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[1]董玥湘,刘岩,靳小石,等.应用CRISPR/Cas9技术敲除SLC5A8基因对黑色素瘤的影响[J].天津医科大学学报,2024,30(02):128-131.[doi:10.20135/j.issn.1006-8147.2024.02.0128]
　DONG Yuexiang,LIU Yan,JIN Xiaoshi,et al.Effect of knockdown of SLC5A8 gene on melanoma by applying CRISPR/Cas9 technology[J].Journal of Tianjin Medical University,2024,30(02):128-131.[doi:10.20135/j.issn.1006-8147.2024.02.0128]
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应用CRISPR/Cas9技术敲除SLC5A8基因对黑色素瘤的影响(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
30卷
期数:
2024年02期
页码:
128-131
栏目:
肿瘤疾病专题
出版日期:
2024-03-20

文章信息/Info

Title:
Effect of knockdown of SLC5A8 gene on melanoma by applying CRISPR/Cas9 technology
文章编号:
1006-8147（2024）02-0128-04
作者:
董玥湘1; 刘岩2; 靳小石3; 刘雅涵3; 谢天皓3; 矫政洧3
（1.河北大学临床医学院，保定071000；2.邢台市人民医院急诊科，邢台054000；3.河北大学附属医院普通外科，保定071000）
Author(s):
DONG Yuexiang1; LIU Yan 2; JIN Xiaoshi3; LIU Yahan3; XIE Tianhao3; JIAO Zhengwei3
（1. Hebei University School of Clinical Medicine，Baoding 071000，China；2. Departement of Emergency Emergency， Xingtai Pepole′s Hospital，Xingtai 054000，China；3. Department of General Surgery， Affiliated Hospital of Hebei University，Baoding 071000，China）
关键词:
CRISPR/Cas9; SLC5A8基因; 黑色素瘤
Keywords:
CRISPR/Cas9;  SLC5A 8 gene;  melanoma
分类号:
R73-3
DOI:
10.20135/j.issn.1006-8147.2024.02.0128
文献标志码:
A
摘要:
目的：采用CRISPR/Cas9技术研究SLC5A8基因对肿瘤细胞的影响。方法：通过CRISPR/Cas9技术建立SLC5A8基因敲除模型，将C57小鼠分为两组各4只，分别为敲除SLC5A8基因负瘤鼠实验组（KO组）和普通负瘤鼠对照组（WT组）。对比两组的肿瘤时间-生长曲线、肿瘤体积、肿瘤重量及病理学改变。结果：与WT组相比，KO组黑色素瘤生长速度更快，肿瘤体积显著增大（t=7.845，P<0.01）。KO组肿瘤重量较WT组显著增加（t=3.804，P<0.01）。KO组小鼠肿瘤细胞表现出更深层次的异型性，细胞密度不均，结构复杂、形态多样，且存在大量炎细胞浸润。结论：敲除SLC5A8基因影响了C57负瘤鼠黑色素瘤细胞的发展，SLC5A8基因是黑色素瘤进展过程中的负调控因子。
Abstract:
Objective：To investigate the effect of the SLC5A8 gene on tumor cells using CRISPR/Cas9 technology. Methods：A CRISPR/Cas9-induced SLC5A8 gene knockout model was created. Eight C57 mice were divided into the knockout group（KO group） with the SLC5A8 gene knocked out in tumor-bearing mice，and the wild-type control group（WT group），with 4 mice in each group. Tumor growth curves，tumor volume，tumor weight，and pathological changes were compared between the two groups. Results：Compared to the WT group，the KO group showed an accelerated melanoma growth rate，a marked increase in tumor volume（t=7.845，P<0.01）. Compared with the WT group，the tumor weight significantly increased in mice within the KO group（t=3.804，P<0.01）. Tumor cells in KO group showed deeper cellular atypia，uneven cell density，complex and diverse morphology，and abundant infiltration of inflammatory cells. Conclusion：Knocking out the SLC5A8 gene affects the development of melanoma cells in C57 tumor-bearing mice，and the SLC5A8 gene functions as a negative regulator in the progression of melanoma.

参考文献/References:

[1] THANGARAJU M，GOPAL E，MARTIN P M，et al. SLC5A8 triggers tumor cell apoptosis through pyruvate-dependent inhibition of histone deacetylases[J]. Cancer Res，2006，66（24）：11560-11564.
[2] GARRAWAY L A. Genomics-driven oncology：framework for an emerging paradigm[J]. J Clin Oncol，2013，31（15）：1806-1814.
[3] VERMA M. Personalized medicine and cancer[J]. J Pers Med，2012， 2（1）：1-14.
[4] GUERNET A，GRUMOLATO L. CRISPR/Cas9 editing of the geno-me for cancer modeling[J]. Methods，2017，121：130-137.
[5] MARTINEZ-LAGE M，PUIG-SERRA P，MENENDEZ P，et al. CR-ISPR/Cas9 for cancer therapy：hopes and challenges[J]. Biome-dicines，2018，6（4）：105.
[6] RODRIGUEZ A M，PERRON B，LACROIX L，et al. Identification and characterization of a putative human iodide transporter located at the apical membrane of thyrocytes[J]. J Clin Endocr Metab，2002， 87（7）：3500-3503.
[7] ELANGOVAN S，PATHANIA R，RAMACHANDRAN S，et al. Mo-lecular mechanism of SLC5A8 inactivation in breast cancer[J]. Mol Cell Biol，2013，33（19）：3920-3935.
[8] THANGARAJU M，CRESCI G，ITAGAKI S，et al. Sodium-coupled transport of the short chain fatty acid butyrate by SLC5A8 and its relevance to colon cancer[J]. J Gastrointest Surg，2008，12：1773-1782.
[9] GUPTA N，MARTIN P M，PRASAD P D，et al. SLC5A8 （SMCT1）-mediated transport of butyrate forms the basis for the tumor suppressive function of the transporter[J]. Life Sci，2006，78（21）：2419-2425.
[10] PARK J Y，KIM D，YANG M，et al. Gene silencing of SLC5A8 identified by genome-wide methylation profiling in lung cancer[J]. Lung Cancer，2013，79（3）：198-204.
[11] SHAIN A H，YEH I，KOVALYSHYN I，et al. The genetic evolution of melanoma from precursor lesions[J]. N Engl J Med，2015，373（20）：1926-1936.
[12] MENEZES M E，TALUKDAR S，WECHMAN S L，et al. Prospects of gene therapy to treat melanoma[J]. Adv Cancer Res，2018，138：213-237.
[13] VIOLA J R，RAFAEL D F，WAGNER E，et al. Gene therapy for adva-nced melanoma：selective targeting and therapeutic nucleic acids[J]. J Drug Deliv，2013：2013：897348.
[14] ANBAZHAGAN A N，PRIYAMVADA S，KUMAR A，et al. miR-29a，b，and c regulate SLC5A8 expression in intestinal epithelial cells[J]. AM J PHYSIOL-GASTR L，2021，321（2）：G223-G231.
[15] ZHANG X M，MENG Q H，KONG F F，et al. SLC5A8 regulates the biological behaviors of cervical cancer cells through mediating the Wnt signaling pathway[J]. Eur Rev Med Pharmaco，2020，24（9）：4679-4686.
[16] 刘岩. 基于CRISPR/Cas9基因编辑技术探讨SLC5A8基因对黑色素瘤微环境细胞免疫功能的影响[D].河北大学，2020.

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备注/Memo

备注/Memo:
基金项目 河北省重点研发计划（21377773D）
作者简介 董玥湘（1998-），女，硕士在读，研究方向：外科学；董玥湘和刘岩为共同第一作者；通信作者：靳小石，E-mail：doctorjinxiaoshi@126.com。
更新日期/Last Update: 2024-03-20