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Pancreatic Neoplasms: HELP
Articles by Z. Fang
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Z. Fang wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article PKR2 and β-catenin genes regulates pancreatic cancer chemosensitivity. 2017

Zhong, R-L / Li, Y / Fang, Z / Fang, K-F / Wang, L. ·Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. liwang1456@hotmail.com. ·Eur Rev Med Pharmacol Sci · Pubmed #28121357.

ABSTRACT: OBJECTIVE: Pancreas is a well developed glandular organ lying behind the stomach. Cancer arises in this organ are difficult to identify in the initial stages, even in advanced stages it shows non-specific symptoms, and it is difficult to prognosis. Since they are identified and treated in the last stage, they are less responsive to chemotherapy. Therefore, it is important to study the proteins that are involved in regulating chemosensitivity and chemoresistance. MATERIALS AND METHODS: Initially, using KRAS mutant mice, we developed initial and advanced stage of pancreatic cancer. And we analyzed the expression of PKR2 and β-catenin in different pathological stages of pancreatic cancer using Immunohistology and Western blotting. RESULTS: The histology of the tissue nature confirms and helps to categorize cancer, which shows enlarged nucleus in initial stages and shows clustering of cells in advanced stages. Immunohistological and Western blotting analyzes show prominent increasing in the expression of PKR2 and β-catenin as the tumor develops to the next stages. On the course of initial treatment with cisplatin we find out that PKR2 and β-catenin regulate the chemosensitivity with under-expression when compared with respective controls. In the advanced stages of pancreatic cancer with cisplatin treatment, we observed chemoresistance behavior with overexpression, especially for β-catenin. CONCLUSIONS: The results conclude that using PKR2 and β-catenin we are able to assess the chemosensitivity and chemoresistance nature of pancreatic cancer.

2 Article Profilin 1 potentiates apoptosis induced by staurosporine in cancer cells. 2013

Yao, W / Cai, X / Liu, C / Qin, Y / Cheng, H / Ji, S / Xu, W / Wu, C / Chen, T / Xu, J / Long, J / Fang, Z / Qu, B / Hoth, M / Ni, Q / Zha, X / Yu, X. ·Department of Pancreas and Hepatobiliary Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, P.R. China. ·Curr Mol Med · Pubmed #23331014.

ABSTRACT: The correlation between the loss of Profilin 1 (Pfn1) with tumor progression indicated that Pfn1 is a tumor suppressor in human carcinoma. The molecular mechanisms underlying Pfn1 tumor suppression has yet to be elucidated. In this study, we showed that Pfn1 overexpression sensitizes cancer cells to apoptosis through the typical intrinsic apoptotic pathway. Mechanistically, the increased Pfn1 expression mediated the upregulation of p53R273H, one of the most common tumor-associated hotspot mutations of p53, with transactivation deletion in tumorigenesis and increased localization of p53R273H in cytoplasm. Further studies showed that mutant p53R273H was involved in apoptosis induced by Staurosporine (STS) via transcription-independent mitochondrial functions. We observed (i) the increased cytosolic localization of p53R273H, (ii) the activation of phosphorylation at Ser15, (iii) its mitochondrial localization; Pfn1 acted as a positive regulator of these processes. We also found that Pfn1 interacted with p53R273H and thus facilitated its exertion over the transcription-independent activity in the cytoplasm during drug action. Our results define a new function and mechanism of Pfn1 demonstrating that the combined effect with apoptotic agents led to a synergistic increase in apoptosis. In addition, p53R273H abrogating DNA binding was found to play a major role in the Pfn1- sensitized apoptosis through a transactivation-independent and cytosolic activity.