CXCL12 alone is enough to Reprogram Normal Fibroblasts into Cancer-Associated Fibroblasts.

ABSTRACT: Cancer-associated fibroblasts (CAFs) are critical components of the tumor microenvironment (TME), playing significant roles in regulating cancer progression. However, the underlying mechanism of CAFs activation remains elusive. In this study, we aim to investigates the mechanisms by which CAFs promote the conversion of normal fibroblasts (NFs) to CAFs in lung cancer, with a focus on the role of p53 mutations and the CXCL12/STAT3 signaling axis. We found that CAFs significantly induced NFs to acquire CAFs properties (called CEFs), including upregulation of α-SMA and Vimentin, enhanced proliferation and migration, and increased ability to promote lung cancer cell migration. In vivo, CEFs accelerated A549 xenograft growth and induced spontaneous lung metastasis. CXCL12 was identified as a key

SUBMITTER: Ma Z 

PROVIDER: S-EPMC11978793 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature