Postn-flox Mouse

Postn, also known as periostin, is an extracellular matrix protein. It is involved in multiple biological processes, such as extracellular matrix remodeling, and is associated with pathways like Wnt/β -catenin, NF -κB, and IL -6/STAT3. It plays a significant role in various biological contexts, including tissue fibrosis, tumor development, and immune regulation [3,6-9]. Genetic models, especially KO/CKO mouse models, can be valuable in further understanding its functions.

In cancer, POSTN + cancer-associated fibroblasts (CAFs) act as immune response barriers. In hepatocellular carcinoma, they hinder T-cell infiltration and reduce immunotherapy efficacy, and interact with SPP1 + macrophages via the IL -6/STAT3 signaling pathway [1]. In non-small cell lung cancer, POSTN + CAFs are enriched in advanced tumors, associate with SPP1 + macrophages, and are related to immune suppression and poor prognosis [2]. In gastric cancer, POSTN secreted by CAFs enhances macrophage chemotaxis through the Akt signaling pathway, leading to immune checkpoint blockade resistance [8]. In acne keloidalis, communication between POSTN + fibroblasts and SPP1 + myeloid cells via the SPP1 axis may contribute to pathogenesis [3].

In idiopathic pulmonary fibrosis, POSTN is up-regulated and may contribute to fibrosis, as knockdown of POSTN attenuates fibrotic marker expression in response to TGF -β1 stimulation [4]. In neuroblastoma, ALK drives tumorigenesis in part through a feedforward loop between POSTN and WNT signaling, and knockdown of POSTN delays adhesion and suppresses proliferation of ALK/MYCN tumors [5]. In intervertebral disc degeneration, POSTN promotes nucleus pulposus cell senescence and extracellular matrix metabolism via activating the Wnt/β -catenin and NF -κB signal pathway, and its inhibition can ameliorate the disease progression [6]. In heart failure, interactions between C-C chemokine receptor type 2 (CCR2) macrophages and fibroblasts mediated by interleukin-1β (IL-1β) signalling drive the emergence of FAP/POSTN fibroblasts, and targeting this signaling reduces myocardial fibrosis and improves cardiac function [7].

In conclusion, Postn is crucial in processes like extracellular matrix remodeling, immune regulation, and tissue fibrosis. Model-based research, especially KO/CKO mouse models, has revealed its role in various diseases, including cancer, fibrosis-related diseases, and heart failure. Understanding Postn provides insights into disease mechanisms and potential therapeutic targets.