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- 저자 : Gao Huijie (검색결과 2 건)
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The upregulation of keratocan promotes the progression of human pancreatic cancer
Gao Huijie,Qian Ruikun,Ren Qiang,Zhang Litao,Qin Wei,Zhou Caiju,Wang Huiyun,Liu Chao,Zhang Yuntao 대한독성 유전단백체 학회 2024 Molecular & cellular toxicology Vol.20 No.2
Background The role of the extracellular matrix (ECM) in oncogenic contexts has been studied previously, but the expression patterns and functional role of keratocan, a classical small leucine-rich proteoglycan found in the ECM, in tumors remain poorly understood. As pancreatic cancer (PC) is characterized by desmoplasia in the ECM, this study sought to assess the significance of keratocan in PC. Objective In this study, Gene Expression Profiling Interactive Analysis (GEPIA) was first used to analyze the expression pattern of keratocan in PC. Keratocan, P53, and P21 levels were evaluated in PDAC patient tissues and the role of keratocan was additionally directly assessed via transfecting PDAC cell lines with a pENTER-human keratocan construct. Results Patients with PC showing high levels of keratocan had low survival rates. A significantly upregulated expression of keratocan was observed in the PC tumor tissues in comparison to healthy paracancerous tissues. Keratocan upregulation in BxPC-3 and PANC-1 cells markedly enhanced their proliferation and migration, but reduced cellular apoptosis. Furthermore, the P53 and P21 expression levels were significantly reduced in pancreatic ductal adenocarcinoma cells overexpressing keratocan. P53 and P21 were downregulated in PC tumor tissues. Conclusions All results showed that keratocan played important roles in the promoting of PC. Background The role of the extracellular matrix (ECM) in oncogenic contexts has been studied previously, but the expression patterns and functional role of keratocan, a classical small leucine-rich proteoglycan found in the ECM, in tumors remain poorly understood. As pancreatic cancer (PC) is characterized by desmoplasia in the ECM, this study sought to assess the significance of keratocan in PC. Objective In this study, Gene Expression Profiling Interactive Analysis (GEPIA) was first used to analyze the expression pattern of keratocan in PC. Keratocan, P53, and P21 levels were evaluated in PDAC patient tissues and the role of keratocan was additionally directly assessed via transfecting PDAC cell lines with a pENTER-human keratocan construct. Results Patients with PC showing high levels of keratocan had low survival rates. A significantly upregulated expression of keratocan was observed in the PC tumor tissues in comparison to healthy paracancerous tissues. Keratocan upregulation in BxPC-3 and PANC-1 cells markedly enhanced their proliferation and migration, but reduced cellular apoptosis. Furthermore, the P53 and P21 expression levels were significantly reduced in pancreatic ductal adenocarcinoma cells overexpressing keratocan. P53 and P21 were downregulated in PC tumor tissues. Conclusions All results showed that keratocan played important roles in the promoting of PC.
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Shi Si,Gu Huijie,Xu Jinyuan,Sun Wan,Liu Caiyin,Zhu Tong,Wang Juan,Gao Furong,Zhang Jieping,Ou Qingjian,Jin Caixia,Xu Jingying,Chen Hao,Li Jiao,Xu Guotong,Tian Haibin,Lu Lixia 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Excessive osteoclast activation, which depends on dramatic changes in actin dynamics, causes osteoporosis (OP). The molecular mechanism of osteoclast activation in OP related to type 1 diabetes (T1D) remains unclear. Glia maturation factor beta (GMFB) is considered a growth and differentiation factor for both glia and neurons. Here, we demonstrated that Gmfb deficiency effectively ameliorated the phenotype of T1D-OP in rats by inhibiting osteoclast hyperactivity. In vitro assays showed that GMFB participated in osteoclast activation rather than proliferation. Gmfb deficiency did not affect osteoclast sealing zone (SZ) formation but effectively decreased the SZ area by decreasing actin depolymerization. When GMFB was overexpressed in Gmfb-deficient osteoclasts, the size of the SZ area was enlarged in a dose-dependent manner. Moreover, decreased actin depolymerization led to a decrease in nuclear G-actin, which activated MKL1/SRF-dependent gene transcription. We found that pro-osteoclastogenic factors (Mmp9 and Mmp14) were downregulated, while anti-osteoclastogenic factors (Cftr and Fhl2) were upregulated in Gmfb KO osteoclasts. A GMFB inhibitor, DS-30, targeting the binding site of GMFB and Arp2/3, was obtained. Biocore analysis revealed a high affinity between DS-30 and GMFB in a dose-dependent manner. As expected, DS-30 strongly suppressed osteoclast hyperactivity in vivo and in vitro. In conclusion, our work identified a new therapeutic strategy for T1D-OP treatment. The discovery of GMFB inhibitors will contribute to translational research on T1D-OP.
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