Abstract
Lung cancer is the most common malignancy worldwide and is characterized by rapid progression, aggressive behavior, frequent recurrence, and poor prognosis. The TCGA database indicates that chondroitin polymerizing factor (CHPF) is overexpressed in human lung cancer tissues compared with normal tissues and this overexpression corresponds to shorter overall survival in lung cancer patients. In this study, to investigate the function of CHPF in lung cancer, lentiviral vectors expressing CHPF shRNA were stably transduced into A549 and H1299 cells. Compared to shCtrl cells, CHPF knockdown cells had significantly reduced proliferation. Furthermore, the silencing of CHPF in A549 and H1299 cells resulted in apoptotic induction, which led to decreased colony formation. Wound healing and transwell invasion assays revealed that CHPF could positively regulate the migration of lung cancer cells. The tumorigenic role of CHPF was also validated in nude mouse xenograft models. Affymetrix gene chip analysis indicated that CHPF regulated the proliferation and invasion of lung cancer cells through CDH1, RRM2, MKI67, and TNFRSF10B. We thus highlight CHPF as a novel target for lung cancer treatment.
Highlights
Lung cancer is one of the most lethal and common malignancies in humans, with a 5-year survival rate of p20% [1,2]
chondroitin polymerizing factor (CHPF) mRNA levels were assessed in lung cancer cell lines including A549, 95-D, NCI-H1299, H1688, and NCI-H460 by quantitative real-time PCR (qRT-PCR)
CHPF silencing inhibited lung cancer cell proliferation More than 80% of the A549 and H1299 cells that were infected with shCtrl or shCHPF lentivirus at 6 Â 108 TU/mL exhibited green fluorescence, indicating successful lentiviral infection (Figure 2A and B)
Summary
Lung cancer is one of the most lethal and common malignancies in humans, with a 5-year survival rate of p20% [1,2]. This poor survival rate is related to an unclear pathogenesis and a lack of effective early diagnosis and treatment methods [3,4]. Knowledge of the molecular and cellular mechanisms that govern lung cancer development can improve future diagnostics and therapies [5,6,7]. Kinase-targeted therapies and immune check-point inhibitors have shown increased efficacy in lung cancer treatment compared to standard chemotherapy [6,8,9]. Characterized drug targets are required to overcome these barriers
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