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[1]葉洲杰,王心睿.應(yīng)用CRISPR/Cas9技術(shù)敲除甲狀腺乳頭狀癌B-CPAP細(xì)胞FHL1基因及轉(zhuǎn)錄組分析[J].福建醫(yī)藥雜志,2023,45(04):101-106.
　YE Zhoujie,WANG Xinrui.FHL1 gene knockout and transcriptome analysis with CRISPR/Cas9 in human thyroid papillary carcinoma B-CPAP cells[J].FUJIAN MEDICAL JOURNAL,2023,45(04):101-106.
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應(yīng)用CRISPR/Cas9技術(shù)敲除甲狀腺乳頭狀癌B-CPAP細(xì)胞FHL1基因及轉(zhuǎn)錄組分析()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
45
期數(shù):
2023年04期
頁(yè)碼:
101-106
欄目:
基礎(chǔ)研究
出版日期:
2023-08-15

文章信息/Info

Title:
FHL1 gene knockout and transcriptome analysis with CRISPR/Cas9 in human thyroid papillary carcinoma B-CPAP cells
文章編號(hào):
1002-2600(2023)04-0101-06
作者:
葉洲杰; 王心睿1
福建省婦產(chǎn)醫(yī)院 福建省婦幼保健院醫(yī)學(xué)研究中心(福州 350001)
Author(s):
YE Zhoujie;  WANG Xinrui
Fujian Provincial Hospital of Obstetrics and Gynecology,Medical Research Center, Fujian Maternity and Child Health Hospital, Fuzhou, Fujian 350001, China
關(guān)鍵詞:
甲狀腺乳頭狀癌;  FHL1;  RNA-Seq;  CRISPR/Cas9
Keywords:
papillary thyroid carcinoma;  FHL1;  RNA-Seq;  CRISPR/Cas9
分類號(hào):
R736.1
文獻(xiàn)標(biāo)志碼:
A
摘要:
目的 探究FHL1在甲狀腺瘤細(xì)胞中參與的細(xì)胞生物學(xué)功能,為后續(xù)研究FHL1基因介導(dǎo)甲狀腺癌發(fā)生發(fā)展的分子機(jī)制提供依據(jù)。方法 運(yùn)用CRISPR/Cas9基因編輯技術(shù)在甲狀腺乳頭狀癌B-CPAP細(xì)胞系中大片段敲除FHL1基因,CCK-8實(shí)驗(yàn)測(cè)定B-CPAPFHL1-/-細(xì)胞活率,細(xì)胞劃痕實(shí)驗(yàn)計(jì)算B-CPAPFHL1-/-細(xì)胞遷移率,抽提B-CPAP細(xì)胞和B-CPAPFHL1-/-細(xì)胞RNA用于轉(zhuǎn)錄組高通量測(cè)序,并進(jìn)行表達(dá)差異基因KEGG與GO富集分析。結(jié)果 實(shí)驗(yàn)結(jié)果顯示B-CPAP細(xì)胞中FHL1基因缺失35 995 bp,導(dǎo)致蛋白功能被破壞。B-CPAPFHL1-/-細(xì)胞與B-CPAP細(xì)胞相比增殖速率、遷移能力加快。B-CPAP與B-CPAPFHL1-/-細(xì)胞轉(zhuǎn)錄組高通量測(cè)序分析結(jié)果表明,與B-CPAP細(xì)胞相比,B-CPAPFHL1-/-細(xì)胞蛋白編碼基因表達(dá)量分析檢測(cè)到1 813個(gè)差異基因,其中1 125個(gè)基因上調(diào),688個(gè)基因下調(diào)。KEGG通路富集分析發(fā)現(xiàn)細(xì)胞外基質(zhì)受體交互作用、腫瘤信號(hào)通路、細(xì)胞黏附分子信號(hào)通路基因表達(dá)明顯較高,這3條信號(hào)通路對(duì)腫瘤信號(hào)轉(zhuǎn)導(dǎo)、侵襲及轉(zhuǎn)移具有重要作用。對(duì)差異表達(dá)基因進(jìn)行GO富集分析,發(fā)現(xiàn)上述3條信號(hào)通路的多種上調(diào)和下調(diào)表達(dá)基因。結(jié)論 B-CPAPFHL1-/-細(xì)胞可能通過(guò)胞外基質(zhì)受體交互作用、腫瘤信號(hào)通路、細(xì)胞黏附分子等信號(hào)通路上調(diào)相關(guān)基因表達(dá),從而提升細(xì)胞增殖、遷移能力。
Abstract:
Objective To explore the cellular biological function of FHL1 in thyroid tumor cells,and to provide a basis for further research on the molecular mechanism of FHL1 gene mediating the occurrence and development of thyroid cancer. Methods Using CRISPR/Cas9 gene editing technology,FHL1 gene was knocked out in large fragments of thyroid papillary carcinoma B-CPAP cell line,B-CPAPFHL1-/- cell viability was determined by CCK-8 assay,and B-CPAPFHL1-/-cell mobility was calculated by cell scratch assay. B-CPAP cells and B-CPAPFHL1-/- cell RNA were extracted for high-throughput transcriptome sequencing and enrichment analysis of expression differential genes KEGG and GO.Results The results showed a 35 995 bp deletion of the FHL1 gene in B-CPAP cells,resulting in a breakdown of the proteins function. B-CPAPFHL1-/- cells had faster proliferation and migration than B-CPAP cells. High-throughput sequencing analysis of B-CPAP and B-CPAPFHL1-/- cell transcriptome showed that 1 813 differential genes were detected in B-CPAPFHL1-/- cell transcriptome compared with B-CPAP cells,among which 1 125 genes were up-regulated and 688 genes were down-regulated. KEGG pathway enrichment analysis showed that the gene expressions of extracellular matrix receptor interaction,tumor signaling and cell adhesion molecule signaling pathways were significantly higher,and the three signaling pathways played an important role in tumor signal transduction,invasion and metastasis. GO enrichment analysis of differentially expressed genes showed that a variety of up-regulated and down-regulated genes were found in the above three signaling pathways.Conclusion B-CPAPFHL1-/- cells may up-regulate the expression of related genes through signaling pathways such as extracellular matrix receptor interaction,tumor signaling,and cell adhesion molecules,thereby enhancing cell proliferation and migration.

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備注/Memo

備注/Memo:
基金項(xiàng)目:福建省衛(wèi)生健康青年科研課題項(xiàng)目(2019-1-14)
1 通信作者,E-mail:[email protected]
更新日期/Last Update: 2023-08-15