Department of Gastrointestinal Surgery 2 Section, The First Hospital Affiliated to Fujian Medical University, Fuzhou 350005, China; Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Fujian Medical University, Fuzhou 350000, China.
Department of Gastrointestinal Surgery 2 Section, The First Hospital Affiliated to Fujian Medical University, Fuzhou 350005, China.
Life Sci. 2019 Oct 15;235:116831. doi: 10.1016/j.lfs.2019.116831. Epub 2019 Sep 2.
TRAF6 is an intracellular signal adapter molecule plays a significant role in tumor development. However, the specific mechanism causes and promotes of colorectal cancer keep largely unknown. Therefore, we sought to investigate the roles and the molecular mechanisms of TRAF6 in regulation colorectal cancer.
The immunohistochemistry analyzed the expression of TRAF6 in colorectal cancer samples and analyzed the effects of expression of TRAF6 on the prognosis in colorectal cancer. The roles of TRAF6 in regulating colorectal cancer cell proliferation, colony formation, cell migration, cell wound healing and cell invasion were evaluated in vitro. Animal studies were performed to investigate the effects of TRAF6 on tumor growth. mRNA abundance of key genes was analyzed via qPCR. Protein level of TRAF6 and NF-κB/AP-1 signaling pathways was examined by Western blot. Luciferase reporter and Immunofluorescence assays were used to identify the activities NF-κB/AP-1 signaling pathways.
TRAF6 high expression in colorectal cancer tissues. And colorectal cancer patients with high expression of TRAF6 had a poor survival rate. TRAF6 knockdown can inhibit proliferation, migration, and invasion of colorectal cancer cells in vitro and in vivo experiments. TRAF6 activates the TRAF6-NF-κB/AP-1 signaling pathway by entering the nucleus, causing biobehavioral changes in colorectal cancer cells.
TRAF6 plays a vital role in the progression of colorectal cancer. What's more, research elucidating the biological mechanisms of TRAF6 can treated as potential therapeutic target for colorectal cancer.
TRAF6 是一种细胞内信号接头分子，在肿瘤发展中发挥重要作用。然而，结直肠癌发生和促进的确切机制在很大程度上仍不清楚。因此，我们试图研究 TRAF6 在调节结直肠癌中的作用和分子机制。
免疫组织化学分析了 TRAF6 在结直肠癌样本中的表达，并分析了 TRAF6 表达对结直肠癌预后的影响。体外评估了 TRAF6 对结肠癌细胞增殖、集落形成、细胞迁移、细胞伤口愈合和细胞侵袭的调节作用。进行动物研究以研究 TRAF6 对肿瘤生长的影响。通过 qPCR 分析关键基因的 mRNA 丰度。通过 Western blot 检测 TRAF6 和 NF-κB/AP-1 信号通路的蛋白水平。使用荧光素酶报告和免疫荧光测定来鉴定 NF-κB/AP-1 信号通路的活性。
TRAF6 在结直肠癌组织中高表达。结直肠癌患者中 TRAF6 高表达者生存率低。TRAF6 敲低可抑制结直肠癌细胞的体外增殖、迁移和侵袭，体内实验也得到了验证。TRAF6 通过进入细胞核激活 TRAF6-NF-κB/AP-1 信号通路，导致结直肠癌细胞发生行为变化。
TRAF6 在结直肠癌的进展中起着至关重要的作用。此外，研究阐明 TRAF6 的生物学机制可以作为结直肠癌的潜在治疗靶点。
