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Publication : Growth of B16F10 cells is enhanced in DJ-1-deficiency pancreas.

First Author  Chien CH Year  2023
Journal  Biochem Biophys Res Commun Volume  682
Pages  359-364 PubMed ID  37839104
Mgi Jnum  J:342354 Mgi Id  MGI:7548050
Doi  10.1016/j.bbrc.2023.10.039 Citation  Chien CH, et al. (2023) Growth of B16F10 cells is enhanced in DJ-1-deficiency pancreas. Biochem Biophys Res Commun 682:359-364
abstractText  Association between cancer risk and Parkinson's disease is still debated. DJ-1, a Parkinson's disease (PD)-related gene, is encoded by PARK-7 gene and its deficiency causes early-onset PD. In our last studies, it was found that the immunosuppressive microenvironment established in DJ-1 knockout (KO) mice can enhance metastasis of melanoma cells to lungs. Therefore, we wanted to further examine whether there were some niche in other organs of DJ-1-deficiency mouse to facilitate cell growth of tumors. We used in vivo tissue-specific models of tumor growth and in vitro cellular model to verify the hypothesis. We also used protein blot assay, cell-adhesion assay and bioinformatic tools to conduct experiments. In the mouse model of subcutaneous injection, there was no difference on tumor growth between WT and DJ-1 KO mice. Moreover, the results of experimental liver metastasis by intrasplenic injection model showed that there was no difference of nodules number in both mice, but a dramatic enhancement of nodule formation and increased mucin4 levels were found in pancreas of DJ-1 KO mice. In cell cultures, we further found that B16F10 cells indeed tended to adhere well to primary DJ-1-deficiency pancreatic epithelial cells, which had higher protein levels of mucin4. Notably, a human database also showed the inverse relationship in human pancreas between DJ-1 and mucin4, and mucin4 down-regulation can reverse the enhanced cellular adhesion in DJ-1 KO pancreatic epithelial cells. These results indicated that DJ-1 KO pancreatic tissue creating an appropriate microenvironment benefited development of the cancer cells.
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