Background The various pathogenesis between Clear cell renal carcinoma (CCRCC) and Chromophobe renal carcinoma (CHRCC) contributes to the different tumor growth rate and metastasis. In this study, we explored the distinct proteomic profiles between these two cancers and found different expression of glycogen phosphorylases in two cancers. Methods We explored novel targets by proteomics. Five CCRCC cases and five CHRCC cases were selected for tandem mass tag-labeling liquid chromatography-mass spectroscopy (LC-MS). Gene ontology and KEGG pathway were applied for bioinformatic analysis. Glycogen phosphorylases were detected by Western blotting. Results CHRCC were younger, more commonly female, and had larger tumors compared to those with CCRCC. 101 differentially expressed proteins (DEPs) in CCRCC and 235 DEPs in CHRCC were detected by LC-MS. It was found that disruption of metabolic pathways, epithelial cell differentiation, and cell response were the common characters for two tumor types. Activation of cell-cell adhesion and oxidation-reduction process stimulate CCRCC growth and epithelial cell differentiation and transferrin transport was involved in CHRCC growth, We also found that oxidative phosphorylation is activated in CHRCC and inhibited in CCRCC. More importantly, we found and confirmed that upregulation of glycogen phosphorylase liver type in CCRCC and glycogen phosphorylase brain type in CHRCC mediated differential glycogenolysis in the two tumor types, which could serve as potential therapeutic targets. Conclusion We found different expression of glycogen phosphorylases in CCRCC and CHRCC by quantitative proteomics, which provides potential therapeutic targets in the future.

中文翻译：

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肾透明细胞肾癌和嫌色细胞肾癌中糖原磷酸化酶的不同表达。


背景 透明细胞肾癌（CCRCC）和嫌色肾癌（CHRCC）之间不同的发病机制导致了不同的肿瘤生长速度和转移。在这项研究中，我们探索了这两种癌症之间不同的蛋白质组谱，并发现两种癌症中糖原磷酸化酶的表达不同。方法我们通过蛋白质组学探索新的靶标。选择 5 个 CCRCC 病例和 5 个 CHRCC 病例进行串联质量标签标记液相色谱-质谱 (LC-MS)。应用基因本体论和KEGG通路进行生物信息分析。通过蛋白质印迹法检测糖原磷酸化酶。结果 与 CCRCC 患者相比，CHRCC 患者更年轻，女性更常见，且肿瘤更大。 LC-MS检测到CCRCC中101个差异表达蛋白（DEP）和CHRCC中235个DEP。研究发现，代谢途径、上皮细胞分化和细胞反应的破坏是两种肿瘤类型的共同特征。细胞间粘附和氧化还原过程的激活刺激CCRCC生长和上皮细胞分化，转铁蛋白转运参与CHRCC生长，我们还发现氧化磷酸化在CHRCC中被激活而在CCRCC中被抑制。更重要的是，我们发现并证实了CCRCC肝型糖原磷酸化酶和CHRCC脑型糖原磷酸化酶的上调介导了两种肿瘤类型的差异糖原分解，这可以作为潜在的治疗靶点。结论 我们通过定量蛋白质组学发现CCRCC和CHRCC中糖原磷酸化酶的不同表达，为未来提供潜在的治疗靶点。