CD164, also known as endolyn, is a sialomucin. It is highly expressed by primitive hematopoietic progenitor cells and is implicated in mediating or regulating hematopoietic precursor cell adhesion to stroma, and may serve as a negative regulator of hematopoietic progenitor cell proliferation [2]. It has also been found to be involved in multiple biological processes related to diseases, such as allergic inflammation, viral entry, and tumorigenesis [1,3,4,5,7,8].

In allergic inflammation, allergen-induced CD164 upregulation on basophils shows promise as a diagnostic marker for pollen and potentially other allergies [1]. In terms of tumor-related research, in glioblastoma, depletion of CD164 with siRNA reduced cell proliferation, migration, and invasiveness, and it was proposed as a potential molecular marker and therapeutic target [4]. In bladder cancer, silencing CD164 inhibited tumor progression both in vitro and in vivo, suggesting it may be an effective treatment target [5]. In glioma, knockdown of CD164 inhibited cell proliferation and promoted apoptosis, likely via the PTEN/PI3K/AKT pathway [7]. In ovarian cancer, CD164 overexpression promoted tumorigenesis through the SDF-1α/CXCR4 axis [8]. Also, CD164 is associated with clonal hematopoiesis as genes at new loci implicate it in hematopoietic stem cell migration/homing [6].

In conclusion, CD164 plays diverse and important roles in biological processes, especially in allergic inflammation, tumorigenesis, and hematopoietic-related events. The findings from functional studies, such as knockdown experiments in various cell lines representing different disease models, highlight its potential as a diagnostic marker and therapeutic target in diseases like allergies, glioblastoma, bladder cancer, glioma, and ovarian cancer. These studies contribute to a better understanding of the underlying mechanisms of these diseases and may offer new strategies for treatment.

References:

1. Wolanczyk-Medrala, Anna, Barg, Wojciech, Medrala, Wojciech. . CD164 as a Basophil Activation Marker. In Current pharmaceutical design, 17, 3786-96. doi:. https://pubmed.ncbi.nlm.nih.gov/22103850/

2. Watt, S M, Chan, J Y. . CD164--a novel sialomucin on CD34+ cells. In Leukemia & lymphoma, 37, 1-25. doi:. https://pubmed.ncbi.nlm.nih.gov/10721766/

3. Bakkers, Mark J G, Moon-Walker, Alex, Herlo, Rasmus, Kirchhausen, Tomas L, Whelan, Sean P J. 2022. CD164 is a host factor for lymphocytic choriomeningitis virus entry. In Proceedings of the National Academy of Sciences of the United States of America, 119, e2119676119. doi:10.1073/pnas.2119676119. https://pubmed.ncbi.nlm.nih.gov/35235462/

4. Wang, Chung-Ching, Hueng, Dueng-Yuan, Huang, Ai-Fang, Huang, Shih-Ming, Yi-Hsin Chan, James. 2019. CD164 regulates proliferation, progression, and invasion of human glioblastoma cells. In Oncotarget, 10, 2041-2054. doi:10.18632/oncotarget.26724. https://pubmed.ncbi.nlm.nih.gov/31007847/

5. Zhang, Xiao-Guang, Zhang, Tong, Li, Chang-Ying, Zhang, Ming-Hao, Chen, Fang-Min. 2018. CD164 promotes tumor progression and predicts the poor prognosis of bladder cancer. In Cancer medicine, 7, 3763-3772. doi:10.1002/cam4.1607. https://pubmed.ncbi.nlm.nih.gov/30022623/

6. Kar, Siddhartha P, Quiros, Pedro M, Gu, Muxin, Burgess, Stephen, Vassiliou, George S. 2022. Genome-wide analyses of 200,453 individuals yield new insights into the causes and consequences of clonal hematopoiesis. In Nature genetics, 54, 1155-1166. doi:10.1038/s41588-022-01121-z. https://pubmed.ncbi.nlm.nih.gov/35835912/

7. Tu, Ming, Cai, Lin, Zheng, Weiming, Chen, Yong, Qi, Songtao. 2017. CD164 regulates proliferation and apoptosis by targeting PTEN in human glioma. In Molecular medicine reports, 15, 1713-1721. doi:10.3892/mmr.2017.6204. https://pubmed.ncbi.nlm.nih.gov/28259931/

8. Huang, Ai-Fang, Chen, Min-Wei, Huang, Shih-Ming, Lai, Hung-Cheng, Chan, James Yi-Hsin. 2013. CD164 regulates the tumorigenesis of ovarian surface epithelial cells through the SDF-1α/CXCR4 axis. In Molecular cancer, 12, 115. doi:10.1186/1476-4598-12-115. https://pubmed.ncbi.nlm.nih.gov/24094005/