目的 研究SOCS6/STAT6通路在前列腺细胞炎性增殖作用中的调控作用。方法 使用人前列腺细胞株RWPE-1建立炎症模型,将细胞分为对照（CON）组和炎症刺激（INF）组,后者通过添加脂多糖（LPS）模拟炎症环境。采用ELISA检测白细胞介素-1β（IL-1β）-1β、白细胞介素-6（IL-6）和白细胞介素-8（IL-8）表达水平,蛋白免疫印迹法检测细胞因子信号抑制物-6（SOCS6）、信号转导和转录激活因子-6（STAT6）及磷酸化STAT6蛋白的表达水平。结果 经过LPS处理后,RWPE-1细胞中的SOCS6蛋白表达水平显著下降（P<0.01）,而磷酸化STAT6表达水平上升（P<0.01）。结论 SOCS6/STAT6通路可能通过调节炎症环境下STAT6的磷酸化水平,参与调节前列腺细胞的炎性增殖作用。

Objective To explore the regulatory role of SOCS6/STAT6 pathway in the inflammatory proliferation of prostate cells．Methods The human prostate cell line RWPE-1 was used to establish an inflammation model．Cells were divided into a control（CON）group and an inflammation-stimulated（INF）group,with the latter subjected to lipopolysaccharide（LPS）treatment to simulate an inflammatory environment．The expression levels of interleukin（IL）-1β、IL-6 and IL-8 were detected by ELISA,and the expression levels of suppressor of cytokine signaling 6（SOCS6）,signal transducer and activator oftranscription-6,（STAT6）,and phosphorylated STAT6 proteins were detected by Western blot．Results The results showed that after LPS treatment,the expression of SOCS6 protein in RWPE-1 cells significantly decreased,while the expression of phosphorylated STAT6 increased．Conclusions The SOCS6/STAT6 pathway may be involved in regulating the inflammatory proliferation of prostate cells by modulating the phosphorylation level of STAT6 under inflammatory conditions．

目的 探讨微RNA-29b（miR-29b）对子宫内膜癌细胞增殖、迁移和侵袭的影响。方法 子宫内膜癌HEC-1-B细胞分为miR-29b模拟物组（MM组）、miR-29b阻遏物组（MR组）和阴性对照物组（MNC组）,分别转染miR-29b拟似物、miR-29b阻遏物和miR-29b阴性对照物,每组设置6个复孔。以实时定量逆转录PCR检测miR-29b表达,以水溶性四氮唑（WST-1）检测miR-29b对HEC-1-B子宫内膜癌细胞增殖的影响,以Transwell小室检测HEC-1-B子宫内膜癌细胞迁移和侵袭的影响,以Western blot法检测磷酸酶张力蛋白同源物（PTEN）-蛋白激酶 B（AKT）通路蛋白表达水平。结果 MNC组、MM组、MR组miR-29b相对表达量分别为（2 032.1±873.4）、（19 272.8±2 087.9）、（472.7±105.6）,组间比较差异有统计学意义（P<0.05）。MM组0、3、5、7 d时OD值分别为（0.32±0.06）、（0.53±0.08）、（1.13±0.12）和（1.92±0.14）,MNC组0、3、5、7 d时OD值分别为（0.34±0.09）、（0.71±0.08）、（1.67±0.21）和（3.49±0.24）,MR组0、3、5、7 d时OD值分别为（0.38±0.09）、（0.84±0.18）、（2.43±0.24）和（5.67±0.15）,3组0 d时OD值比较差异无统计学意义（P=0.216）,三组3 d、5 d、7 d时OD值比较差异存在统计学意义（P<0.001）。MNC组、MM组和MR组迁移细胞数分别为（403.9±23.8）（102.6±15.7）和（685.7±46.8）个,上述3组侵袭细胞数分别为（82.1±12.7）（38.2±10.6）和（124.6±21.6）个,MM组和MNC组上述指标比较差异均有统计学意义（P<0.05）,MR组和MM组上述指标比较差异均有统计学意义（P<0.05）。MNC组、MM组、MR组PTEN蛋白相对表达量分别为（0.25±0.08）、（0.69±0.11）、（0.11±0.05）,上述3组p-AKT蛋白相对表达量分别为（0.58±0.10）、（0.13±0.06）和（0.79±0.08）,上述3组AKT蛋白相对表达量分别为（0.38±0.09）、（0.37±0.11）和（0.37±0.08）,MM组与MNC组PTEN、p-AKT水平比较差异有统计学意义（P<0.05）,AKT水平比较差异无统计学意义（P>0.05）;MR组与MNC组、MM组PTEN、p-AKT水平比较差异有统计学意义（P<0.05）,AKT水平比较差异无统计学意义（P>0.05）。结论 过表达miR-29b对子宫内膜癌细胞增殖、迁移和侵袭具有抑制作用,靶向PTEN-AKT可能是其重要作用途径。

Objective To investigate the effects of microRNA-29b on proliferation,migration and invasion of endometrial cancer cells．Methods The endometrial cancer HEC-1-B cells were divided into micro29b mimetic group（MM group）,micro29b repressor group（MR group）and negative control group（MNC group）,and the micro29b mimetic,micro29b repressor and micro29b negative control were transfected into each group,six compound holes with each group．The real-time quantitative reverse transcription polymerase chain reaction（RT-PCR）was used to detect the expression of mi29b,WST-1 was used to detect the effect of mi29b on the proliferation of HEC-1-B endometrial cancer cells,Transwell chamber was used to detect the migration and invasion of HEC-1-B endometrial cancer cells,and Western blot was used to detect the expression level of PTEN-AKT pathway protein．Results The relative expression levels of microRNA-29b in MNC group,MM group and MR group were（2 032.1±873.4）,（19 272.8±2 087.9）and（472.7±105.6）,respectively,and there were significant differences between groups（P<0.05）．OD values of MM group at 0 d,3 d,5 d and 7 d were（0.32±0.06）,（0.53±0.08）,（1.13±0.12）and（1.92±0.14）respectively．The OD values of MNC group at 0,3,5 and 7 days were（0.34±0.09）,（0.71±0.08）,（1.67±0.21）and（3.49±0.24）respectively．The OD values of MR group at 0 d,3 d,5 d and 7 d were（0.38±0.09）,（0.84±0.18）,（2.43±0.24）and（5.67±0.15）respectively．There was no significant difference in OD value between the three groups on day 0 （P=0.216）．There were significant differences in OD value between the three groups on day 3,day 5 and day 7（P<0.001）．The number of migrating cells in MNC group,MM group and MR group were（403.9±23.8）cells,（102.6±15.7）cells and（685.7±46.8）cells,respectively．The number of invasive cells in the above three groups were（82.1±12.7）cells,（38.2±10.6）cells and（124.6±21.6）cells．There were significant differences in the above indexes between MM group and MNC group（P<0.05）,also between MR group and MM group（P<0.05）．The relative expression levels of PTEN protein in MNC group,MM group and MR group were（0.25±0.08）,（0.69±0.11）and（0.11±0.05）．The relative expression levels of p-AKT protein in the above three groups were（0.58±0.10）,（0.13±0.06）and（0.79±0.08）．The relative expression levels of AKT protein in the above three groups were（0.38±0.09）,（0.37±0.11）and（0.37±0.08）,respectively．Compared with MNC group,the levels of PTEN and p-AKT in MM group had statistical significance（P<0.05）,but there was no statistical difference in AKT level（P>0.05）．Compared with MNC group and MM group,the levels of PTEN and p-AKT in MR group had statistical significance（P<0.05）,and there was no statistical difference in AKT level（P>0.05）．Conclusions Overexpression of microRNA-29b can inhibit the proliferation,migration and invasion of endometrial cancer cells,and targeting PTEN-AKT may be an important pathway．

目的 探讨柚皮素对人乳腺癌细胞株MCF-7和小鼠乳腺癌细胞系4T1的作用机制。方法 选择人乳腺癌细胞株MCF-7和小鼠乳腺癌细胞系4T1为实验对象,设置对照组和柚皮素组,其中柚皮素组分为20、40、80 和120 μmol/L 4个浓度,利用CCK-8、平板克隆形成实验检测柚皮素对乳腺癌细胞的增殖作用,应用流式细胞术检测柚皮素对乳腺癌细胞的凋亡作用。建立乳腺癌移植瘤模型,应用柚皮素作用于模型小鼠,探讨柚皮素在体内抗肿瘤作用。通过荧光定量PCR和蛋白免疫印迹实验检测自噬相关基因,分析其作用机制。结果 经柚皮素处理后,乳腺癌细胞的增殖明显受到抑制,正常乳腺癌细胞增殖情况变化不大,MCF-7乳腺癌细胞和小鼠乳腺癌4T1均出现明显的凋亡（P<0.001）。结论 柚皮素可以抑制乳腺癌细胞的增殖,且对正常乳腺细胞无明显毒副作用。柚皮素通过凋亡和自噬方式促进乳腺癌细胞的死亡,体内实验结果显示柚皮素具有抗肿瘤作用,并可促进其坏死。

目的 探讨不同浓度的青藤碱对肾癌细胞增殖、细胞周期及凋亡的影响。方法 以不同浓度的青藤碱处理肾癌细胞786-O,采用四氮唑蓝盐法检测细胞增殖能力,流式细胞术检测细胞周期分布,Annexin-v FITC/PI双染流式细胞分析仪检测细胞凋亡率;采用实时荧光定量PCR及蛋白免疫印迹(WB)检测c-myc、Bax、Caspase-3等细胞周期、凋亡相关基因表达情况。结果 青藤碱显著抑制786-O细胞的增殖能力,诱导细胞周期G1/S期阻滞及细胞凋亡;且随着青藤碱浓度的增加,其抑制率也逐渐增加;青藤碱显著下调c-myc蛋白表达,而诱导凋亡蛋白Bax、Caspase-3表达上调。结论 青藤碱可以显著抑制786-O细胞中c-myc表达,使其增殖能力减弱,诱导细胞周期阻滞及凋亡。青藤碱可能具有潜在的抑制肾癌生长作用。

Objective To investigate the effects of different concentrations of sinomenine on proliferation, cell cycle and apoptosis of renal carcinoma cells. Methods The renal carcinoma cells were treated with different concentrations of sinomenine. MTS was used to analyze the effects of sinomenine on proliferation in 786-O renal carcinoma cells, the cell cycle changes were determined using flow cytometry, while the changes of apoptosis were detected by Annexin V-FITC / PI double staining. The expression of apoptosis-related proteins such as c-myc, Bax and Caspase-3 were detected by Western blot. Results Sinomenine significantly inhibited the proliferation of 786-O cells and induced cell cycle arrest and apoptosis in G1/S phase. With the increase of sinomenine concentration, the inhibition rate increased gradually. Sinomenine significantly down-regulated the expression of c-myc protein, while the expressions of the apoptotic protein Bax, Caspase-3 were up-regulated. Conclusions Sinomenine can significantly inhibit the expression of c-myc in 786-O cells, reduce proliferation ability, and induce cell cycle arrest and apoptosis. Sinomenine may have a potential therapeutic effect on renal cancer.

目的 体外细胞实验检测吴茱萸碱对骨肉瘤HOS细胞株细胞周期及体外增殖能力的影响。方法 通过利用浓度为0、3、6、12 μmol/L吴茱萸碱处理骨肉瘤HOS细胞48 h后,Hoechst-33258荧光染色观察不同浓度吴茱萸碱处理后HOS细胞核的形态学变化。利用流式细胞术检测3 μmol/L的吴茱萸碱处理后骨肉瘤HOS细胞的细胞周期分布变化。结果 3、6、12 μmol/L的骨肉瘤吴茱萸碱处理细胞,细胞呈现凋亡核碎裂等典型变化,而且随药物剂量增加而更趋明显。呈剂量依赖性抑制其体外增殖能力。3 μmol/L吴茱萸碱处理骨肉瘤HOS细胞0、24、48、72 h,各组细胞周期变化如下:G0/G1期:对照组(51.12±2.13)%、24 h(19.17±1.02)%、48 h(16.94±1.67)%、72 h(11.05±1.25)%;S期:对照组(32.92±0.73)%、24 h(31.00±1.42)%、48 h(32.38±3.03)%、72 h(29.18±2.87)%;G2/M期:对照组(16.01±2.26)%、24 h(49.82±0.62)%、48 h(50.6767±2.80)%、72 h(59.56±1.97)%。结论 吴茱萸碱可诱导人骨肉瘤HOS细胞发生G2/M期阻滞,而S期变化不明显。说明吴茱萸碱可以抑制骨肉瘤细胞的增殖能力,并阻滞细胞周期于G2/M期。

Objective Using transcriptome sequencing and in vitro cell assay to detect the effect of evodiamine on cell cycle and proliferation in osteosarcoma HOS cell line. Methods HOS cells were treated with evodiamine at 0, 3, 6, and 12 μmol/L for 48 hours, Hoechst-33258 fluorescence staining was used to observe the morphological changes of HOS nuclei after treatment with different concentrations of evodiamine.The cell cycle distribution of HOS cells treated with 3 μmol/L evodiamine was detected by flow cytometry. Results 3,6,12 μmol/L osteosarcoma treated with evodiamine, the cells showed typical changes such as apoptotic nuclear fragmentation, and it became more obvious with the increase of drug dosage. Inhibition of proliferation in vitro in a dose-dependent manner.HOS cells were treated with 3 μmol/L evodiamine for 0, 24, 48, 72 h. The cell cycle changes of each group were as follows: G0/G1 phase: control group(51.12±2.13)%, 24 h(19.17±1.02)%, 48 h(16.94±1.67) %, 72 h(11.05±1.25)%;S phase: control group(32.92±0.73)%, 24 h(31.00±1.42)%, 48 h(32.38±3.03)%, 72 h(29.18±2.87)%;G2/M period: control group(16.01±2.26)%, 24 h(49.82±0.62)%, 48 h(50.6767±2.80)%, 72 h(59.56±1.97)%. Conclusion Analysis of the above results revealed that evodiamine can induce G2/M phase arrest in human osteosarcoma HOS cells, but the S phase changes are not obvious. It indicated that evodiamine would inhibit the proliferation of osteosarcoma cells and block the cell cycle in G2/M phase.

目的 研究过表达miR-29a-3p对IL-22诱导的HaCaT细胞增殖的影响。方法 将HaCaT细胞分为Cell组、IL-22组、IL-22+NC组和IL-22+ miR-29a-3p组,荧光定量PCR检测miR-29a-3p的表达水平,CCK8检测细胞的活力,流式细胞仪检测细胞凋亡及周期。结果 与0 μg/L组相比,25 μg/L组、50 μg/L组和100 μg/L组HaCaT细胞的增殖率在24 h、48 h和72 h均出现升高(F值分别为33.27、36.19、52.29,均P<0.000 1)。与0 μg/L组相比,miR-29a-3p在50 μg/L组和100 μg/L组HaCaT中的表达水平降低(F=129,P<0.000 1),分别降低83%和80%。与IL-22+NC组相比,IL-22+ miR-29a-3p组的增殖率在24 h、48 h和72 h均降低(P值分别为0.002 1、0.001 6、0.023 1),细胞总凋亡率增加(6.67±1.06 vs 30.55±1.86,P=0.000 1),G1期细胞比例增加(P=0.000 1),S期细胞比例降低(P=0.000 1)。结论 IL-22可降低HaCaT中miR-29a-3p的表达量,过表达miR-29a-3p通过促进凋亡和引起细胞G1期阻滞抑制IL-22诱发的HaCaT细胞过度增生。

Objective To investigate the effect of miR-29a-3p overexpression on IL-22-induced proliferation of HaCaT cells. Methods HaCaT cells were divided into four groups, Cell group, IL-22 group, IL-22 +NC group and IL-22+miR-29a-3p group. The expression level of miR-29a-3p was detected by fluorescence quantitative PCR. Cell viability was detected by CCK8. Apoptosis and cell cycle were detected by flow cytometry. Results Compared with the 0 g/L group, the proliferation rate of HaCaT cells in the 25 μg/L group, 50 μg/L group and 100 μg/L group was increased at 24 h, 48 h and 72 h (F value was 33.27, 36.19, 52.29,respectively, all P<0.000 1). Compared with the 0 μg/L group, miR-29a-3p expression level in HaCaT in 50 μg/L and 100 μg/L groups was decreased (F=129, P<0.000 1), with a decrease of 83% and 80%, respectively. Compared with the IL-22+NC group, proliferation rate of IL-22+miR-29a-3p group was decreased at 24 h, 48 h and 72 h (P value was 0.002 1, 0.001 6, 0.023 1, respectively), total apoptosis rate was increased (6.67±1.06 vs 30.55±1.86, P=0.000 1), cell proportion in G1 phase was increased (P=0.000 1), and the cell proportion in S phase was decreased (P=0.000 1). Conclusion Il-22 can reduce miR-29a-3p expression level in HaCaT, and miR-29a-3p overexpression can inhibit the excessive proliferation induced by IL-22 in HaCaT cells by promoting apoptosis and inducing G1 phase arrest.

目的 本研究从细胞生物学角度检测二甲双胍对小鼠胰岛瘤MIN6的影响,并探讨此过程中包含的分子生物学机制。方法 MTT法检测不同浓度二甲双胍(1、2、5、10、20 mmol/L)对MIN6细胞活力的影响,细胞划痕实验检测二甲双胍对MIN6细胞迁移的影响,免疫印记实验检测此过程中细胞凋亡相关蛋白Bcl-2、Bax、caspase3表达的变化,及AMPK和JNK信号通路蛋白磷酸化水平的变化。结果 二甲双胍浓度大于10 mmol/L时可以抑制MIN6细胞的活力(P<0.01),降低其迁移能力(P<0.01),高浓度二甲双胍可以上调细胞内凋亡蛋白Bax(P<0.05)和p-AMPK的表达(P<0.05),降低抗凋亡蛋白Bcl-2的表达,增加caspase3剪切体(P<0.05)。同时,二甲双胍可以降低MIN6细胞内JNK信号通路的磷酸化水平(P<0.05)。结论 高浓度二甲双胍可以抑制MIN6细胞的增殖和迁移,其作用可能与降低了JNK信号的通路活化有关。

Objective This study aims to investigate the effect of metformin on proliferation and migration of MIN6 cells, and to explore the underlying mechanism. Methods The viability of MIN6 cells that were treated with various metformin (1,2,5,10 and 20 mmol/L) was detected by MTT assay. The migration of MIN6 cells was determined by wound-healing assay. Meanwhile, the proteins expression of Bcl-2, Bax, caspase3 and the phosphorylation of AMPK, JNK was detected by western bolt assay. Results The cell viability and the migration of MIN6 cells were decreased when the concentration of metformin above 10 mmol/L(P<0.01). The expression of apoptosis-related protein Bax(P<0.05) and p-AMPK(P<0.05)was up-regulated, anti-apoptosis-related protein Bcl-2 was down-regulated and cleaved caspase3 (P<0.05)was increased after high metformin treatment. At the same time, the phosphorylation of JNK was down-regulated by metformin(P<0.05). Conclusion High concertration of metformin may inhibit the proliferation and migration of MIN6 cells through suppressing the activation of JNK signaling pathway.

目的 探索蟾毒灵对舌鳞状细胞癌Tca8113细胞增殖、凋亡的影响及可能作用机制。方法 以人舌鳞癌Tca8113细胞为研究对象,MTT法检测10、20、40、80、160 nmol/L浓度蟾毒灵体外抑制Tca8113细胞增殖的活性;检测蟾毒灵干预下肿瘤细胞Na⁺-K⁺-ATP酶活性的变化;Western blot发检测Bcl-2、Bax、caspase-3蛋白表达。结果 蟾毒灵有抑制Tca8113细胞的活性,且呈剂量-时间依赖性;在蟾毒灵干预下Tca8113细胞Na⁺-K⁺-ATP酶收到抑制;Western blot结果显示凋亡相关Bax、caspase-3蛋白表达上调,Bcl-2蛋白表达下调。结论 蟾毒灵通过抑制细胞膜Na⁺-K⁺-ATP酶活性,通过调节Bcl-2凋亡通路的相关蛋白,最终激活caspase-3,诱导人舌鳞癌Tca8113细胞凋亡。

Objective To explore the effects of bufalin on proliferation and apoptosis of tongue squamous cell carcinoma Tca8113 cells and its possible mechanism. Methods Tca8113 cells were treated with 10, 20, 40, 80 and 160 nmol/L Tca8113 cells in vitro. MTT assay was used to detect the inhibitory effect of bufalin on the proliferation of Tca8113 cells; And the activity of Na⁺-K⁺-ATPase in tumor cells was detected by the interference of bufalin; The expression of Bcl-2, Bax and caspase-3 protein was detected by Western blot. Results Bufalin inhibited the activity of Tca8113 cells in a dose-and time-dependent manner; Na⁺-K⁺-ATPase in Tca8113 cells was inhibited by bufalin; The results of Western blot showed that the expression of Bax and caspase-3 protein was up-regulated and the expression of Bcl-2 protein was down-regulated. Conclusion Bufalin induced the apoptosis of human tongue squamous cell carcinoma Tca8113 cells by inhibiting the activity of Na⁺-K⁺-ATPase and regulating the related proteins of Bcl-2 apoptosis pathway, finally activating caspase-3.

目的 观察紫河车提取物联合顺铂对人脑胶质瘤细胞增殖与凋亡的影响。方法 把正常培养传代后的U251胶质瘤细胞按随机分配的方法分为四组,A组仅加普通培养液,B、C、D组各加紫河车提取物(400 mg/mL)2 mL、顺铂(1 mg/mL)0.01 mL、紫河车提取物(400 mg/mL)2 mL＋顺铂(1 mg/mL)0.01 mL;MTT法观察U251细胞增殖情况,流式细胞仪检测U251细胞凋亡率。结果 培养12、24、36、48、60 h,B、C、D组细胞增殖指数逐渐下降,与A组进行比较,各组P值均小于0.05;其中,将D组与B、C组进行比较,P值小于0.05。将各组培养24 h后上机,测得A、B、C、D各组细胞的凋亡率分别为(0.3±0.2)%,(10.6±1.5)%,(35.9±2.8)%,(52.1±4.1)%。其中,B、C、D各组和A组进行比较,P值均小于0.05;将D组与B、C组两组进行比较,P值也均小于0.05。结论 紫河车提取物联合顺铂可抑制人脑胶质瘤U251细胞增殖,并诱导其凋亡。

Objective To observe the effect of cisplatin combinated with the placental immunoregulating polypeptide (PIP) on proliferation and apoptosis of glioma cells. Methods Randomly we divide the normal handed U251 glioma cells into four groups. We added ordinary nutrient solution to group A, while added activated PIP(400 mg/mL)2 mL to group B, cisplatin (1 mg/ml) 0.01 ml to group C, PIP 400 mg/mL)2 mL and cisplatin (1 mg/mL) 0.01 mL to group D. We surveyed the proliferation rate of gliobma cells by MTT experimental method and analyzed the apoptosis of U251 glioma cells by flow cytometry. Results The index of cell proliferation of group B,C,D declined gradually with the training of 12 h,24 h,36 h,48 h,60 h. Compared B, C,D group with A group, P<0.05,and compared group D with group B and group C, P< 0.05. Put groups culturing of 24 hour on flow cytometer, the glioma cells apoptosis rate of each group was 0.3%±0.2%、10.6%±1.5%、35.9%±2.8%、52.1%±4.1% respectively. Compared group B,C,D with group A, P<0.05,and compared group D with group B and group C, P<0.05. Conclusion Placental immunoregulatingpPolypeptide combined with cisplatin may restrain the proliferation of human glioma cells, meanwhile increase the apoptosis of glioma cells.

       目的   研究SOCS6/STAT6通路在前列腺细胞炎性增殖作用中的调控作用。方法  使用人前列腺细胞株RWPE-1建立炎症模型，将细胞分为对照（CON）组和炎症刺激（INF）组，后者通过添加脂多糖（LPS）模拟炎症环境。采用ELISA检测白细胞介素-1β（IL-1β）-1β、白细胞介素-6（IL-6）和白细胞介素-8（IL-8）表达水平，蛋白免疫印迹法检测细胞因子信号抑制物-6（SOCS6）、信号转导和转录激活因子-6（STAT6）及磷酸化STAT6蛋白的表达水平。结果  经过LPS处理后，RWPE-1细胞中的SOCS6蛋白表达水平显著下降（P＜0.01），而磷酸化STAT6表达水平上升（P＜0.01）。结论  SOCS6/STAT6通路可能通过调节炎症环境下STAT6的磷酸化水平，参与调节前列腺细胞的炎性增殖作用。

       Objective   To explore the  regulatory  role of  SOCS6/STAT6  pathway in the inflammatory  proliferation of 

prostate cells．Methods  The human prostate cell line RWPE-1 was used to establish an inflammation model．Cells were divided into a control（CON）group and an inflammation-stimulated（INF）group，with the latter subjected to lipopolysaccharide（LPS）treatment to simulate an inflammatory environment．The expression levels of interleukin（IL）-1β、IL-6 and  IL-8 were detected by ELISA，and the expression levels of suppressor of cytokine signaling 6（SOCS6），signal transducer and activator oftranscription-6，（STAT6），and phosphorylated STAT6 proteins were detected by Western blot．Results  The  results showed that after LPS treatment，the expression of SOCS6 protein in RWPE-1 cells significantly decreased，while the expression of phosphorylated STAT6 increased．Conclusions  The SOCS6/STAT6 pathway may be involved in  regulating the inflammatory proliferation of prostate cells by modulating the phosphorylation level of STAT6 under inflammatory conditions．