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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:

25卷

期数:

2019年03期

页码:

275-278

栏目:

临床医学

出版日期:

2019-05-20

文章信息/Info

Title:

Expression and significance of SRSF2、HMGA2 and Caspase-3 in high grade serous ovarian carcinoma and precursor lesions

文章编号:

1006-8147(2019)03-0275-04

作者:

汪红燕; 宋文静

（天津医科大学基础医学院病理学教研室，天津300070）

Author(s):

WANG Hong-yan;  SONG Wen-jing

（Department of Pathology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China）

关键词:

高级别浆液性癌; SRSF2; HMGA2; Caspase-3; 凋亡

Keywords:

high grade serous carcinoma; SRSF2; HMGA2; Caspase-3; apoptosis

分类号:

R365

DOI:

-

文献标志码:

A

摘要:

目的：观察富含丝氨酸/精氨酸剪接因子2（SRSF2）、HMGA2和Caspase-3在卵巢高级别浆液性癌（HGSOC）及其前驱病变中的表达并探讨其意义。方法：收集输卵管分泌型上皮细胞过度生长（SCOUT）20例、P53印记13例、浆液性输卵管上皮内癌（STIC）18例、输卵管高级别浆液性癌37例和HGSOC 48例，应用免疫组化技术检测SRSF2、HMGA2和Caspase-3在5组中的表达，分析3个指标间及其与临床病理参数间的关系。结果：在5组中SRSF2和Caspase-3呈递减性表达，HMGA2呈递增性表达（P均<0.05）。3个指标在STIC、输卵管高级别浆液性癌和HGSOC中的表达无显著差异（P均>0.05）。在HGSOC及其前驱病变中，SRSF2与Caspase-3的表达呈正相关，SRSF2与HMGA2、 Caspase-3与HMGA2的表达均呈负相关（r分别为0.618、-0.329和-0.373，P均<0.05）。3个指标的表达与肿瘤FIGO分期、肿瘤大小及年龄无关。结论：SRSF2和HMGA2蛋白异常表达可能协同参与调控HGSOC肿瘤细胞凋亡。

Abstract:

Objective: To examine the expression of SRSF2, HMGA2 and Caspase-3 in high grade serous ovarian carcinoma and precursor lesions,and to discuss their relevant meanings. Methods: The expressions of SRSF2, HMGA2 and Caspase-3 in the tissue inclding high grade serous ovarian carcinoma（HGSOC，48 cases）, fallopian tube high grade serous fallopian tube carcinoma（37 cases）, serous tubal intraepithelial carcinoma-STIC（18 cases）, P53 signature（13 cases）and secretory cell outgrowths（SCOUT，20 cases）were detected using immunohistochemical method． Relations between the three markers as well as relations beween markers and clinical pathological parameters were analyzed. Results: （1）The expressions of SRSF2 and Caspase-3 in the SCOUT, P53 signature, STIC, ovarian/ fallopian tube high grade serous carcinoma showed a decreasing trend, while the expressions of HMGA2 showed an increasing trend. The differences were statistically significant (P<0.05). There were no significant differences in expressions of the three markers between STIC, fallopian tube high grade serous carcinoma and HGSOC. （2）In HGSOC and its precursor lesion, positive correlation between the expression of SRSF2 and Caspase-3，and negative correlations beween SRSF2 and HMGA2, Caspase-3 and HMGA2 were obtained（They values 0.618、-0.329 and -0.373 respectively，P<0.05）；There was no correlation between the expressions of the three markers and FIGO stage, tumor size and age. Conclusion: The abnormal expressions of SRSF2 and HMGA2 may be involed in regulating apoptosis pathway synergisticly in HGSOC.

参考文献/References:

[1] Chen W, Zheng R, Baade P D, et al. Cancer statistics in China, 2015[J]. CA Cancer J Clin, 2016,66(2):115
[2] Miller K D, Siegel R L, Lin C C, et al. Cancer treatment and survivorship statistics, 2016[J]. CA Cancer J Clin, 2016,66(4):271
[3] Lee Y, Miron A, Drapkin R, et al. A candidate precursor to serous carcinoma that originates in the distal fallopian tube[J]. J Pathol,2007,211(1):26
[4] Sebestyén E, Zawisza M, Eyras E. Detection of recurrent alternative splicing switches in tumor samples reveals novel signatures of cancer[J]. Nucleic Acids Res, 2015, 43(3):1345
[5] Latorre E, Harries L W. Splicing regulatory factors, ageing and age-related disease[J]. Ageing Res Rev, 2017,(36): 165
[6] Luo C, Cheng Y, Liu Y, et al. SRSF2 Regulates Alternative Splicing to Drive Hepatocellular Carcinoma Development[J]. Cancer Res,2017, 77(5):1168
[7] K?誰dzierska H, Poplawski P, Hoser G, et al. Decreased expression of SRSF2 splicing factor inhibits apoptotic pathways in renal cancer[J]. Int J Mol Sci, 2016,17(10):1598
[8] Tan E J, Kahata K, Id?覽s O, et al. The high mobility group A2 protein epigenetically silences the Cdh1 gene during epithelial-to-mesenchymal transition[J]. Nucleic Acids Res, 2015, 43(1): 162
[9] Mahajan A, Liu Z, Gellert L, et al. HMGA2: a biomarker significantly overexpressed in high-grade ovarian serous carcinoma[J]. Mod Pathol, 2010, 23(5): 673
[10] 银铎,刘彤，陆景明. caspase3表达及其与卵巢上皮性肿瘤组织细胞凋亡和增殖的关系[J] .肿瘤防治杂志，2004，11(6):622
[11] Lee J M, Nobumori C, Tu Y, et al. Modulation of LMNA splicing as a strategy to treat prelamin A diseases[J]. J Clin Invest, 2016, 126(4):1592
[12] Hahn C N, Venugopal P, Scott H S, et al. Splice factor mutations and alternative splicing as drivers of hematopoietic malignancy[J]. Immunol Rev, 2015, 263(1): 257
[13] Iborra S, Hirschfeld M, Jaeger M, et al. Alterations in expression pattern of splicing factors in epithelial ovarian cancer and its clinical impact[J]. Int J Gynecol Cancer, 2013, 23(6): 990
[14] Milena S N，Monica S，Alessandra D A, et al. SRSF2 mutations in epithelial ovarian cancer [J]. Cancer Break News, 2017, 5(3): 25
[15] Aubrey B J, Kelly G L, Janic A, et al. How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression?[J]. Cell Death Differ, 2018, 25(1): 104
[16] Cancer Genome Atlas Research Network. Integrated genomic analyses of ovarian carcinoma[J]. Nature, 2011, 474(7353): 609
[17] Natarajan S, Hombach-Klonisch S, Dr?觟ge P, et al. HMGA2 inhibits apoptosis through interaction with ATR-CHK1 signaling complex in human cancer cells[J]. Neoplasia, 2013, 15(3): 263
[18] Wu J, Wei J J. HMGA2 and high-grade serous ovarian carcinoma[J]. J Mol Med (Berl), 2013, 91(10): 1155
[19] Chen L, Chen J Y, Huang Y J, et al. The augmented R-Loop is a unifying mechanism for myelodysplastic syndromes induced by high-risk splicing factor mutations[J]. Mol Cell, 2018, 69(3): 412
[20] Karnezis A N, Cho K R, Gilks C B, et al. The disparate origins of ovarian cancers:pathogenesis and preventionstrategies[J]. Nat Rev Cancer, 2017, 17(1): 65
[21] Haldar K, Crawford R. The role of peritoneal cytology at risk-reducing salpingo-oophorectomy(RRSO) in women at increased risk of familial ovarian/tubal cancer: Is the evidence strong enough?[J]. Gynecol Oncol, 2013,128(1): 148
[22] Labidi-Galy S I, Papp E, Hallberg D, et al. High grade serous ovarian carcinomas originate in the fallopian tube[J]. Nat Commun,2017, 8(1): 1093

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备注/Memo

备注/Memo:

作者简介 汪红燕（1982-），女，硕士在读，研究方向：女性生殖系统肿瘤；通信作者：宋文静，E-mail：songwenjing2004@aliyun.com。

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更新日期/Last Update: 2019-07-03