| Autor: |
CHUN Caipu, CUI Xiaobin, HU Jianming, JIA Wei, LYU Xinling |
| Jazyk: |
čínština |
| Rok vydání: |
2022 |
| Předmět: |
|
| Zdroj: |
陆军军医大学学报, Vol 44, Iss 23, Pp 2409-2420 (2022) |
| Druh dokumentu: |
article |
| ISSN: |
2097-0927 |
| DOI: |
10.16016/j.2097-0927.202204176 |
| Popis: |
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 (P < 0.05). CRIP1 knockdown distinctly hindered the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of EC cells (P < 0.05). PGK1 expression was also enhanced in EC cells as compared with normal cells (P < 0.05), while CRIP1 binding to PGK1 as well as CRIP1 knockdown notably inhibited the expression of PGK1 (P < 0.05). However, overexpression of PGK1 in CRIP1 knockdown cells partially restored the malignant phenotypes of EC cells (P < 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. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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