Ctse, also known as cathepsin E, is an intracellular, hydrolytic aspartic protease. It is expressed in cells of the immune and gastrointestinal systems, lymphoid tissues, erythrocytes, and cancer cells. While its precise functions are not fully understood, it may be involved in antigen presentation in dendritic cells by cleaving bacterial peptides [6].

In cancer research, Ctse has emerged as a significant factor. In bladder cancer, it was part of a disulfidptosis-related gene prognostic model, and POU5F1 can transactivate Ctse, promoting cell proliferation and metastasis [1]. In rectal cancer, its overexpression is related to concurrent chemoradiotherapy (CCRT) resistance and inferior survival [2]. In intrahepatic cholangiocarcinoma, the co-location of MARCO+ tumor-associated macrophages and Ctse+ tumor cells determined a poor prognosis [3]. In liver hepatocellular carcinoma, higher Ctse levels are linked to poorer survival, and siRNA-mediated knockdown suppressed cell proliferation [4]. Also, Ctse may be a potential early biomarker for pancreatic ductal adenocarcinoma (PDAC), and its activity shows potential for PDAC detection [5]. In the context of allogeneic hematopoietic stem cell transplantation, Ctse deficiency ameliorated graft-versus-host disease and modified dendritic cell motility [6].

In conclusion, Ctse is involved in multiple biological processes and diseases, especially cancers. Research on Ctse, including through gene-knockout models as seen in the graft-versus-host disease study, helps to understand its role in disease development and progression, potentially providing new targets for diagnosis and treatment in various cancer types.

References:

1. Chen, Hualin, Yang, Wenjie, Li, Yingjie, Ma, Lin, Ji, Zhigang. 2023. Leveraging a disulfidptosis-based signature to improve the survival and drug sensitivity of bladder cancer patients. In Frontiers in immunology, 14, 1198878. doi:10.3389/fimmu.2023.1198878. https://pubmed.ncbi.nlm.nih.gov/37325625/

2. Chou, Chia-Lin, Chen, Tzu-Ju, Tian, Yu-Feng, Li, Chien-Feng, Lai, Hong-Yue. 2021. CTSE Overexpression Is an Adverse Prognostic Factor for Survival among Rectal Cancer Patients Receiving CCRT. In Life (Basel, Switzerland), 11, . doi:10.3390/life11070646. https://pubmed.ncbi.nlm.nih.gov/34357018/

3. Fan, Guangyu, Tao, Changcheng, Li, Lin, Han, Xiaohong, Shi, Yuankai. 2024. The co-location of MARCO+ tumor-associated macrophages and CTSE+ tumor cells determined the poor prognosis in intrahepatic cholangiocarcinoma. In Hepatology (Baltimore, Md.), , . doi:10.1097/HEP.0000000000001138. https://pubmed.ncbi.nlm.nih.gov/39471066/

4. Liu, Qi, Chen, Junyi, Liu, Yuyang, Zhang, Ning, Yang, Zhanyu. 2024. The impact of cathepsins on liver hepatocellular carcinoma: Insights from genetic and functional analyses. In Gene, 935, 149064. doi:10.1016/j.gene.2024.149064. https://pubmed.ncbi.nlm.nih.gov/39486661/

5. Pontious, Corbin, Kaul, Sabrina, Hong, Marcus, Conwell, Darwin L, Cruz-Monserrate, Zobeida. 2019. Cathepsin E expression and activity: Role in the detection and treatment of pancreatic cancer. In Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 19, 951-956. doi:10.1016/j.pan.2019.09.009. https://pubmed.ncbi.nlm.nih.gov/31582345/

6. Mengwasser, Jörg, Babes, Liane, Cordes, Steffen, Reinheckel, Thomas, Penack, Olaf. 2017. Cathepsin E Deficiency Ameliorates Graft-versus-Host Disease and Modifies Dendritic Cell Motility. In Frontiers in immunology, 8, 203. doi:10.3389/fimmu.2017.00203. https://pubmed.ncbi.nlm.nih.gov/28298913/