Distal-less homeobox 5 gives rise to myofibroblastic carcinoma-associated fibroblasts to promote collective breast cancer invasion
Tumor-promoting myofibroblastic carcinoma-associated fibroblasts (myCAFs) are induced by activation of transforming growth factor-{beta} signaling. However, the molecular basis of myCAF-specific transcriptional programs regulated by TGF-{beta} signaling remains poorly understood. Using a meta-analysis of single-cell RNA-seq data from 132 human breast tumor and non-tumor tissues, we show that…
Breast cancer tumors are fueled by specialized fibroblasts known as myofibroblastic carcinoma-associated fibroblasts (myCAFs). These cells, which promote the spread of cancer, are activated by the signaling molecule TGF-beta. A recent study has discovered that a gene called Distal-less homeobox 5 (DLX5) plays a key role in the development of myCAFs.
This gene is a master regulator of skeletal development and is expressed at both epigenetic and transcriptional levels in human breast myCAFs. DLX5's activation of TGF-beta signaling is crucial for myCAF formation and cancer progression. The gene works by interacting with proteins involved in the TGF-beta signaling pathway, allowing them to bind to shared regions of DNA and enhance the signaling process.
Additionally, DLX5-expressing myCAFs increase the production of neuropilin-2, a protein that further promotes collective tumor invasion. The researchers conclude that DLX5 is essential for the transformation of breast cancer fibroblasts into aggressive cells that contribute to the spread of the disease.
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