TGF‑β1 induces CREB1‑mediated miR‑1290 upregulation to antagonize lung fibrosis via Napsin A.

ABSTRACT: The pathologic mechanisms of pulmonary fibrosis (PF), one of the most common chronic pulmonary diseases, remain unclear. Napsin A is an aspartic proteinase that has been regarded as a hallmark of pulmonary adenocarcinoma. The present study aimed to investigate the specific function and molecular mechanisms of Napsin A in PF from the perspective of microRNA (miRNA or miR) regulation. In the present study, it was found that miR‑1290 downregulated the expression of Napsin A by binding to its 3'‑UTR. Cell viability was examined by MTT assay. The protein levels of α‑smooth muscle actin (α‑SMA), Collagen I and Napsin A were examined by western blot analysis. The predicted targeting of Napsin A by miR‑1290 was validated by luciferase reporter assay. The protein content of α‑SMA was examined by imm

SUBMITTER: Guan S 

PROVIDER: S-EPMC7255477 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature