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2. FKBP3 aggravates the malignant phenotype of diffuse large B‐cell lymphoma by PARK7‐mediated activation of Wnt/β‐catenin signalling.

Author

Xing, Xiaojing, Liu, Meichen, Wang, Xuguang, Guo, Qianxue, Wang, Hongyue, and Wang, Wenxue

Subjects
DIFFUSE large B-cell lymphomas, RITUXIMAB, FORKHEAD transcription factors
Abstract

Diffuse large B‐cell lymphoma (DLBCL) is difficult to treat due to the high recurrence rate and therapy intolerance, so finding potential therapeutic targets for DLBCL is critical. FK506‐binding protein 3 (FKBP3) contributes to the progression of various cancers and is highly expressed in DLBCL, but the role of FKBP3 in DLBCL and its mechanism are not clear. Our study demonstrated that FKBP3 aggravated the proliferation and stemness of DLBCL cells, and tumour growth in a xenograft mouse model. The interaction between FKBP3 and parkinsonism associated deglycase (PARK7) in DB cells was found using co‐immunoprecipitation assay. Knockdown of FKBP3 enhanced the degradation of PARK7 through increasing its ubiquitination modification. Forkhead Box O3 (FOXO3) belongs to the forkhead family of transcription factors and inhibits DLBCL, but the underlying mechanism has not been reported. We found that FOXO3 bound the promoter of FKBP3 and then suppressed its transcription, eventually weakening DLBCL. Mechanically, FKBP3 activated Wnt/β‐catenin signalling pathway mediated by PARK7. Together, FKBP3 increased PARK7 and then facilitated the malignant phenotype of DLBCL through activating Wnt/β‐catenin pathway. These results indicated that FKBP3 might be a potential therapeutic target for the treatment of DLBCL. [ABSTRACT FROM AUTHOR]

Published
2024
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7. ZNF259 promotes breast cancer cells invasion and migration via ERK/GSK3β/snail signaling

Author

Xiang Li, Bin Liu, Xu Tonghong, Guo Qianxue, Xiaojing Xing, and Ke Xu

Subjects
0301 basic medicine, MAPK/ERK pathway, Small interfering RNA, U0126, Biology, 03 medical and health sciences, 0302 clinical medicine, Breast cancer, p-ERK, medicine, p-GSK3β, ZO-1, Original Research, Gene knockdown, ZPR1, E-cadherin, Transfection, medicine.disease, 030104 developmental biology, Oncology, Cancer Management and Research, 030220 oncology & carcinogenesis, Cancer cell, Cancer research, Signal transduction, Tyrosine kinase
Abstract

Bin Liu,1 Xiaojing Xing,1 Xiang Li,2 Qianxue Guo,1 Tonghong Xu,1 Ke Xu3 1Medical Oncology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning Province, People’s Republic of China; 2Breast Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning Province, People’s Republic of China; 3Thoracic Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning Province, People’s Republic of China Purpose: Zinc finger protein 259 (ZNF259), also known as ZPR1, is a zinc finger-containing protein that can bind the intracellular tyrosine kinase domain of EGFR. At present, our knowledge on ZNF259 in cancers is limited. Here, we aimed to explore the biological functions of ZNF259 in breast cancer and reveal their mechanisms.Patients and methods: The expression of ZNF259 was measured in 133 cases of breast cancer by immunohistochemistry. The online database Kaplan–Meier (KM) Plotter Online Tool was used to analyze the relationship between ZNF259 expression and breast cancer patient survival prognosis. Plasmid transfection and small interfering RNA and inhibitor treatments were carried out to explore the functions of ZNF259 in breast cancer cell lines and its potential mechanism. Matrigel invasion and wound healing assays were performed to detect the invasion and migration ability of cancer cells. In addition, protein expressions in tissues and cells were determined by Western blotting.Results: ZNF259 expression was much higher in breast cancer cells than in the adjacent normal breast duct glandular epithelial cells (75.94% vs 7.52%, P

Published
2018

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