Crabp2-flox Mouse

CRABP2, or Cellular retinoic acid-binding protein 2, is involved in retinoid partitioning between different nuclear receptors. It participates in various biological processes, potentially influencing cell proliferation, motility, apoptosis, and immune-related pathways. It is associated with pathways like Wnt/β-catenin, integrin/FAK/AKT, and epithelial-mesenchymal transition (EMT) [3,4,5,6].

In melanoma, high CRABP2 levels predicted poor prognosis in PD-1 inhibitor-treated patients, and it may regulate immunotherapy by influencing cancer-associated fibroblasts (CAFs) infiltration [1]. In endometrial cancer, high CRABP2 expression was related to serous EC, reduced overall survival, advanced stage and grade [2]. In Hu sheep dermal papilla cells, overexpression of CRABP2 facilitated cell proliferation via the Wnt/β-catenin pathway [3]. In thyroid cancer, CRABP2 was associated with recurrence and promoted invasion via the integrin/FAK/AKT pathway [4]. In lung cancer, it promoted metastasis via HuR and integrin β1/FAK/ERK signaling [5]. In serous ovarian cancer cells, it accelerated EMT by promoting TRIM16 methylation via upregulating EZH2 expression [6]. In prostate cancer, it facilitated cell migration and invasion by activating PI3K/AKT and MAPK signaling pathways through upregulating LAMB3 [7]. In human osteoblast cells, overexpression of CRABP2 inhibited dexamethasone-induced apoptosis [8]. In breast cancer, it was identified as an oncogene promoting tumour cell proliferation, migration, and invasion [9].

In conclusion, CRABP2 is involved in multiple biological functions including cell proliferation, apoptosis, invasion, and immune-related processes. Studies on CRABP2, especially through in vivo models, have revealed its significant roles in various cancers such as melanoma, endometrial, thyroid, lung, ovarian, prostate, and breast cancers, providing potential biomarker and therapeutic target implications for these disease areas.