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[1]王学敏,吴琼,赵智刚,等.MAPKAPK2抑制剂联合PTX抑制舌鳞状细胞癌进展的研究[J].天津医科大学学报,2025,31(05):459-463.[doi:10.20135/j.issn.1006-8147.2025.05.0459]
　WANG Xuemin,WU Qiong,ZHAO Zhigang,et al.Study on MAPKAPK2 inhibitor combined with PTX to inhibit progression of tongue squamous cell carcinoma[J].Journal of Tianjin Medical University,2025,31(05):459-463.[doi:10.20135/j.issn.1006-8147.2025.05.0459]
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MAPKAPK2抑制剂联合PTX抑制舌鳞状细胞癌进展的研究(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
31卷
期数:
2025年05期
页码:
459-463
栏目:
基础医学
出版日期:
2025-09-20

文章信息/Info

Title:
Study on MAPKAPK2 inhibitor combined with PTX to inhibit progression of tongue squamous cell carcinoma
文章编号:
1006-8147(2025)05-0459-05
作者:
王学敏1; 吴琼1; 赵智刚1; 李春燕2
1．天津市第一中心医院肿瘤内科，天津300192；2.曲靖市第一人民医院肿瘤科，曲靖655000
Author(s):
WANG Xuemin1;  WU Qiong1;  ZHAO Zhigang1;  LI Chunyan2
1.Medical Oncology， Tianjin First Central Hospital， Tianjin 300192， China；2.Medical Oncology， Qujing No.1 Hospital， Qujing 655000， China
关键词:
舌鳞状细胞癌; CRISPR文库; 紫杉醇; MAPKAPK2
Keywords:
tongue squamous cell carcinoma;  CRISPR library;  paclitaxel;  MAPKAPK2
分类号:
R739.8
DOI:
10.20135/j.issn.1006-8147.2025.05.0459
文献标志码:
A
摘要:
目的：探索与紫杉醇（PTX）联合应用可抑制舌鳞状细胞癌进展的新药物。方法：首先舌鳞状细胞癌Scc9细胞感染CRISPR全基因组文库，加入PTX处理后提取DNA，进行测序分析。然后通过分别敲除候选基因并加入PTX观察细胞活力确定研究靶点。最后Scc9细胞分别经对照组、PTX、靶点抑制剂及两药联合的不同处理，通过CCK8实验、平板克隆形成实验和EdU实验检测不同处理方式对细胞增殖活力、克隆形成能力和DNA合成能力的影响。结果：CRISPR文库筛选结果经验证发现敲除丝裂原活化蛋白激酶活化蛋白激酶2（MAPKAPK2）基因后加入PTX，Scc9细胞的增殖活力显著降低（F=21.42，P＜0.05）。与对照组、PTX、MAPKAPK2抑制剂MK2-IN-1单药组相比，两药联合显著抑制细胞增殖活力（F=65.39， P＜0.001）。PTX联合MK2-IN-1组的克隆形成能力明显减弱（F=88.69，P＜0.001）。联合用药组DNA合成能力显著降低（F=38.8，P＜0.001）。结论：MAPKAPK2是促进舌鳞状细胞癌进展的潜在靶点。MAPKAPK2抑制剂联合PTX可抑制舌鳞状细胞癌进展。
Abstract:
Objective： To investigate novel drug combinations with paclitaxel （PTX） that have the potential to suppress the progression of tongue squamous cell carcinoma. Methods： Firstly， Scc9 cells of tongue squamous cell carcinoma were transduced with a genome-wide CRISPR library and subjected to PTX. DNA was extracted for sequencing analysis. Then， a target was determined by CRISPR-mediated gene knockout and cell viability assessment after adding PTX. Finally， Scc9 cells were subjected to control， PTX monotherapy， inhibitor monotherapy and combination therapy，the effects of different treatment methods on cell proliferation activity， clone formation ability， and DNA synthesis ability were evaluated using CCK-8 proliferation assay， platecolony formation assay and EdU assay. Results： Subsequent validation of the CRISPR library screening results revealed that mitogen activated protein kinase activated protein kinase 2 （MAPKAPK2） gene knockout and adding PTX significantly inhibited the cell proliferation viability of Scc9 cells （F=21.42， P＜0.05）. MAPKAPK2 inhibitor MK2-IN-1 combined with PTX demonstrated superior cell proliferation activity inhibition versus control or monotherapies in Scc9 cells （F=65.39， P<0.001）. PTX combined with MK2-IN-1 group significantly reduced colony formation（F=88.69， P＜0.001）. The DNA synthesis ability was significantly inhibited in combination therapy group （F=38.8， P<0.001）.Conclusion： MAPKAPK2 is a potential therapeutic target in promoting the progression of tongue squamous cell carcinoma. MAPKAPK2 inhibitor combined with PTX can inhibit the progression of tongue squamous cell carcinoma.

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备注/Memo

备注/Memo:
基金项目:曲靖市第一人民医院院级课题（2023YJKTB01）
作者简介:王学敏（1991-），女，主治医师，博士，研究方向：头颈部肿瘤的基础与临床；通信作者：李春燕，E-mail： 2378384250@qq.com。
更新日期/Last Update: 2025-10-01