Dstn, also known as Destrin, is a member of the actin-depolymerizing factor family. It regulates actin dynamics by treadmilling actin filaments and increasing globular actin pools, which is crucial for various biological processes such as cell migration, development, and maintaining proper cell and nuclear morphology. It is associated with pathways like the Wnt/β-catenin signaling pathway, and its dysregulation is linked to multiple diseases [3].

In rectal cancer, DSTN hypomethylation leads to its high expression, which promotes radiotherapy resistance by activating the Wnt/β-catenin signaling pathway. High DSTN expression in neoadjuvant radiation-resistant rectal cancer tissues is associated with shorter disease-free survival. Knockdown of DSTN in colorectal cancer cells promotes their sensitivity to radiotherapy, while overexpression promotes resistance [1].

In cardiac hypertrophy, Snrk -/- mice (a model relevant to DSTN study as SNRK binds to DSTN) display worse cardiac function, increased DNA damage, and chromatin compaction. DSTN down-regulation can reverse these changes along with cellular hypertrophy seen with SNRK knockdown [2].

In lung adenocarcinoma, DSTN is highly expressed, and it promotes cell proliferation, invasion, migration, subcutaneous tumor formation, and lung metastasis. It enhances malignancy by facilitating β-catenin nuclear translocation and inducing epithelial-to-mesenchymal transition (EMT) [4].

In HNSCC, DSTN is significantly overexpressed in tumor cells, and its knockdown inhibits tumor cell proliferation, migration, and invasion [5].

In summary, Dstn plays essential roles in actin-related biological functions. Through gene-knockout and related mouse models, its significance in diseases like rectal cancer, cardiac hypertrophy, lung adenocarcinoma, and HNSCC has been revealed. These findings help in understanding disease mechanisms and potentially identifying new therapeutic targets.