Li Chao, An Ming-Xin, Jiang Jing-Yi, Yao Han-Bing, Li Si, Yan Jing, Li Xin-Yu, Wang Hua-Qin
Department of Biochemistry and Molecular Biology, China Medical University, Shenyang, China.
Key Laboratory of Cell Biology, Ministry of Public Health, and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China.
Front Oncol. 2019 Apr 2;9:225. doi: 10.3389/fonc.2019.00225. eCollection 2019.
Pancreatic stellate cells (PSCs) are a subset of pancreatic cancer-associated fibroblasts, which play a critical role in pancreatic fibrosis, a characteristic feature of pancreatic cancer. The interplay between PSCs and pancreatic cancer cells is vital for promotion of tumor progression and metastasis. BAG3 is correlated with poor prognostics in patients with pancreatic ductal adenocarcinoma (PDAC), however, the exact mechanisms remain largely unknown. In this study, we demonstrated that BAG3 downregulation decreased IL6 release by PDACs, and IL6 reduction was, at least partially, responsible for suppression of PSCs activation by PDACs with BAG3 downmodulation. Importantly, BAG3 expression positively correlated with fibrosis in pancreatic cancer tissue. With regard to the underlying mechanism, we demonstrated that BAG3 knockdown facilitated recruitment of Agonaute 2 (Ago2) to IL6 mRNA, resulting in destabilization of IL6 mRNA. In addition, the current study demonstrated that phosphorylation at Serine (Ser) 387 site was required for recruitment of Ago2-containing miRISC to IL6 mRNA and BAG3 knockdown facilitated Ago2 loading to IL6 mRNA via increasing its phosphorylation at Ser 387. This study shed new light on the tumor-promoting role of BAG3 in PDAC tumors, suggesting BAG3 might represent an interesting therapeutic opportunity to PDAC patients.
胰腺星状细胞(PSCs)是胰腺癌相关成纤维细胞的一个亚群,在胰腺纤维化(胰腺癌的一个特征性表现)中起关键作用。PSCs与胰腺癌细胞之间的相互作用对于促进肿瘤进展和转移至关重要。BAG3与胰腺导管腺癌(PDAC)患者的不良预后相关,然而,确切机制仍 largely未知。在本研究中,我们证明BAG3下调会减少PDAC细胞释放白细胞介素6(IL6),并且IL6的减少至少部分地导致了BAG3下调的PDAC细胞对PSCs激活的抑制。重要的是,BAG3表达与胰腺癌组织中的纤维化呈正相关。关于潜在机制,我们证明BAG3敲低促进了AGO2(Ago2)与IL6 mRNA的结合,导致IL6 mRNA不稳定。此外,当前研究表明,丝氨酸(Ser)387位点的磷酸化是含Ago2的miRISC与IL6 mRNA结合所必需的,并且BAG3敲低通过增加其Ser 387位点的磷酸化促进了Ago2加载到IL6 mRNA上。这项研究为BAG3在PDAC肿瘤中的促肿瘤作用提供了新的线索,表明BAG3可能为PDAC患者提供一个有意义的治疗机会。