Lhfpl3, lipoma HMGIC fusion partner-like 3, is involved in multiple biological processes, and its dysregulation is associated with various diseases. Although the references do not explicitly state its core function, gene fusions and interactions with miRNAs and lncRNAs related to Lhfpl3 suggest its role in pathways related to cell growth, polarity, and cancer-associated processes [1,2]. Genetic models could potentially be used to further explore its functions.

In a case of dysembryoplastic neuroepithelial tumor, an in-frame fusion between LHFPL3 and NTRK2 was identified, which likely involves aberrant dimerization and constitutive activation of RTK signaling pathways [1]. In glioma cells, miR-218-5p was found to target LHFPL3, and transfection of miR-218-5p reduced cell activity, proliferation, invasive ability, and inhibited epithelial-mesenchymal transitions [2].

In conclusion, while direct evidence from KO/CKO mouse models is lacking in the provided references, the identified gene fusion and miRNA-target interaction suggest Lhfpl3's potential role in tumor-related biological processes, specifically in neuroepithelial and glioma-associated diseases. Further study using genetic models like KO or CKO mouse models could provide more insights into its functions and implications in disease.

References:

1. Chen, Yanming, Zhu, Qing, Wang, Ye, Xiao, Sheng, Lan, Qing. 2022. Case Report: A novel LHFPL3::NTRK2 fusion in dysembryoplastic neuroepithelial tumor. In Frontiers in oncology, 12, 1064817. doi:10.3389/fonc.2022.1064817. https://pubmed.ncbi.nlm.nih.gov/36531047/

2. Li, Zhixiao, Qian, Rongjun, Zhang, Jiadong, Shi, Xiwen. 2019. MiR-218-5p targets LHFPL3 to regulate proliferation, migration, and epithelial-mesenchymal transitions of human glioma cells. In Bioscience reports, 39, . doi:10.1042/BSR20180879. https://pubmed.ncbi.nlm.nih.gov/30314994/