Department of Translational Medicine Informatics, St. Marianna University School of Medicine, Kawasaki, Kanagawa, 216-8511, Japan.
Biosys Technologies, Inc., Tokyo, Tokyo, 153-8904, Japan.
Sci Rep. 2022 Aug 29;12(1):14709. doi: 10.1038/s41598-022-19182-9.
Pancreatic ductal adenocarcinoma (PDAC) is a multifactorial disease, the molecular profile of which remains unclear. This study aimed at unveiling the disease-related protein networks associated with different outcomes of resectable, node-positive PDAC cases. We assessed laser-microdissected cancerous cells from PDAC tissues of a poor outcome group (POG; n = 4) and a better outcome group (BOG; n = 4). Noncancerous pancreatic duct tissues (n = 5) were used as the reference. We identified four representative network modules by applying a weighted network correlation analysis to the obtained quantitative PDAC proteome datasets. Two network modules that were significant for POG were associated with the heat shock response to hypoxia-related stress; in the latter, a large involvement of the non-canonical Hedgehog pathway (regulated by GLI1), the internal ribosome entry site-mediated cap-independent translation, the inositol requiring enzyme 1-alpha (IRE1α)/X-box binding protein 1 pathway of the unfolding protein response (UPR), and the aerobic glycolysis was observed. By contrast, the BOG characteristic module was involved in the inactivation of the UPR pathway via the synoviolin 1-dependent proteasomal degradation of IRE1α, the activation of SOX2, and the loss of PALB2 (partner and localizer of BRCA2) function, all potentially suppressing malignant tumor development. Our findings might facilitate future therapeutic strategies for PDAC.
胰腺导管腺癌(PDAC)是一种多因素疾病,其分子特征尚不清楚。本研究旨在揭示与可切除、有淋巴结转移的 PDAC 病例不同结局相关的疾病相关蛋白网络。我们评估了来自预后不良组(POG;n=4)和预后较好组(BOG;n=4)的 PDAC 组织中经激光微切割的癌细胞。非癌性胰腺导管组织(n=5)用作参考。我们通过对获得的定量 PDAC 蛋白质组数据集应用加权网络相关分析,确定了四个有代表性的网络模块。与 POG 相关的两个显著网络模块与缺氧相关应激的热休克反应有关;在后一个模块中,非经典的 Hedgehog 途径(受 GLI1 调控)、内部核糖体进入位点介导的无帽依赖性翻译、需要酶 1-α(IRE1α)/X-框结合蛋白 1 的未折叠蛋白反应(UPR)途径和有氧糖酵解的大量参与。相比之下,BOG 特征模块涉及通过滑膜蛋白 1 依赖性蛋白酶体降解 IRE1α 使 UPR 途径失活、SOX2 的激活以及 PALB2(BRCA2 的伴侣和定位子)功能丧失,所有这些都可能抑制恶性肿瘤的发展。我们的研究结果可能为 PDAC 的未来治疗策略提供便利。