顺铂处理后剪接因子SRSF12 mRNA异构体在多种细胞中的变化
Changes of Alternative Splice Variant of the SRSF12 by Cisplatin in Multiple Cells
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摘要: 目的 用梯度浓度顺铂处理多种细胞后检测剪接因子SRSF12的mRNA异构体并分析其变化.方法用梯度浓度顺铂处理肺癌细胞A549和H1299、人胚肾细胞293FT以及宫颈癌细胞系Si Ha、Ca Ski、C33A细胞后提取总RNA, 利用半定量RT-PCR检测分析SRSF12基因mRNA异构体及相对水平的变化.结果 在除Caski细胞外的5种细胞中检测到了2种异构体 (Isoform-a、b) , 且随着处理顺铂浓度的增加, Isoform-a的比例有增加趋势, Isoform-b的比例变化在A549及293FT细胞中变化不明显, 在H1299及C33A细胞中渐弱, 在Siha细胞中表达较弱且2种异构体均有渐弱趋势.结论 在顺铂处理后, SRSF12的表达不仅具有组织特异性还具有细胞特异性.Abstract: Objective To detect the changes of mRNA isoforms in multiple cancer cell lines with dose of cisplatin. Methods Total RNA of the cells treated by cisplatin were abstracted 24 h after the treatment. mRNA isoforms of SRSF12 gene were detected by semiquantitative RT-PCR. The ratios of mRNA isoforms were analyzed by gel image software and statistical analysis. Results Under the cisplatin treatment, 2 mRNA isoforms of SRSF12 were detected in five cells except Caski cells, their ratios and relative mRNA levels were changed. With the increase of dose of cisplatin, the ratio of isoform-a was slightly increased; but the ratio of isoform-b was different, the changes were not obvious in the A549 and 293 FT cells, the weaker expression was expressed in the H1299 and C33 A cells, and the two isoforms were gradually weakening in the Siha cells. Conclution Under the cisplatin treatment in multiple cancer cells, the expression of SRSF12 shows tissue-specific and cell type-specific patterns.
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[1] [1]KIM E, GOREN A, AST G.Insights into the connection between cancer and alternative splicing[J].Trends in Genetics, 2008, 24 (1) :7-10. [2] [2]DAS S, KRAINER A R.Emerging functions of SRSF1, splicing factor and oncoprotein, in RNA metabolism and cancer.[J].Molecular Cancer Research Mcr, 2014, 12 (9) :1195-1204. [3] [3]TWYFFELS L, AL E, SHUTTLING S R.Proteins:more than splicing factors[J].Febs Journal, 2011, 278 (18) :3246-3255. [4] [4]LIU H X, ZHANG M, KRAINER A R.Identification of functional exonic splicing enhancer motifs recognized by individual SR proteins[J].Genes Dev, 1998, 12 (13) :1998-2012. [5] [5]HERTEL K J, GRAVELEY B R.RS.Domains contact the pre-m RNA throughout spliceosome assembly[J].Trends Biochem Sci, 2005, 30 (3) :115-118. [6] [6]VAN D H V O W, NEWTON K, SCREATON G R, et al.Role of SR protein modular domains in alternative splicing specificity in vivo[J].Nucleic Acids Research, 2000, 28 (24) :4822-4831. [7] [7]COWPER A E, CCERES J F, MAYEDA A, et al.Serine-arginine (SR) protein-like factors that antagonize authentic SR proteins and regulate alternative splicing[J].Journal of Biological Chemistry, 2001, 276 (52) :48908-48914. [8] [8]LI Y, LIN Y, LI Q, et al.SRrp35 suppresses cell proliferation and malignancy in hepatocellular carcinoma[J].Hepatology Research the Official Journal of the Japan Society of Hepatology, 2015, 45 (12) :1241-1247. [9]马春霞, 杨梦莉, 李明阳, 等.顺铂处理下肺癌细胞剪接因子SRSF1 m RNA异构体的变化[J].贵州医科大学学报, 2017, 42 (8) :879-884. [10] [10]BOEHME K A, BLATTNER C.Regulation of p53--insights into a complex process[J].Critical Reviews in Biochemistry&Molecular Biology, 2009, 44 (6) :367-392. [11] [11]TOKINO T, NAKAMURA Y.The role of p53-target genes in human cancer.[J].Critical Reviews in Oncology/hematology, 2000, 33 (1) :1-6.
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