Search

Your search keyword '"Ji, Zhaodong"' showing total 22 results
Start Over Author "Ji, Zhaodong"
22 results on '"Ji, Zhaodong"'

10. A NOTCH1 Mutation Found in a Newly Established Ovarian Cancer Cell Line (FDOVL) Promotes Lymph Node Metastasis in Ovarian Cancer

Author

Jiang, Wei, primary, Ouyang, Xueyan, additional, Jiang, Chunjuan, additional, Yin, Lina, additional, Yao, Qianlan, additional, Pei, Xuan, additional, Ji, Zhaodong, additional, Li, Ming, additional, Song, Shaoli, additional, Yang, Wentao, additional, Huang, Shenglin, additional, Yang, Huijuan, additional, and Shan, Boer, additional

Published
2023
Full Text
View/download PDF

20. Identification of Sca-1+Abcg1+bronchioalveolar epithelial cells as the origin of lung adenocarcinoma in Gprc5a-knockout mouse model through the interaction between lung progenitor AT2 and Lgr5 cells

Author

Yin, Huijing, Jiang, Zhengyu, Feng, Xu, Ji, Zhaodong, and Jin, Wei

Abstract

The reason for the reduced efficacy of lung cancer therapy is the existence of lung cancer stem cells (CSCs). Targeting CSCs results in evolved phenotypes with increased malignancy, leading to therapy failure. Here, we propose a new therapeutic strategy: investigating the “transitional” cells that represent the stage between normal lung stem cells and lung CSCs. Identifying and targeting the key molecule that drives carcinogenesis to inhibit or reverse this process would thus provide new perspectives for early diagnosis and intervention in lung cancer. We used Gprc5a-knockout (KO) mice, the first animal model of spontaneous lung adenocarcinoma established by the deletion of a single lung tumor suppressor gene. We investigated the interaction of lung progenitor cells AT2 with Lgr5 cells in the generation of CSCs and related signaling mechanism. In the present study, using Gprc5a-KO mice, we found the initiator Sca-1+Abcg1+subset with a CSC-like phenotype within the lung progenitor AT2 cell population in mice that had not yet developed tumors. We confirmed the self-renewal and tumor initiation capacities of this subset in vitro, in vivo, and clinical samples. Mechanistically, we found that the generation of Sca-1+Abcg1+cells was associated with an interaction between AT2 and Lgr5 cells and the subsequent activation of the ECM1-α6β4-ABCG1 axis. Importantly, Sca-1+Abcg1+and SPA+ABCG1+cells specifically existed in the small bronchioles of Gprc5a-KO mice and patients with pneumonia, respectively. Thus, the present study unveiled a new kind of lung cancer-initiating cells (LCICs) and provided potential markers for the early diagnosis of lung cancer.

Published
2020
Full Text
View/download PDF

21. ASS1 Enhances Anoikis Resistance via AMPK/CPT1A-mediated Fatty Acid Metabolism in Ovarian Cancer.

Author

Feng X, Ji Z, Fan X, Kong Y, Yu Y, Shao Y, Meng J, Zhou X, Tang R, and Yang G

Abstract

Metastasis is the leading cause of death in ovarian cancer (OC), with anoikis resistance being a crucial step for detached OC cells survival. Despite extensive research, targeting anoikis resistance remians a challenge. Here, we identify argininosuccinate synthase 1 (ASS1), a key enzyme in urea cycle, is markedly upregulated in OC cells in detached culture and is associated with increased anoikis resistance and metastasis. Disruption of the AMP/ATP balance by elevated ASS1 activates AMPK and its downstream factor, CPT1A. Then, ASS1 enhances FAO, leading to higher ATP generation and lipid utilization. Inhibition of CPT1A reverses ASS1-induced FAO. Our study gives some new functional insights into OC metabolism and represents a shift from traditional views, expanding ASS1's relevance beyond nitrogen metabolism to fatty acid metabolism. It uncovers how ASS1-induced FAO disrupts the AMP/ATP balance, leading to AMPK activation. By identifying the ASS1/AMPK/CPT1A axis as crucial for OC anoikis resistance and metastasis, our study opens up new avenues for therapeutic interventions., Competing Interests: Declaration of Competing Interest The authors declare no conflicts of interest., (Copyright © 2024. Published by Elsevier B.V.)

Published
2024
Full Text
View/download PDF

22. The deregulation of arachidonic acid metabolism in ovarian cancer.

Author

Xia Q, Gao W, Yang J, Xing Z, and Ji Z

Abstract

Arachidonic acid (AA) is a crucial polyunsaturated fatty acid in the human body, metabolized through the pathways of COX, LOX, and cytochrome P450 oxidase to generate various metabolites. Recent studies have indicated that AA and its metabolites play significant regulatory roles in the onset and progression of ovarian cancer. This article examines the recent research advancements on the correlation between AA metabolites and ovarian cancer, both domestically and internationally, suggesting their potential use as biological markers for early diagnosis, targeted therapy, and prognosis monitoring., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Xia, Gao, Yang, Xing and Ji.)

Published
2024
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results