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釉丛蛋白1表达对结直肠腺癌细胞增殖、凋亡及PI3K/AKT信号通路的影响
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作者 杨慧 孙淼 +1 位作者 王世雄 赵菁 《中国现代普通外科进展》 CAS 2023年第8期594-598,共5页
目的:探究釉丛蛋白1(TUFT1)表达对结直肠腺癌细胞(HCT-15)增殖、凋亡及磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/Akt)信号通路的影响。方法:2019年3月至2021年5月,20例结直肠癌(CRA)患者癌组织及相应癌旁组织。将HCT-15细胞分为对照组、siRNA-N... 目的:探究釉丛蛋白1(TUFT1)表达对结直肠腺癌细胞(HCT-15)增殖、凋亡及磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/Akt)信号通路的影响。方法:2019年3月至2021年5月,20例结直肠癌(CRA)患者癌组织及相应癌旁组织。将HCT-15细胞分为对照组、siRNA-NC组、siRNA-TUFT1组、siRNA-TUFT1+IGF-1(PI3K/Akt通路激活剂25 ng/mL)组;实时荧光定量PCR检测组织及细胞中TUFT1表达;CCK-8法、克隆形成实验检测细胞增殖;流式细胞仪检测细胞周期及凋亡情况;Western blot检测组织及细胞中增殖、凋亡及PI3K/Akt通路相关蛋白表达情况。结果:与癌组织相比,癌旁组织中TUFT1 mRNA及蛋白表达显著增加(P<0.05);与对照组相比,siRNA-TUFT1组细胞增殖抑制率、G0/G1期细胞、细胞凋亡率、Caspase-3、Bax表达水平显著增加,而c-Myc、Cyclin D1表达水平、克隆细胞数、S期和G2/M期细胞、p-PI3K/PI3K、p-Akt/Akt水平显著降低(P<0.05);IGF-1可逆转TUFT1沉默对上述指标的影响。结论:TUFT1表达沉默可能通过抑制PI3K/Akt通路激活来抑制HCT-15细胞增殖、促进凋亡。 展开更多
关键词 结直肠腺癌 釉丛蛋白1 增殖 PI3K/AKT 凋亡
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Oncogenic tuftelin 1 as a potential molecular-targeted for inhibiting hepatocellular carcinoma growth 被引量:4
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作者 Meng-Na Wu Wen-Jie Zheng +5 位作者 Wen-Xin Ye Li Wang Ying Chen Jie Yang Deng-Fu Yao Min Yao 《World Journal of Gastroenterology》 SCIE CAS 2021年第23期3327-3341,共15页
BACKGROUND Abnormal tuftelin 1(TUFT1)has been reported in multiple cancers and exhibits oncogenic roles in tumor progression.However,limited data are available on the relationship between TUFT1 and hepatocellular carc... BACKGROUND Abnormal tuftelin 1(TUFT1)has been reported in multiple cancers and exhibits oncogenic roles in tumor progression.However,limited data are available on the relationship between TUFT1 and hepatocellular carcinoma(HCC),and the exact biological mechanism of TUFT1 is still poorly understood in HCC.AIM To investigate TUFT1 expression in HCC and how interfering TUFT1 transcription affects HCC growth.METHODS TUFT1 in HCC and non-HCC tissues based on databases of the Cancer Genome Atlas and Oncomine were analyzed,and TUFT1 in human HCC tissues on microarray were detected by immunohistochemistry for clinicopathological features,overall survival,and disease-free survival.HCC cells were transfected with constructed vectors of TUFT1 that interfere or over-express TUFT1 for analyzing the biological behaviors of HCC cells.Proliferation,invasion,migration,and apoptosis of cells were detected by cell counting kit-8,scratch assay,transwell tests,and flow cytometry and confirmed by Western blotting,respectively.RESULTS Abnormal TUFT1 levels in databases expressed in HCC at messenger RNA(mRNA)level and HCC tissues were mainly located in cytoplasm and membrane.The level of TUFT1 expression in the HCC group was significantly higher(χ2=18.563,P<0.001)than that in the non-cancerous group,closely related to clinical staging,size,vascular invasion of tumor,hepatitis B e-antigen positive,and ascites(P<0.01)of HCC patients,and negatively to HCC patients’overall survival and disease-free survival(P<0.001).After interfering with TUFT1 transcription at mRNA level in the MHCC-97H cells by the specific TUFT1-short hairpin RNA,cell proliferation,invasion,and metastasis were significantly inhibited with increasing apoptosis rate.In contrast,proliferation,invasion,and migration were significantly enhanced after over-expression of TUFT1 mRNA in Hep3B cells in vitro.CONCLUSION Oncogenic TUFT1 was associated with the progression of HCC and could be a potential molecular-target for inhibiting HCC growth. 展开更多
关键词 Hepatocellular carcinoma Tuftelin 1 PROGNOSIS Molecular-target GROWTH
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