Page 62 - 南京医科大学自然版
P. 62
南京医科大学学报(自然科学版) 第46卷第10期
·1492 · Journal of Nanjing Medical University(Natural Sciences) 2026年10月
·基础研究·
转录因子ZNF326在急性T淋巴细胞白血病细胞中的致病作用
研究
李 易 ,商 艳 ,陆 超 2*
2
1
南京医科大学第三附属医院(常州市第二人民医院)儿科,江苏 常州 213003;南京医科大学第一附属医院儿科,江苏 南
1 2
京 210036
[摘 要] 目的:探讨转录因子锌指蛋白 326(zinc finger protein 326,ZNF326)在急性 T 淋巴细胞白血病(T⁃cell acute lympho⁃
blastic leukemia,T⁃ALL)细胞中的致病作用。方法:使用TARGET 数据库分析ZNF326在T⁃ALL 组织中的表达情况;利用小干
扰 RNA(small interferingRNA,siRNA)技术在 Jurkat 细胞中敲低 ZNF326 和丝氨酸蛋白酶抑制剂 B2(serpin family B member 2,
SERPINB2)的基因表达,用慢病毒转染对 Jurkat 细胞进行 ZNF326 基因过表达,采用逆转录实时荧光定量聚合酶链式反应
(reverse transcription quantitative polymerase chain reaction,RT⁃qPCR)和蛋白质免疫印记实验(Western blot)验证敲低和过表达
效率;CCK⁃8细胞增殖实验分别检测敲低和过表达ZNF326后细胞的增殖能力,并验证敲低其下游靶基因SERPINB2对T⁃ALL
细胞增殖的影响;流式细胞术检测敲低ZNF326对T⁃ALL细胞凋亡以及细胞周期的影响;转录组测序(RNA sequencing,RNA⁃seq)
寻找过表达 ZNF326 的下游靶基因。结果:敲低 ZNF326 可显著抑制 T⁃ALL 细胞的增殖并将细胞周期阻滞在 G1 期;敲低
ZNF326可下调SERPINB2的表达,而特异性敲低SERPINB2同样能够有效抑制T⁃ALL细胞的增殖。结论:ZNF326可能通过调
控SERPINB2的表达,进而促进T⁃ALL细胞的增殖,其可能成为治疗急性T淋巴细胞白血病的新靶点。
[关键词] 急性T淋巴细胞白血病;锌指蛋白326;增殖;凋亡;细胞周期
[中图分类号] R725.2 [文献标志码] A [文章编号] 1007⁃4368(2026)10⁃1492⁃07
doi:10.7655/NYDXBNSN260854
Study on the pathogenic role of transcription factor ZNF326 in acute T⁃cell leukemia cells
2
1
Li Yi ,Shang Yan ,Lu Chao 2*
1 Department of Paediatrics,the Third Affiliated Hospital of Nanjing Medical University(Changzhou Second People’s
Hospital),Changzhou 213003;Department of Paediatrics,the First Affiliated Hospital of Nanjing Medical
2
University,Nanjing 210036,China
[Abstract] Objective:To explore the pathogenic role of transcription factor zinc finger protein 326(ZNF326)in T ⁃ cell acute
lymphoblastic leukemia(T⁃ALL). Methods:The expression of ZNF326 in T⁃ALL tissues was analyzed using the TARGET database.
Small interfering RNA(siRNA)technology was used to knock down the expression of the ZNF326 and serpin family B member 2
(SERPINB2)genes in Jurkat cells,and lentiviral transfection was performed to overexpress ZNF326 gene in Jurkat cells. Reverse
transcription quantitative polymerase chain reaction(RT ⁃ qPCR)and Western blot were used to verify the knockdown and
overexpression efficiency. CCK ⁃ 8 cell proliferation assay was performed to detect the proliferative capacity of cells after ZNF326
knockdown and overexpression,respectively,and to verify the effect of knocking down its downstream target gene SERPINB2 on cell
proliferation. Flow cytometry was used to detect the effect of ZNF326 knockdown on apoptosis and cell cycle in T⁃ALL cells. RNA
sequencing(RNA ⁃ seq)was performed to identify the downstream target genes of ZNF326 overexpression. Results:Knockdown of
ZNF326 significantly inhibited the proliferation of T ⁃ ALL cells and induced G1 phase cell cycle arrest. Knockdown of ZNF326
downregulated the expression of SERPINB2,and specific knockdown of SERPINB2 also effectively inhibited the proliferation of T⁃ALL
cells. Conclusion:ZNF326 may promote the proliferation of T⁃ALL cells by regulating the expression of SERPINB2,and may serve as
[基金项目] 国家自然科学基金(81770162)
通信作者(Corresponding author),E⁃mail:luchaodoctor@163.com(ORCID:0009⁃0004⁃7541⁃0466)
∗

