|本期目录/Table of Contents|

[1]李勇莉,赵秀兰,张宁,等.RSRC2影响三阴性乳腺癌细胞增殖迁移及侵袭的初步研究[J].天津医科大学学报,2020,26(04):313-316,323.
　LI Yong-li,ZHAO Xiu-lan,ZHANG Ning,et al.A preliminary study on the effect of RSRC2 on the proliferation, migration and invasion of triple negative breast cancer cells[J].Journal of Tianjin Medical University,2020,26(04):313-316,323.
点击复制

RSRC2影响三阴性乳腺癌细胞增殖迁移及侵袭的初步研究(PDF)
分享到：

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

卷:
26卷
期数:
2020年04期
页码:
313-316,323
栏目:
基础医学
出版日期:
2020-07-15

文章信息/Info

Title:
A preliminary study on the effect of RSRC2 on the proliferation, migration and invasion of triple negative breast cancer cells
文章编号:
1006-8147(2020)04-0313-04
作者:
李勇莉; 赵秀兰; 张宁; 董学易; 班新超; 廖诗晗; 刘铁菊
（天津医科大学基础医学院病理学教研室，天津300070）
Author(s):
LI Yong-li;  ZHAO Xiu-lan;  ZHANG Ning;  DONG Xue-yi;  BAN Xin-chao;  LIAO Shi-han;  LIU Tie-ju
（Department of Pathology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China）
关键词:
三阴性乳腺癌; RSRC2; 增殖; 迁移; 侵袭
Keywords:
triple-negative breast cancer; RSRC2; proliferation; migration; invasion
分类号:
R737.9
DOI:
-
文献标志码:
A
摘要:
目的：探究富含精氨酸/丝氨酸卷曲螺旋2（RSRC2）对三阴性乳腺癌细胞生物学行为的影响。方法：将RSRC2过表达、降表达和空载体质粒通过慢病毒包装转染至三阴性乳腺癌细胞MDA-MB-231中，通过Western blot检测转染效果，通过Transwell 迁移实验、侵袭实验、划痕实验检测RSRC2对MDA-MB-231细胞迁移、侵袭能力的影响，通过平板克隆形成实验检测RSRC2对MDA-MB-231细胞增殖能力的影响。结果：Western blot结果显示RSRC2过表达和降表达质粒成功转染至MDA-MB-231细胞中，Transwell迁移实验、侵袭实验、划痕实验、平板克隆实验显示，RSRC2过表达的MDA-MB-231细胞其迁移、侵袭及增殖能力减弱，RSRC2降表达的MDA-MB-231细胞其迁移、侵袭及增殖能力增强（均P<0.05）。结论：RSRC2在三阴性乳腺癌细胞增殖、迁移及侵袭过程中起着重要的负调控作用。
Abstract:
Objective: To explore the effect of arginine/serine-rich coiled-coil 2(RSRC2) on the biological behavior of triple-negative breast cancer cells. Methods: RSRC2 overexpression, interference and empty vector plasmids were transfected into triple-negative breast cancer cell line MDA-MB-231 by the lentiviral packaging system. Western blot was used to detect the protein expression level of RSRC2. Transwell assay and wound-healing assay were used to examine the effect of RSRC2 on the migration and invasion of MDA-MB-231 cells. The effect of RSRC2 on the proliferation of MDA-MB-231 cells was tested by plate clone formation assay. Results: Cellular function experiments showed that with the overexpression of RSRC2, the proliferation, migration and invasion abilities of triple-negative breast cancer cell line MDA-MB-231 were weakened compared with the control group. Compared with the control group, knockdown of RSRC2 enhanced proliferation, invasion, and migration of triple-negative breast cancer cell line MDA-MB-231（all P<0.05）. Conclusion：RSRC2 plays an important negative regulatory role in the proliferation, migration and invasion of triple-negative breast cancer cells.

参考文献/References:

[1] Zheng R, Zeng H, Zhang S, et al. Estimates of cancer incidence and mortality in China, 2013[J]. Chin J Cancer, 2017,36(1):66
[2] Marra A, Viale G, Curigliano G. Recent advances in triple negative breast cancer: the immunotherapy era[J]. BMC Med, 2019,17(1):90
[3] Jiang Y Z, Ma D, Suo C, et al. Genomic and transcriptomic landscape of triple-negative breast cancers: subtypes and treatment strategies[J]. Cancer Cell, 2019,35(3):428
[4] Wolf M, Korja M, Karhu R, et al. Array-based gene expression, CGH and tissue data defines a 12q24 gain in neuroblastic tumors with prognostic implication[J]. BMC Cancer, 2010,10:181
[5] Kurehara H, Ishiguro H, Kimura M, et al. A novel gene, RSRC2, inhibits cell proliferation and affects survival in esophageal cancer patients[J]. Int J Oncol, 2007,30(2):421
[6] Camorani S, Granata I, Collina F, et al. Novel aptamers selected on living cells for specific recognition of triple-negative breast cancer[J]. iScience, 2020,23(4):100979
[7] Damaskos C, Garmpi A, Nikolettos K, et al. Triple-negative breast cancer: the progress of targeted therapies and future tendencies[J]. Anticancer Res, 2019,39(10):5285
[8] He J, McLaughlin R P, van der Noord V, et al. Multi-targeted kinase inhibition alleviates mTOR inhibitor resistance in triple-negative breast cancer[J]. Breast Cancer Res Treat, 2019,178(2):263
[9] Lee K L, Kuo Y C, Ho Y S, et al. Triple-negative breast cancer: current understanding and future therapeutic breakthrough targeting cancer stemness[J]. Cancers (Basel), 2019,11(9):1334
[10] Dong X, Wang J, Tang B, et al. The role and gene expression profile of SOCS3 in colorectal carcinoma[J]. Oncotarget, 2018,9(22):15984
[11] Lin X M, Chen H, Zhan X L. MiR-203 regulates JAK-STAT pathway in affecting pancreatic cancer cells proliferation and apoptosis by targeting SOCS3[J]. Eur Rev Med Pharmacol Sci, 2019,23(16):6906
[12] Li H, Zhang B, Ding M, et al. C1QTNF1-AS1 regulates the occurrence and development of hepatocellular carcinoma by regulating miR-221-3p/SOCS3[J]. Hepatol Int, 2019,13(3):277
[13] Jin W. Role of JAK/STAT3 signaling in the regulation of metastasis, the transition of cancer stem cells, and chemoresistance of cancer by epithelial-mesenchymal transition[J]. Cells, 2020,9(1):217
[14] Li G, Martinez-Bonet M, Wu D, et al. High-throughput identification of noncoding functional SNPs via type IIS enzyme restriction[J]. Nat Genet, 2018,50(8):1180
[15] Richards D M, Sefrin J P, Gieffers C, et al. Concepts for agonistic targeting of CD40 in immuno-oncology[J]. Hum Vaccin Immunother, 2020,16(2):377
[16] Pang X, Zhang L, Wu J, et al. Expression of CD40/CD40L in colon cancer, and its effect on proliferation and apoptosis of SW48 colon cancer cells[J]. J BUON, 2017,22(4):894
[17] Georganaki M, Ramachandran M, Tuit S, et al. Tumor endothelial cell up-regulation of IDO1 is an immunosuppressive feed-back mechanism that reduces the response to CD40-stimulating immunotherapy[J]. Oncoimmunology, 2020,9(1):1730538
[18] Carrigan P E, Bingham J L, Srinvasan S, et al. Characterization of alternative spliceoforms and the RNA splicing machinery in pancreatic cancer[J]. Pancreas, 2011,40(2):281
[19] Liu T, Sun H, Zhu D, et al. TRA2A promoted paclitaxel resistance and tumor progression in triple-negative breast cancers via regulating alternative splicing[J]. Mol Cancer Ther, 2017,16(7):1377
[20] Yu J, Zayas J, Qin B, et al. Targeting DNA methylation for treating triple-negative breast cancer[J]. Pharmacogenomics, 2019,20(16):1151
[21] Hernandez-Vargas H, Ouzounova M, Le Calvez-Kelm F, et al. Methylome analysis reveals JAK-STAT pathway deregulation in putative breast cancer stem cells[J]. Epigenetics, 2011,6(4):428

相似文献/References:

[1]刘俊汝,郁春艳,郑小燕,等.富脂微环境通过PPARγ/ABCG2途径促进三阴性乳腺癌细胞的多药耐药[J].天津医科大学学报,2023,29(03):280.
　LIU Jun-ru,YU Chun-yan,ZHENG Xiao-yan,et al.The adipocyte-rich microenvironment promotes multidrug resistance in triple-negative breast cancer cells via the PPARγ/ABCG2 pathway[J].Journal of Tianjin Medical University,2023,29(04):280.

备注/Memo

备注/Memo:
基金项目 国家自然科学基金面上项目（81672870）
作者简介 李勇莉（1992-），女，硕士在读，研究方向：肿瘤病理学；
通信作者：刘铁菊，E-mail:liutieju@tmu.edu.cn。
更新日期/Last Update: 2020-07-15