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@# Objective: To investigate the effect of Baohuoside-Ⅰ on the proliferation, invasion, migration and apoptosis of colon cancer cell lines SW480 and RKO and the relative mechanism. Methods: Colon cancer cell lines SW480 and RKO were respectively treated with different concentrations of Baohuoside-Ⅰ (0, 5, 10, 20 μg/ml). Cell proliferation was detected by MTT assay; The ability of cell clone formation was tested by cell clone formation experiments; The migration and invasion of cells were detected by Transwell assay; The apoptosis and cell cycle was detected by Flow cytometry; and the protein expression levels of cleaved PARP, cleaved Caspase-3 and Bcl-2 were detected by Western blotting. TheeffectsofBaohuoside-Ⅰontranscriptomeandpossiblesignaling pathways were detected by RNA-Seq technology. Results: Baohuoside-Ⅰ could inhibit the proliferation, invasion and migration of SW480 and RKO cells, and induce cell apoptosis and G0/G1 phase block. Baohuoside-Ⅰ could also up-regulate the protein expressions of cleaved PARP and cleaved Caspase-3 but down-regulate the protein expression of Bcl-2 in SW480 and RKO cell lines. In addition, RNA-Seq data analysis showed that DNAreplication and transcription of ERBB signaling pathway related genes were both affected by Baohuoside-Ⅰ. Conclusion: Baohuoside-Ⅰ could induce apoptosis and G0/G1 phase block of colon cancer cell lines SW480 and RKO by affecting the expression of apoptosis related proteins, as well as cellular DNA replication and ERBB signaling pathways, thus inhibiting the malignant phenotypes of SW480 and RKO.
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@#可变剪接指从单个基因产生多种mRNA同种型，是转录后调控的重要方式之一。可变剪接不仅影响人体正常生长发 育过程，而且在包括癌症在内的多种疾病发生发展中扮演重要角色。癌组织的剪接变化通常是全局的而不是基因特异性的， 异 常的剪接模式控制癌症的主要特征。遗传、表观遗传、剪接因子网络差异表达及选择性转录起始或终止等多种途径巩固了特定 促癌或抑癌同种型的优势表达，进而影响癌症进程。此外，近年来研究，证明呈组织或阶段特异性表达的剪接同种型有作为癌症 生物标志物及治疗靶标的潜能。本文通过全局剪接变化影响肿瘤进展、可变剪接影响癌症进展的途径及可变剪接提示癌症监控 和治疗新策略3个方面进行综述。
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@#Objective: To investigate the expression of metastasis-associated protein 2 (MTA2) in human bladder cancer tissues and its effect on the malignant biological behaviors of bladder cancer T24 cells, as well as to explore the effect of MTA2 on the progression of bladder cancer. Methods: Sixty-two cases of human bladder cancer tissues and 28 cases of normal bladder tissues (from patients with cystitis, and pathologically confirmed as normal tissue) were collected at People’s Hospital of Hebei Province during December 2012 and December 2014. The expression of MTA2 in bladder cancer tissues and normal bladder tissues was detected by immunohistochemical staining, and the correlation between MTA2 expression and clinicopathological characteristics of patients was also analyzed. The bladder cancer T24 cell line stably expressing MTA2 was constructed. The effects of MTA2 on the proliferation, colony formation, migration and invasion of bladder cancer T24 cells were detected by MTS, clone formation, scratch healing and Transwell assay, respectively. Results: Immunohistochemical staining showed that MTA2 expression was significantly up-regulated in bladder cancer tissues as compared with normal bladder tissues (P<0.01). The high expression of MTA2 in bladder cancer tissues was not related to gender, age and tumor volume (P>0.05), but was associated with higher TNM stage, histological grade, and lymphatic infiltration and metastasis (all P<0.05). After over-expression of MTA2 in bladder cancer T24 cell line, the proliferation activity of the cells was significantly increased (P<0.05), and the colony formation, scratch healing, migration and invasion ability were significantly increased (all P<0.01). Conclusions: MTA2 is up-regulated in human bladder cancer tissues and can promote the proliferation, tumor formation, migration and invasion of T24 cells.
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@#Objective: To investigate the expression of miR-1269a in esophageal squamous cell carcinoma (ESCC) tissues and its effect on the malignant biological behaviors of ESCC KYSE30 cells, as well as to explore the underlying mechanism. Methods: Ninety specimens of ESCC tissues and adjacent para-cancerous tissues were obtained from patients underwent surgery in Fourth Hospital, Hebei Medical University. In addition, normal esophageal immortalized epithelial cells and esophageal cancer cell lines were also collected. The expression level of miR-1269a in above mentioned tissues and cell lines was examined by Real-time fluorescent quantitative PCR. After being transfected with miR-1269a mimics and inhibitors, the effects of miR-1269a on proliferation, migration, invasion and colony formation of KYSE30 cells were detected by MTS, Transwell and colony formation assay, respectively. The bioinformatics tool was used to predict the possible target genes of miR-1269a. Then the regulation effect of miR-1269a on target gene expression was validated by WB and Dual-luciferase reporter assay. After being transfected with SOX6 plasmid, the effects of SOX6 on the proliferation, migration, invasion and colony formation of KYSE30 cells were detected by MTS, Transwell and colony formation assay, respectively. At last, rescue assay was used to confirm the results. Results: The expression level of miR-1269a in ESCC tissues was significantly higher than that in adjacent para-cancerous tissues (P<0.05), and the expression level of miR-1269a in ESCC cell lines was significantly elevated compared with the normal epithelial cells (P<0.05 or P<0.01). The capacities of proliferation, invasion, migration and colony formation of KYSE30 cells in miR-1269a mimics transfection group were obviously higher than those in mimics NC group, while those abilities in miR-1269a inhibitor transfection group were significantly lower than those in inhibitor NC group (P<0.05 or P<0.01). Bioinformatics analysis showed that miR-1269a could combine with 3’UTR region at SOX6 gene; and after miR-1269a over-expression, the expression level of SOX6 and luciferase activity in KYSE30 cells were significantly reduced (P<0.05). Rescue assay showed that miR1269a over-expression could promote the proliferation, invasion and migration of KYSE 30 cells, while simultaneous transfection of SOX6 could partially reverse the promotion effect of miR-1269a mimics. Conclusion: The expression level of miR-1269a in ESCC tissues and cell lines is significantly increased, and it could enhance proliferation, migration, invasion and colony formation of KYSE30 cell line.And its mechanism may be related to the suppression of its target gene SOX6.