of human carcinoma cell lines with differing growth rates and levels of KGF receptor (KGFR) expression. METHODS: Potential effects of repifermin on in vitro cell proliferation were evaluated by alamarBlue and/or [(3)H]-thymidine incorporation assays under a range of serum conditions. In vivo tumor growth was evaluated by implanting KGFR(+) carcinomas subcutaneously into nude mice and measuring tumor growth over time in mice injected intravenously (i.v.) or intraperitoneally (i.p.) with repifermin or placebo. RESULTS: In vitro, none of the 30 human carcinoma cell lines tested demonstrated a substantial increase in proliferation in response to repifermin over the concentration range 0.01 to 1000 ng/ml. In vivo results showed no significant tumor growth-promoting activity when single- or multiple-cycle intravenous injections of repifermin (1 mg/kg) were given to athymic nude mice inoculated with human KGFR(+) tumors of the pharynx (Detroit 562, FaDu), colon (Caco-2), salivary gland (A-253) or tongue (SCC-25, CAL 27). In addition, repifermin (0.2 or 2 mg/kg) injected i.p. for 2 weeks had no effect on the growth of eight other human carcinomas including those of the ovary (NIH:OVCAR-3, SK-OV 3, PA-1), bladder (SCaBER), epidermis (A 431), lung (SW 900), breast (MDA-MB-231) and cervix (SiHa). CONCLUSIONS: Repifermin had no in vitro or in vivo proliferative effects on KGFR(+) human epithelial-like tumors. This failure to stimulate tumor cell growth highlights the ability of repifermin to specifically target normal epithelial tissue. This is critical to the safety profile of repifermin, since it is currently in phase II clinical trials for the treatment of cancer patients with mucositis resulting from chemo- or radiotherapy.     

The effect of somatostatin and SSTR3 on proliferation and apoptosis of gastric cancer cells

In the present study, we detected the expression of SSTR3 protein in 40 patients with gastric adenocarcinoma and 40 cases of normal gastric mucosa by immunoperoxidased staining. SSTR3 mRNA and protein were also examined in gastric cancer cell lines and eternal gastric epithelial cell line by RT-PCR, immunofluorescence and Western blot. The effect of octreotide on the growth of gastric cancer cells was examined by MTT test, and the apoptosis by flow cytometry. Competitive protein binding method was also used to evaluate the role of SSTR3. The results were: (1) SSTR3 protein existed in the membrane of gastric cancer cells. In normal gastric mucosa, SSTR3 protein distributed to the cellular membrane and cytoplasm or interstitial tissue in submucosa. The expression of SSTR3 protein was significantly lower in gastric cancer compared with normal mucosa. Moreover, the poor-differentiated adenocarcinoma was lower than the well-differentiated adenocarcinoma, and the similar result in cell lines. (2) Octreotide could inhibit the growth and induce the apoptosis of gastric cancer and normal epithelial cells that expressed SSTR3, but didn't affect the cells with no or weakly expression of SSTR3. (3) When the cells were administrated octreotide in combination of SSTR3 antibody, the effect of octreotide decreased dramatically. The preliminary study suggested that SSTR3 might play a role in the growth and apoptosis of gastric cancer. In those gastric cancers that expressed SSTR3, octreotide could be effective in inhibiting cell growth and inducing cell apoptosis through mediation of SSTR3.