Protein tyrosine phosphatase PTPL1 suppresses lung cancer through Src/ERK/YAP1 signaling

Abstract

Background: To reveal the function of protein tyrosine phosphatase-L1 (PTPL1) in lung adenocarcinoma.

Methods: Lung cancer cell lines were transfected with short hairpin RNA against PTPL1 (shPTPL1 group) or negative control (shmock group). Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were used to verify the transfection efficacy. Cell proliferation was analyzed by ethynyldeoxyuridine (EdU), Cell counting kit 8 (CCK8), and colony formation assay after PTPL1 or PTPL1 and yes-associated protein (YAP1) knockdown. The effect of PTPL1 on tumor growth was examined in a xenograft lung cancer model.

Results: PTPL1 was downregulated in various types of lung cancer cell lines. The EdU, CCK8, colony formation assays and investigation using a xenograft lung cancer model indicated that PTPL1 knockdown increased the proliferation of lung cancer cells. Mechanistically, PTPL1 knockdown induced the activation of the Proto-oncogene tyrosine-protein kinase SRC (Src)/Extracellular regulated MAP kinase (ERK) pathway and thereby promoted yes-associated protein (YAP1) nuclear translocation and activation.

Conclusions: In our study, PTPL1 played a crucial suppressive role in the pathogenesis of lung cancer potentially through counteracting the Src/ERK/YAP1 pathway.

Keywords: PTPL1; non-small cell lung cancer; proliferation.