银杏双黄酮对未分化型甲状腺癌细胞顺铂耐药性的影响与机制研究

目的:探究银杏双黄酮对未分化型甲状腺癌（ATC）细胞顺铂（DDP）耐药性的影响与分子机制。方法:体外培养人ATC细胞8505C,并构建8505C DDP耐药细胞株（8505C/DDP）。用不同浓度的DDP（1.25、2.5、5、10、20 μg/mL）或银杏双黄酮（1.25、2.5、5、10、20 μmol/L）处理后,CCK-8法检测DDP、银杏双黄酮对8505C、8505C/DDP细胞的毒性作用以及两者联合对8505C/DDP细胞的毒性作用。将8505C/DDP细胞分为DDP组、DDP+银杏双黄酮组、DDP+AMPK抑制剂组、DDP+银杏双黄酮+AMPK抑制剂组,CCK-8法检测细胞增殖活力;Annexin V-FITC/PI双染法检测细胞凋亡情况;划痕愈合实验检测细胞迁移能力;Transwell实验检测细胞侵袭能力;Western Blot检测AMPK/mTOR信号通路相关蛋白表达。结果:DDP对8505C/DDP细胞的半数抑制浓度（IC50）高于8505C细胞（P＜0.05）;银杏双黄酮对8505C/DDP、8505C细胞的IC50无明显差异（P>0.05）;银杏双黄酮可增强DDP对8505C/DDP细胞的敏感性（P＜0.05）。与8505C细胞比较,8505C/DDP细胞中p-AMPK/AMPK比值降低,p-mTOR/mTOR比值升高（P＜0.05）;银杏双黄酮可上调8505C细胞和8505C/DDP细胞中p-AMPK/AMPK比值,降低p-mTOR/mTOR比值（P＜0.05）。与DDP组比较,DDP+银杏双黄酮组8505C/DDP细胞增殖活力、划痕愈合率、侵袭数量、p-mTOR/mTOR比值降低,凋亡率、p-AMPK/AMPK比值升高（P＜0.05）;与DDP+银杏双黄酮组比较,DDP+银杏双黄酮+AMPK抑制剂组细胞增殖活力、划痕愈合率、侵袭数量、p-mTOR/mTOR比值升高,凋亡率、p-AMPK/AMPK比值降低（P＜0.05）。结论:银杏双黄酮可降低8505C/DDP细胞对DDP的耐药性,增强DDP对8505C/DDP细胞增殖、迁移和侵袭的抑制作用以及对细胞凋亡的诱导作用,其作用机制可能与激活AMPK/mTOR信号通路有关。     

菊苣酸通过FOXO3-FOXM1信号轴抑制肺癌细胞增殖和化疗敏感性并促进凋亡

目的:研究菊苣酸调节叉头框蛋白O3(FOXO3)-叉头蛋白M1(FOXM1)信号轴对肺癌细胞增殖、凋亡和化疗敏感性的影响。方法:构建人肺癌细胞顺铂(DDP)耐药细胞A549/DDP,用不同浓度菊苣酸处理后通过MTT法测定细胞活力,以不显著降低细胞活力的最大浓度作为菊苣酸的最佳作用浓度。将A549细胞随机分为对照组、空载组、菊苣酸组、菊苣酸+FOXO3敲低组,分组处理后分别采用MTT法、集落生成实验及流式细胞实验测定各组A549细胞增殖及凋亡;采用免疫印迹法检测各组A549细胞FOXO3-FOXM1通路、增殖(PCNA)与凋亡(Bcl-2、Bax)相关蛋白表达。将A549/DDP细胞随机分为对照组、DDP组、DDP+空载组、DDP+菊苣酸组、DDP+菊苣酸+FOXO3敲低组,分组处理后分别采用MTT法、集落生成实验及流式细胞实验测定各组A549/DDP细胞增殖及凋亡;采用免疫印迹法检测各组A549/DDP细胞FOXO3-FOXM1通路、增殖、耐药[P-糖蛋白(P-gp)]与凋亡相关蛋白表达。结果:与对照组相比,空载组A549细胞各指标无明显变化(P>0.05);菊苣酸组A549细胞...     

连翘苷通过激活Hippo-YAP信号通路抑制结肠癌LS180细胞的恶性生 物学行为

目的：探究连翘苷（Phi）通过调控Hippo/YAP信号通路对结肠癌LS180细胞增殖、迁移和侵袭的影响。方法：用不同浓度（0、5、10、20、40、80 μmol/L）的Phi处理人结肠癌LS180细胞,MTT法检测24、48 和72 h时的细胞活力。将LS180细胞分为对照组、Phi-L（5 μmol/L Phi）组、Phi-M（10 μmol/L Phi）组、Phi-H（20 μmol/L Phi）组、Phi-H+YAP抑制剂维替泊芬（VP）组（20 μmol/L Phi+5 μmol/L VP）,各组均处理24 h。EdU法检测Phi对各组细胞增殖的影响,划痕愈合实验、Transwell小室法分别检测Phi对细胞迁移和侵袭的影响,免疫荧光法和WB 法检测 Phi 对细胞 Ki-67 表达率和LATS1、YAP和p-YAP、MMP-2、MMP-9、E-cadherin、N-cadherin表达的影响。构建LS180细胞移植瘤裸鼠模型,观察Phi对移植瘤体积和质量的影响,免疫荧光法和WB法检测移植瘤组织中Ki-67表达率和LATS1、YAP和p-YAP蛋白的表达水平。结果：与对照组比较,Phi-L、Phi-M和Phi-H组LS180细胞EdU阳性率、划痕愈合率、侵袭细胞数、Ki-67阳性率、MMP-2、MMP-9、N-cadherin表达均显著降低（均P<0.05）,E-cadherin、LATS1和p-YAP/YAP表达均显著升高（均P<0.05）;同时使用VP则部分逆转了Phi对LS180细胞增殖、迁移与侵袭的抑制作用（均 P<0.05）Phi显著抑制裸鼠移植瘤生长,与对照组比较,Phi组裸鼠移植瘤体积、质量和 Ki-67 阳性率均显著降低（均 P<0.05）,LATS1和 p-YAP/YAP 水平均显著升高（均P<0.05）。结论：Phi可能通过激活Hippo/YAP信号通路抑制结肠癌LS180细胞的恶性生物学行为。     

布托啡诺通过Hippo/YAP信号通路影响骨肉瘤MG-63 细胞增殖、迁移和侵袭

目的：探讨布托啡诺（BPH）对骨肉瘤（OS）细胞增殖、迁移和侵袭的影响及其相关的作用机制。方法：将MG-63细胞分为对照组、YAP抑制剂组（维替泊芬组）和BPH低、中、高浓度组,MTT法、克隆形成实验、FCM术、划痕愈合实验、Transwell 实验、qPCR法、WB法和移植瘤实验分别检测处理后各组细胞的增殖活性、克隆形成数、细胞凋亡率、划痕愈合率,以及上皮钙黏蛋白（E-cadherin）、神经钙黏蛋白（N-cadherin）、波形蛋白（vimentin）mRNA的表达和YAP、TAZ蛋白的表达,同时观察BPH和维替泊芬对移植瘤生长的影响。结果：与对照组相比,维替泊芬组和BPH低、中、高浓度组细胞增殖活性、克隆数、划痕愈合率、侵袭细胞数,以及N-cadherin 和vimentin mRNA 水平、YAP和TAZ蛋白表达及移植瘤体积均显著降低（均P<0.05）,细胞凋亡率、E-cadherin mRNA水平及对移植瘤的抑瘤率均升高（均P<0.05）,且BPH 高浓度组与维替泊芬组之间各项指标均无明显差异（均P>0.05）。结论：BPH可能通过抑制Hippo/YAP信号通路来抑制OS细胞MG-63增殖、迁移和侵袭。     

miRNA-139-5p通过靶向调控CXCR4/CXCL12信号通路逆转非小细胞肺癌A549细胞顺铂耐药

目的:探讨miRNA-139-5p对非小细胞肺癌A549细胞顺铂（cisplatin,DDP）耐药的影响,及其可能的分子机制。方法:采用DDP浓度递增法诱导A549细胞建立DDP耐药细胞株A549/DDP,将miR-139-5p mimics、无义序列（mimics-NC）、CXCR4过表达质粒（pcDNA3.1-CXCR4）、pcDNA3.1空载质粒（Vector）转染至A549/DDP细胞中,将细胞分为mimics-NC组（转染无义序列）、mimics组（转染miR-139-5p mimics）、mimics+Vector组（共转染miR-139-5p mimics和空载质粒）和mimics+CXCR4组（共转染miR-139-5p mimics和CXCR4过表达质粒）,另设置空白对照组（blank）。不同浓度DDP处理,MTT法检测细胞增殖活性,并计算IC50值和耐药指数（resistance index,RI）;qRT-PCR法检测细胞中miR-139-5p和CXCR4 mRNA表达水平;流式细胞术检测细胞凋亡率;Western blot法检测细胞中耐药相关蛋白P-糖蛋白（P-gp）、多药耐药相关蛋白1（MRP1）及CXCR4/CXCL12信号通路相关蛋白表达水平;双荧光素酶报告基因实验验证miR-139-5p与CXCR4的靶向关系。结果:不同浓度DDP处理24 h后,耐药株A549/DDP及其亲本A549细胞IC50值分别为（208.87±27.89）μmol/L和（31.66±6.30）μmol/L,RI=6.59。与亲本A549细胞比较,耐药株A549/DDP中miR-139-5p的表达水平明显降低（P＜0.05）,而CXCR4 mRNA和蛋白表达水平明显升高（P＜0.05）。与mimics-NC组比较,mimics组A549/DDP细胞增殖活性明显降低（P＜0.05）,细胞凋亡率明显升高（P＜0.05）,细胞中CXCR4 mRNA和蛋白以及P-gp、MRP1、PI3K（p110α）和p-AKT/AKT等蛋白表达水平显著降低（P＜0.05）。与mimics+Vector组比较,mimics+CXCR4组A549/DDP细胞增殖活性显著升高（P＜0.05）,细胞凋亡率显著降低（P＜0.05）,而细胞中CXCR4、P-gp、MRP1、PI3K（p110α）和p-AKT等蛋白表达水平显著升高（P＜0.05）。双荧光素酶报告基因实验证实,miR-139-5p靶向负调控CXCR4表达。结论:miRNA-139-5p通过靶向下调CXCR4表达,提高非小细胞肺癌DDP耐药细胞株A549/DDP对DDP的药物敏感性。     

Hippo信号通路中TAZ、P-TAZ、Mst1/2与

摘 要：［目的］ 检测Hippo信号通路相关蛋白TAZ、磷酸化TAZ、Mst1/2、磷酸化Mst1/2在口腔鳞状细胞癌组织中的表达,探讨其对口腔鳞状细胞癌术后肿瘤复发的影响。［方法］ 收集51例口腔鳞癌患者临床病理资料及癌组织标本,用免疫组化法检测口腔鳞癌组织中的TAZ蛋白和P-TAZ蛋白、Mst1/2蛋白和P- Mst1/2蛋白的表达情况,样本率的比较采用χ2检验,对可能影响口腔鳞癌治疗后复发的因素采用Cox比例风险回归分析,绘制TAZ、Mst1/2蛋白的表达情况与口腔鳞癌治疗后的生存曲线。TAZ与Mst1/2相关性研究采用Spearman秩相关分析。［结果］ TAZ在口腔鳞癌组织中阳性表达主要位于细胞核与细胞质中,P-TAZ、Mst1/2、P-Mst1/2阳性表达位于细胞质中。TAZ阳性表达与肿瘤大小、肿瘤组织分化程度、淋巴结有无转移有关（χ2分别为4.488,5.888,4.638,P＜0.05）;Mst1/2阳性表达与肿瘤的大小、肿瘤组织分化程度有关（χ2分别为4.961,10.232,P＜0.05）。肿瘤的大小是影响口腔鳞癌患者术后复发的危险因素（P＜0.05）。TAZ与Mst1/2表达呈负相关（r=-0.480,P＜0.05）。［结论］ Hippo信号通路参与口腔鳞癌的发生、发展。TAZ、P-TAZ、Mst1/2、P- Mst1/2蛋白与口腔鳞癌的预后情况相关。     

冬凌草甲素逆转黑色素瘤细胞顺铂耐药的作用及机制

目的：探讨冬凌草甲素（Ori）逆转人黑色素瘤细胞顺铂（DDP）耐药的作用及其机制。方法：分别将黑色素瘤DDP耐药细胞A375/DDP和M14/DDP分为对照组、2μmol/L Ori组、4 mg/L DDP组和2μmol/L Ori+4 mg/L DDP组。CCK-8法、Transwell实验、Annexin Ⅴ-FITC/PI染色流式细胞术分别检测各组细胞的增殖活力、侵袭和迁移能力及凋亡水平，透射电子显微镜观察自噬小体，免疫荧光染色法观察微管相关蛋白轻链3(LC3)点状结构，WB法检测A375/DDP细胞自噬相关蛋白Beclin-1、p62、LC3Ⅱ和LC3Ⅰ的表达。结果:与4 mg/L DDP组相比，2μmol/L Ori+4 mg/L DDP组细胞增殖活力、迁移和侵袭能力均显著下降（均P<0.01），凋亡水平显著升高（P<0.01）。4 mg/L DDP组细胞中可见大量自噬小体以及LC3点状染色，但2μmol/L Ori+4 mg/L DDP组仅可见少量。与对照组相比，4 mg/L DDP组细胞中Beclin-1和LC3Ⅱ/LC3Ⅰ的蛋白表达水平均显著升高（均P<...     

下调Beclin1 抑制卵巢癌A2780/DDP细胞对顺铂的耐药性

目的：探究敲减Beclin1 表达对卵巢癌细胞A2780 对顺铂耐药的影响及其相关机制。方法：以Western blotting 及qPCR 检测卵巢癌细胞株A2780 及耐药细胞株A2780/DDP 中Beclin1 的表达情况；A2780/DDP 细胞转染Beclin1 siRNA 后，用MTT法检测细胞对顺铂敏感性的变化，克隆形成实验检测各组细胞的克隆形成情况，流式细胞术检测各组细胞的凋亡，MDC荧光染色检测细胞的自噬情况，Western blotting 检测自噬相关蛋白、溶酶体相关膜蛋白Lamp-2 以及组织蛋白酶Cathepsin B的表达情况。结果：顺铂耐药细胞株A2780/DDP 中Beclin1 mRNA及蛋白的表达水平均明显高于A2780 细胞株（均P<0.05），在A2780细胞中加入顺铂刺激后Beclin1 蛋白的表达水平显著升高（P<0.05）。敲减Beclin1 表达可促进顺铂诱导的A2780/DDP 细胞的凋亡（P<0.05）、抑制细胞自噬的发生（P<0.05）、减少细胞克隆形成（P<0.05）和增加细胞对顺铂的敏感性（P<0.05）；Western blotting结果显示，敲减Beclin1 可上调A2780/DDP 细胞中cleaved-caspase 3 和Cathepsin B的蛋白水平，下调Atg3、Atg7、LC3Ⅱ/Ⅰ、Lamp-2的表达水平（均P<0.05）。结论：敲减Beclin1 表达可提高A2780/DDP细胞对顺铂的敏感性，其机制可能与调节自噬相关蛋白表达抑制细胞保护性自噬和影响溶酶体功能，从而促进顺铂诱导耐药细胞凋亡有关。     

柚皮苷逆转人卵巢癌耐药SKOV3／DDP细胞耐药性及逆转机制的研究

目的 研究柚皮苷对卵巢癌顺铂（DDP）耐药细胞SKOV3／DDP体外增殖的影响及耐药逆转作用,并初步探讨相关耐药机制。方法采用MTT法测定DDP对SKOV3和SKOV3／DDP细胞的半数抑制浓度（IC₅₀）,柚皮苷对SKOV3／DDP细胞的增殖抑制作用及柚皮苷联合DDP对SKOV3／DDP细胞的增殖抑制作用。筛选出非细胞毒性的柚皮苷浓度,将实验细胞分为空白对照组、2.5 μg／ml DDP组、10 μmol/L柚皮苷组、10 μmol/L柚皮苷联合2.5 μg／ml DDP组,分别采用RT-PCR和Western blotting测定各组作用48 h后耐药基因MDR1 mRNA及MRP2 mRNA的表达及其相应的表达产物P-gp、MRP2蛋白的表达水平。结果1～32 μg／ml DDP处理SKOV3及SKOV3／DDP细胞48 h后,SKOV3细胞的IC₅₀为5.48 μg／ml,SKOV3／DDP细胞为14.93 μg／ml,耐药指数为2.72。柚皮苷对SKOV3／DDP细胞有明显的增殖抑制作用,且呈剂量和时间依赖性。选取10 μmol／L柚皮苷作为逆转耐药实验浓度,10 μmol／L柚皮苷联合DDP作用48 h后,SKOV3／DDP细胞对DDP的耐药指数为1.62,逆转倍数为1.68。RT-PCR及Western blotting检测显示,柚皮苷联合DDP组与DDP单药组比较,MDR1 mRNA、MRP2 mRNA表达及P-gp、MRP2蛋白表达均明显下降,差异有统计学意义（P＜0.05）。结论柚皮苷对卵巢癌SKOV3／DDP细胞的体外增殖具有明显抑制作用,并能逆转SKOV3／DDP细胞的耐药性,其逆转耐药的机制可能与下调耐药基因MDR1 mRNA及MRP2 mRNA及相应的P-pg、MRP2蛋白的表达有关。     

Effects of the Hippo Signaling Pathway in Human Gastric Cancer

Background/Aim: The Hippo signaling pathway is a newly discovered and conserved signaling cascade,which regulates organ size control by governing cell proliferation and apoptosis. This study aimed to investigateits effects in human gastric cancer. Methods: Tumor tissues (n=60), adjacent non-tumor tissues (n=60) andnormal tissues (n=60) were obtained from the same patients with primary gastric cancer (GC). In addition,70 samples of chronic atrophic gastritis (CAG) tissues were obtained from patients with intestinal metaplasia(IM) by endoscopic biopsy. Hippo signaling molecules, including Mst1, Lats1, YAP1, TAZ, TEAD1, Oct4 andCDX2, were determined by quantitative polymerase chain reaction (qPCR). Protein expression of Mst1, Lats1,YAP1, TEAD1 and CDX2 was assessed by immunohistochemistry and Western blotting. Results: Mst1, Lats1and Oct4 mRNA expression showed an increasing tendency from GC tissues to normal gastric tissues, while themRNA expression of YAP1, TAZ and TEAD1 was up-regulated (all P<0.01). Mst1 and Lats1 protein expressionpresented a similar trend with their mRNA expression. In addition, YAP1 and TEAD1 protein expression in GCwas significantly higher than in the other groups (all P<0.01). CDX2 mRNA and protein expression in the CAGgroup were higher than in the other groups (all P<0.01). In GC, mRNA expression of Mst1, Lats1, Oct4, YAP1,TAZ, TEAD1 and CDX2 had a close correlation with lymphatic metastasis and tumor TNM stage (all P<0.01).Furthermore, protein expression of Mst1, Lats1 ,YAP1, TAZ, TEAD1 and CDX2 had a close correlation betweeneach other (P<0.05). Conclusion: The Hippo signaling pathway is involved in the development, progression andmetastasis of human gastric cancer. Therefore, manipulation of Hippo signaling molecules may be a potentialtherapeutic strategy for gastric cancer.     

AJUBA调控MST1 YAP1和TAZ因子促进食管鳞状细胞癌细胞体外增殖 迁移和侵袭

  目的  探讨AJUBA在食管鳞状细胞癌（esophageal squamous cell carcinoma,ESCC）细胞中表达以及是否通过调控MST1、YAP1和TAZ因子影响细胞增殖、侵袭和迁移。  方法  采用Western blot 法检测AJUBA 蛋白在食管癌细胞系KYSE30、KYSE150与KYSE450中的表达水平,构建shRNA 干扰载体AJUBA转染至KYSE150食管癌细胞系;通过体外克隆形成实验、流式细胞术、划痕实验和Transwell实验探究AJUBA对KYSE150细胞的增殖、周期、迁移和侵袭能力的影响。采用RT-PCR和Western blot检测MST1、YAP1和TAZ mRNA和蛋白的表达;核质分离实验检测AJUBA、YAP1和TAZ蛋白表达情况。  结果  稳定干扰AJUBA基因后,平板克隆实验结果显示,与阴性对照组相比,shAJUBA组的细胞克隆形成数量明显减少,差异具有统计学意义（P<0.001）;流式细胞周期实验结果显示,shAJUBA组中的细胞阻滞于G₀/G₁期,G₂/M期与S期细胞显著减少（P<0.05）;划痕实验和Transwell侵袭实验结果显示,与AJUBA空染组相比,shAJUBA组细胞迁移能力和侵袭能力均明显减弱（P<0.001）;RT-PCR与Western blot实验结果显示,shAJUBA组细胞中的MST1、YAP1、TAZmRNA与蛋白表达水平均显著降低,差异具有统计学意义（P<0.05）。核质分离实验结果提示AJUBA蛋白在正常食管鳞状上皮细胞株（SHEE）细胞核中表达,而在KYSE150细胞胞质与胞核中表达;YAP1和TAZ蛋白在SHEE细胞中不表达,在KYSE150细胞质与细胞核中表达,上述结果差异均具有统计学意义（均P<0.05）。  结论  AJUBA促进食管癌细胞的增殖、侵袭与迁移,可能与激活MST1、YAP1、TAZ因子的表达而影响食管鳞状细胞癌进展有关。      

HBV preS2 promotes the expression of TAZ via miRNA-338-3p to enhance the tumorigenesis of hepatocellular carcinoma

Transactivators encoded by HBV, including HBx and preS2, play critical role in hepatocellular carcinoma (HCC). YAP, a downstream effector of the Hippo pathway, is involved in hepatocarcinogenesis mediated by HBx. Here, we investigated whether preS2, another transactivator encoded by HBV, regulates the Hippo pathway to promote HCC. We found that preS2 overexpression upregulated TAZ, a downstream effector of the Hippo pathway, at protein level but not at mRNA level. preS2 suppressed miRNA-338-3p expression in HCC cell lines. miRNA-338-3p mimics downregulated TAZ, while miRNA-338-3p inhibitor restored the expression of TAZ, suggesting that TAZ is a direct target of miRNA-338-3p. TAZ overexpression stimulated growth of HCC cell lines. Knockdown of TAZ dampened preS2-promoted HCC proliferation and migration. Thus, preS2 upregulates TAZ expression by repressing miRNA-338-3p. TAZ is necessary for preS2-promoted HCC proliferation and migration     

Statin attenuates cell proliferative ability via TAZ (WWTR1) in hepatocellular carcinoma

Diabetes and obesity are associated with non-alcoholic steatohepatitis and an increased incidence of hepatocellular carcinoma (HCC). TAZ and YAP are equivalently placed downstream effectors of the Hippo pathway with oncogenic roles in human cancers. Statins are commonly used to patients with metabolic problems as hypercholesterolemia. Statins also have anti-cancer properties, and the cross-talk between mevalonate pathway and Hippo pathway was known. The aim of this study is to confirm the statin’s anti-cancer effects on HCC cells and its survival benefits in HCC patients with curative surgery. TAZ expression level in HCC cell lines was analyzed by western blot. Two cell lines (HLF and HuH1) were used in this study. Then the mechanism of statin’s anti-proliferative effect was examined in HLF and HuH1 cells. In clinical setting, overall survival and recurrence-free survival (RFS) rate were examined in comparison between statin intake and statin non-intake group. The proliferation assay using four different statins (atorvastatin, pravastatin, fluvastatin, simvastatin). Simvastatin and fluvastatin showed very strong growth suppressive effects, and induced apoptosis in HLF cells, but not HuH1 cells. TAZ expression was suppressed in HLF cells by fluvastatin and simvastatin treatment. The similar change pattern was confirmed in p-ERK1/2 and ERK. In HuH1 cells, such expression change was not confirmed. In clinical setting, statin intake was significantly associated with longer RFS in the HCC patients with hepatectomy (P = 0.038). The statin had the anti-proliferative effects and induced apoptosis in HCC cells and improved the prognosis of HCC patients.     

Effects of YAP1 and SFRP2 overexpression on the biological behavior of colorectal cancer cells and their molecular mechanisms

BackgroundColorectal cancer (CRC) is one of the most common malignancies worldwide and has a high mortality rate. With the development of tumor molecular biology, more and more attention is being paid to the mechanisms of cell pathways in colorectal carcinogenesis, such as the Hippo/Yes-associated protein 1 (YAP1) and Wnt/β-catenin signaling pathways. The abnormal expression of YAP1 and β-catenin have been reported in CRC, and can lead to excessive cell proliferation, and eventually, tumor formation. Secreted frizzled-related protein 2 (SFRP2) levels have been found to be decreased in a variety of cancers, and SFRP2 is an antagonist that binds directly to Wnt signal. At present, the molecular basis of colorectal tumors is still not fully understood. In the present study, we sought to identify the molecular mechanisms underlying YAP1 and SFRP2 in the development of CRC.MethodsWe constructed CRC cell lines that stably overexpressed YAP1 and SFRP2 using lentivirus packaging and cell infection. The levels of expression of the proteins were evaluated by western blot and immunofluorescence assays. Protein complex immunoprecipitation (Co-IP) was used to detect the interaction between YAP1, SFRP2, and β-catenin. The functional roles of YAP1 and SFRP2 in CRC was determined by a Cell Counting Kit-8 (CCK8) proliferation assay and flow cytometric apoptosis assay.ResultsThe data of the present study showed that the overexpression of SFRP2 promoted the expression of YAP1 and β-catenin protein, and the overexpression of YAP1 promoted the expression of β-catenin protein. YAP1 overexpression promoted cell proliferation, while SFRP2 overexpression inhibited cell proliferation and promoted cell apoptosis.ConclusionsOur findings showed that the expression of YAP1, SFRP2, and β-catenin is correlated in CRC cells. The Hippo pathway and Wnt pathway interact with each other in the pathogenesis of CRC, and YAP1 and SFRP2 are involved in the formation and development of CRC.