[Abstract] Objective: To investigate the expression of transgelin (TAGLN) in colorectal cancer (CRC) tissues and its effect on the proliferation, migration and invasion of CRC SW480 cells. Methods: Surgically resected CRC tissues and corresponding para-cancerous tissues of 97 CRC patients from May 2015 to August 2016 in the Affiliated Tumor Hospital of Zhengzhou University were collected; In addition, CRC cell lines SW620, SW480, HCT116 and normal colorectal mucosal cell line FHC were also collected for this study. Immunohistochemical staining was used to detect the expression of TAGLN in CRC tissues, and the correlation between TAGLN and patients’ clinicopathological features was analyzed. Quantitative Real-time quantitative polymerase chain reaction (qPCR) and Western blotting (WB) were used to detect the mRNA and protein expressions of TAGLN in CRC cell lines. si-TAGLN and si-Ctrl were respectively transfected into SW480 cells by liposome transfection method. The effects of silencing TAGLN on the proliferation, migration and invasion of SW480 cells were detected by CCK-8, Wound-healing assay and Transwell assay, respectively; and the expression of EMT-related proteins E-cadherin, N-cadherin and vimentin were detected by WB. Results: The positive expression rate of TAGLN in CRC tissues was significantly higher than that in para-cancerous tissues (P<0.01), and TAGLN expression was correlated with TNM stage, degree of tumor differentiation and lymph node metastasis in CRC patients (P<0.05 or P<0.01). The mRNA and protein expression levels of TAGLN in SW480 cells were significantly higher than those in FHC cells (all P<0.01). After TAGLN silence, the proliferation, invasion and migration ability of SW480 cells were significantly reduced (all P<0.01), the expression level of E-cadherin in SW480 cells was increased, while the expression levels of N-cadherin and vimentin were decreased (all P<0.01). Conclusion: TAGLN is highly expressed in CRC tissues and cells. Silencing TAGLN can inhibit the proliferation, invasion and migration of CRC cells, suggesting that TAGLN plays an important role in the occurrence and development of CRC.

［摘要］ 目的：探讨lncRNA HOTTIP 对肺癌细胞增殖、凋亡及EMT 的影响及其作用机制。方法：利用qPCR 检测lncRNA HOTTIP、miR-637 和KLK4 在肺癌SPC-A-1、正常肺上皮BEAS-2B细胞中的表达量；siRNA干扰SPC-A-1 细胞中lncRNA HOTTIP 的表达后，分别通过CCK-8、Transwell、流式细胞术和WB法检测SPC-A-1 细胞增殖、侵袭、凋亡和EMT能力的变化。miRanda 软 件和双荧光素酶报告基因实验分析lncRNA HOTTIP 和miR-637 之间的靶向关系，RNA pull-down 实验检测lncRNA HOTTIP 和 miR-637 的吸附作用，检测lncRNA HOTTIP 通过miR-637 对SPC-A-1 细胞增殖、侵袭、凋亡和EMT的调控。利用TargetScan 软件 分析miR-637 与KLK4 的相关性，双荧光素酶报告基因实验检测miR-637 与KLK4 mRNA 之间的相互作用；检测miR-637 通过 KLK4 mRNA对SPC-A-1 细胞增殖、侵袭、凋亡和EMT 的调控。下调lncRNA HOTTIP 和miR-637 表达后，利用qPCR和WB检测 KLK4 mRNA 和蛋白表达水平的变化。结果：与BEAS-2B 细胞比，在SPC-A-1 细胞中lncRNA HOTTIP 呈高表达（P<0.01）， miR-637 呈低表达（P<0.01），KLK4 呈高表达（P<0.01）。下调lncRNA HOTTIP 后，SPC-A-1 细胞增殖、侵袭与EMT能力显著减弱， 细胞凋亡率显著上升（P<0.01）；lncRNA HOTTIP 与miR-637 具有靶向关系；下调miR-637 表达后，SPC-A-1 细胞增殖、侵袭与EMT 能力显著上升，细胞凋亡率显著降低（P<0.01）。miR-637 与KLK4 3'UTR特异性结合。miR-637 通过KLK4 显著促进了SPC-A-1 细胞增殖、侵袭与EMT，细胞凋亡率显著上升（P<0.01）。下调lncRNA HOTTIP 使KLK4 表达显著降低，而下调miR-637 可促进 KLK4 表达（P<0.05）。结论：上调lncRNA HOTTIP 可通过miR-637/KLK4 轴促进肺癌SPC-A-1 细胞的增殖、侵袭与EMT 而抑制 癌细胞凋亡。

[摘 要] 目的：探讨NOD样受体蛋白3（NLRP3）炎症小体的活化在子宫内膜异位症（EMT）进展为EMT相关性卵巢癌（EAOC）过程中的作用及其机制。方法：选取2018年4月至2019年6月上海市长宁区幼保健院收治的EAOC、EMT、正常子宫内膜（CON组）组织标本各15例及患者的临床资料，利用免疫组织化学染色法、WB法检测EAOC、EMT和CON组织中NLRP3、caspase-1和IL-1β及含BRCA1/BRCA2的复杂亚基3（BRCC3）的表达水平。构建过表达BRCC3质粒和si-NLRP3质粒并转染EMT细胞CRL-7566，通过WB法检测转染后细胞中BRCC3蛋白的表达水平，利用MTT法、流式细胞术及Transwell实验分别检测转染后细胞增殖、凋亡、迁移与侵袭能力的变化。对过表达BRCC3组细胞进行干扰NLRP3实验，通过WB法检测干扰后BRCC3和NLRP3蛋白的表达水平，检测干扰后细胞增殖、凋亡、迁移与侵袭能力的变化。结果：EAOC和EMT组织中NLRP3、caspase-1、IL-1β和BRCC3的表达水平较CON组均呈明显升高（均P<0.01），且EAOC组织中NLRP3与BRCC3的表达呈正相关（r=0.65，P<0.01）。在CRL-7566细胞中过表达BRCC3显著促进细胞的增殖、迁移和侵袭并抑制细胞凋亡（均P<0.01），敲减NLRP3则抑制CRL-7566细胞的上述表型（均P<0.01），过表达BRCC3增强NLRP3的表达水平（P<0.01），而干扰BRCC3则抑制NLRP3表达（P<0.01）；干扰NLRP3可以部分逆转BRCC3对细胞凋亡的抑制作用（P<0.01）、对细胞迁移（P<0.05）和侵袭（P<0.01）的促进作用。结论：EAOC和EMT组织中NLRP3和BRCC3均呈高表达，过表达BRCC3可促进CRL-7566细胞的增殖、迁移和侵袭并抑制细胞凋亡，与EMT向EAOC转化有关，BRCC3/NLRP3是潜在的EAOC炎癌转化预测标志物及治疗靶点。