CRIP1参与子宫内膜癌细胞增殖、侵袭、迁移及EMT的作用

淳彩璞; 崔晓宾; 胡建明; 贾薇; 吕新玲; 李美峰; 吴小双

doi:10.16016/j.2097-0927.202204176

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CRIP1参与子宫内膜癌细胞增殖、侵袭、迁移及EMT的作用

基础医学 | 更新时间：2026-01-09

- CRIP1参与子宫内膜癌细胞增殖、侵袭、迁移及EMT的作用
- Roles of cysteine rich protein 1 in proliferation, invasion, migration and epithelial-mesenchymal transition of endometrial cancer cells
- 陆军军医大学学报 2022年44卷第23期页码：2409-2420
- 作者机构：
  
  1.843000 新疆阿克苏，新疆石河子大学医学院第四附属医院病理科
  2.832000 新疆石河子，新疆石河子大学医学院第一附属医院病理科
  3.833200 新疆奎屯，新疆伊犁州奎屯医院病理科
- 作者简介：
  
  [淳彩璞，E-mail: Ccaipu09@163.com CHUN Caipu, E-mail: Ccaipu09@163.com
- 基金信息：
- DOI：10.16016/j.2097-0927.202204176
  中图分类号： R341;R73-37;R737.33
- 收稿：2022-04-24，
  
  修回：2022-08-10，
  
  纸质出版：2022-12-15
- 稿件说明：
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淳彩璞, 崔晓宾, 胡建明, 等. CRIP1参与子宫内膜癌细胞增殖、侵袭、迁移及EMT的作用[J]. 陆军军医大学学报, 2022,44(23):2409-2420.

Caipu CHUN, Xiaobin CUI, Jianming HU, et al. Roles of cysteine rich protein 1 in proliferation, invasion, migration and epithelial-mesenchymal transition of endometrial cancer cells[J]. Journal of Army Medical University, 2022, 44(23): 2409-2420.
淳彩璞, 崔晓宾, 胡建明, 等. CRIP1参与子宫内膜癌细胞增殖、侵袭、迁移及EMT的作用[J]. 陆军军医大学学报, 2022,44(23):2409-2420. DOI： 10.16016/j.2097-0927.202204176.

Caipu CHUN, Xiaobin CUI, Jianming HU, et al. Roles of cysteine rich protein 1 in proliferation, invasion, migration and epithelial-mesenchymal transition of endometrial cancer cells[J]. Journal of Army Medical University, 2022, 44(23): 2409-2420. DOI： 10.16016/j.2097-0927.202204176.

摘要

目的

探究半胱氨酸丰富蛋白1(cysteine rich protein 1，CRIP1)通过与磷酸甘油酸激酶1(phosphoglycerate kinase 1，PGK1)结合对子宫内膜癌(endometrial cancer

EC)细胞体外增殖及转移的调控作用。

方法

收集新疆石河子大学医学院第四附属医院(新疆生产建设兵团第一师医院)2019年2月至2020年12月收治的20例EC患者的组织及癌旁组织标本，GEO2R在线分析CRIP1在EC组织中的表达，RT-qPCR、Western blot检测CRIP1及PGK1在EC细胞和组织中的表达。将EC细胞Ishikawa分为空白对照组、干扰对照组、CRIP1干扰组-1、CRIP1干扰组-2、CRIP1干扰组+过表达对照组、CRIP1干扰组+PGK1过表达组。CCK-8和EdU法分析细胞活性；划痕、transwell实验、Western blot和免疫荧光(immunofluorescence，IF)评估细胞转移；Biogrid数据库和免疫共沉淀(Co-IP)实验分别预测并验证CRIP1与PGK1两者关系。

结果

肿瘤组织和肿瘤细胞中的CRIP1表达水平较正常组织和细胞增加(

0.05)。CRIP1敲低可明显削弱EC细胞增殖、迁移、侵袭和EMT能力(

0.05)。EC细胞中的PGK1表达水平较正常细胞增加(

0.05)。CRIP1与PGK1结合且干扰CRIP1可抑制PGK1表达(

0.05)。在CRIP1敲低的细胞中过表达PGK1可部分恢复EC细胞的恶性行为表型(

0.05)。

结论

敲低CRIP1可显著减弱EC增殖、迁移、侵袭和EMT能力，其机制可能与结合PGK1有关。

Abstract

Objective

To investigate the regulatory roles of cysteine rich protein 1 (CRIP1) in the proliferation and metastasis of endometrial cancer (EC) cells

in vitro

through binding to phosphoglycerate kinase 1 (PGK1).

Methods

The EC tissue samples and adjacent normal tissues were collected from 20 patients admitted in the Fourth Hospital Affiliated to Medical College of Shihezi University (First Division Hospital of Xinjiang Production and Construction Corps) between February 2019 and December 2020. NCBI online database was used to analyze CRIP1 expression in EC tissues. RT-qPCR and Western blotting were also performed to test the levels of CRIP1 and PGK1 in EC cells and tissues. Subsequently

EC Ishikawa cells were divided into control group

CRIP1 interference (shRNA-CRIP1-1 and shRNA-CRIP1-2) groups and control (shRNA-NC) group

CRIP1 interference+PGK1 overexpression (shRNA-CRIP1+Ov-PGK1) group and its control (shRNA-CRIP1+Ov-NC) group. Cell viability was detected by CCK-8 assay and EdU assay. Wound healing

transwell assay

Western blotting and immunofluorescence (IF) assay were conducted to detect the proliferation and metastasis of cells. The relationship between CRIP1 and PGK1 was predicted with Biogrid platform and then verified by co-immunoprecipitation (IP) assay.

Results

The expression level of CRIP1 was increased in the EC tissues and cells than the normal tissues and cells (

0.05). CRIP1 knockdown distinctly hindered the proliferation

migration

invasion and epithelial-mesenchymal transition (EMT) of EC cells (

0.05). PGK1 expression was also enhanced in EC cells as compared with normal cells (

0.05)

while CRIP1 binding to PGK1 as well as CRIP1 knockdown notably inhibited the expression of PGK1 (

0.05). However

overexpression of PGK1 in CRIP1 knockdown cells partially restored the malignant phenotypes of EC cells (

0.05).

Conclusion

CRIP1 deficiency significantly attenuates the proliferation

migration

invasion and EMT of EC cells

and its mechanism may be associated with its binding to PGK1.

关键词

Keywords

references

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