As a cell surface proteoglycan anchored by glycosyl-phosphatidylinositol, Glypican-3 (GPC3) is reported to be highly expressed in hepatocellular carcinoma (HCC) and to promote cell proliferation and tumorigenesis through activating Wnt/β-catenin signalling. GPC3 is also overexpressed in lung squamous cell carcinoma (SCC), but its effects and mechanisms in the progression of lung SCC remain unknown. The present study aims to explore the role and molecular mechanism of GPC3 in the occurrence and development of lung SCC. Immunohistochemistry, Western blot (WB) and real-time PCR (RT-PCR) assays were used to determine the expression patterns of GPC3 in lung SCC tissues and cells. MTT, flow cytometry and in vivo xenotransplantation assays were used to evaluate the influence of GPC3 on the growth, apoptosis and tumorigenesis of lung SCC cells. The results showed that GPC3 expression levels in lung SCC tissues and cells were significantly elevated, and the high expression of GPC3 significantly promoted cell growth and tumorigenesis and repressed cell apoptosis, as well as increased β-catenin expression. Moreover, knockdown of β-catenin obviously weakened GPC3 role in the promotion of cell proliferation and tumorigenesis, as well as the inhibition of cell apoptosis. In conclusion, the present study demonstrates that up-regulation of GPC3 accelerates the progression of lung SCC in a β-catenin-dependent manner. Our study provides a theoretical basis for GPC3/β-catenin as a novel diagnostic marker and therapeutic target for lung SCC.
This study assessed whether C-reactive protein (CRP) and procalcitonin (PCT) levels can discriminate between infectious fever and tumor fever (TF) in non-neutropenic patients with nonsmall cell lung cancer (NSCLC).This retrospective clinical study included 96 adults with NSCLC who were admitted to the Third Hospital of Hebei Medical University between July 2015 and July 2017. Febrile, non-neutropenic patients were enrolled. CRP and PCT levels, neutrophil count, and antimicrobial response were evaluated.This study included 26 patients with TF, 49 with localized bacterial infection (LBI), and 21 with bloodstream infection (BSI). CRP levels in BSI were significantly higher than in TF (P < .05) and LBI (P < .05). No statistically significant difference was found between patients with TF and LBI (P > .05). PCT levels were significantly higher in BSI and LBI than in TF (P < .05). CRP and PCT levels in patients with stage IV disease were significantly higher than in those with stage II to III disease (P < .05). CRP and PCT levels declined significantly in patients with BSI who were responding to antimicrobials (P < .05).Compared with CRP levels, PCT levels can discriminate between TF and infectious fever more accurately. PCT and CRP levels may predict different stages of lung cancer.
Hydrogen gas (H2) has been identified to play an anti-tumor role in several kinds of cancers, but the molecular mechanisms remain largely unknown. In our previous study, our project group found that H2 could decrease the expression of CD47 in lung cancer A549 cells via the next-generation sequencing, indicating that CD47 might be involved in H2-mediated lung cancer repression. Therefore, the present study aimed to explore the effects of CD47 on H2-induced lung cancer repression. Western blotting and real-time PCR (RT-PCR) assays were used to detect the levels of proteins and mRNAs, respectively. Cell proliferation, invasion, migration and apoptosis were detected by using the cell counting kit-8 (CCK-8), Transwell chambers, wound healing and flow cytometry assays, respectively. The results showed that H2 treatment caused decreases in the expression levels of CD47 and cell division control protein 42 (CDC42) in a dose-dependent manner. Up-regulation of CD47 abolished H2 roles in promoting lung cancer cell apoptosis and repressing cell growth, invasion and migration in both A549 and H1975 cell lines. However, knockdown of CD47 enhanced H2 role in lung cancer inhibition. Moreover, we also observed that H2 treatment induced obvious inhibitions in the expression levels of CDC42 and CD47 in mice tumor tissues, as well as reinforced macrophage-mediated phagocytosis in A549 and H1975 cells. In conclusion, the current study reveals that H2 inhibits the progression of lung cancer via down-regulating CD47, which might be a potent method for lung cancer treatment.
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