[Retracted] Total flavonoids suppress lung cancer growth via the COX­2­mediated Wnt/ß­catenin signaling pathway.

[This retracts the article DOI: 10.3892/ol.2020.11271.].

Effects of high-quality nursing care on quality of life, survival, and recurrence in patients with advanced nonsmall cell lung cancer.

BACKGROUND: Postoperative nursing can improve the quality of life (QoL) and functional prognosis for lung cancer patients. The purpose of this study was to evaluate the effects of high-quality nursing on inflammation and prognosis in postoperative patients with advanced nonsmall cell lung cancer (NSCLC). METHODS: A total of 372 patients with NSCLC were enrolled between the May 2014 and June 2016. Patients were randomly received high-quality nursing (n = 192) or normal nursing (n = 180). Symptom management, QoL, hospital stay, inflammatory score, survival time, recurrence rate, symptoms, anxiety, depression scale and psychological distress were assessed at baseline and 5-year follow up. RESULTS: High-quality nursing significantly shortened hospital stay, improved postoperative inflammation, symptom management, QoL compared to patients received normal nursing. Compare with normal nursing, high-quality nursing decreased anxiety, depression scale and psychological distress for postoperative patients with advanced NSCLC. Outcomes showed that high-quality nursing increased the survival time and decreased recurrence rate for postoperative patients with advanced NSCLC. CONCLUSION: In conclusion, data in the current study indicate that high-quality nursing can decrease inflammation and improve prognosis for the postoperative patients with NSCLC.

Melittin suppresses growth and induces apoptosis of non-small-cell lung cancer cells via down-regulation of TGF-ß-mediated ERK signal pathway

The purpose of this study was to investigate the anti-cancer effect of melittin on growth, migration, invasion, and apoptosis of non-small-cell lung cancer (NSCLC) cells. This study also explored the potential anti-cancer mechanism of melittin in NSCLC cells. The results demonstrated that melittin suppressed growth, migration, and invasion, and induced apoptosis of NSCLC cells in vitro. Melittin increased pro-apoptotic caspase-3 and Apaf-1 gene expression. Melittin inhibited tumor growth factor (TGF)-β expression and phosphorylated ERK/total ERK (pERK/tERK) in NSCLC cells. However, TGF-β overexpression (pTGF-β) abolished melittin-decreased TGF-β expression and pERK/tERK in NSCLC cells. Treatment with melittin suppressed tumor growth and prolonged mouse survival during the 120-day observation in vivo. Treatment with melittin increased TUNEL-positive cells and decreased expression levels of TGF-β and ERK in tumor tissue compared to the control group. In conclusion, the findings of this study indicated that melittin inhibited growth, migration, and invasion, and induced apoptosis of NSCLC cells through down-regulation of TGF-β-mediated ERK signaling pathway, suggesting melittin may be a promising anti-cancer agent for NSCLC therapy.

Melittin suppresses growth and induces apoptosis of non-small-cell lung cancer cells via down-regulation of TGF-ß-mediated ERK signal pathway.

The purpose of this study was to investigate the anti-cancer effect of melittin on growth, migration, invasion, and apoptosis of non-small-cell lung cancer (NSCLC) cells. This study also explored the potential anti-cancer mechanism of melittin in NSCLC cells. The results demonstrated that melittin suppressed growth, migration, and invasion, and induced apoptosis of NSCLC cells in vitro. Melittin increased pro-apoptotic caspase-3 and Apaf-1 gene expression. Melittin inhibited tumor growth factor (TGF)-ß expression and phosphorylated ERK/total ERK (pERK/tERK) in NSCLC cells. However, TGF-ß overexpression (pTGF-ß) abolished melittin-decreased TGF-ß expression and pERK/tERK in NSCLC cells. Treatment with melittin suppressed tumor growth and prolonged mouse survival during the 120-day observation in vivo. Treatment with melittin increased TUNEL-positive cells and decreased expression levels of TGF-ß and ERK in tumor tissue compared to the control group. In conclusion, the findings of this study indicated that melittin inhibited growth, migration, and invasion, and induced apoptosis of NSCLC cells through down-regulation of TGF-ß-mediated ERK signaling pathway, suggesting melittin may be a promising anti-cancer agent for NSCLC therapy.

Total flavonoids suppress lung cancer growth via the COX-2-mediated Wnt/ß-catenin signaling pathway.

The aim of the present study was to explore the anti-cancer effects of total flavonoids (TF) on lung cancer and to investigate the underlying mechanism. The inhibitory effect of TF on the proliferation of A549 cells in vitro was measured using an MTT assay. The apoptotic rate of TF-treated A549 cells was analyzed using flow cytometry and terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling. Migration and invasion assays were performed to investigate the anti-migration effect of TF on A549 cells. Reverse-transcription quantitative PCR was used to analyze BCL2-like 2, BCL2, Bax, Bad, cyclooxygenase 2 (COX-2), Wnt and ß-catenin mRNA expression levels in A549 cells. The in vivo anti-cancer effect of TF was investigated in a subcutaneous xenograft model of lung cancer in BALB/c nude mice. The results obtained in the present study revealed that TF exerted a significant inhibitory effect on the proliferation of A549 cells in a dose-dependent manner (P<0.01). TF induced apoptosis of A549 cells, which exhibited increased and decreased expression of pro- and anti- apoptotic genes, respectively. Furthermore, TF had a significant inhibitory effect on the migration and invasion of A549 cells (P<0.01). The mRNA expression levels of COX-2, Wnt and ß-catenin were significantly downregulated in TF-treated A549 cells compared with controls. Additionally, treatment with TF inhibited tumor growth in mice, with a tumor inhibition rate of 64.07% compared with the controls. TF exhibited significant tumor inhibitory effects in vivo by promoting the apoptosis of tumor cells. In conclusion, the results suggested that TF may regulate lung cancer growth via the COX-2-Wnt/ß-catenin signaling pathway. TF may serve as a novel anti-cancer agent for the treatment of lung cancer.

Therapeutic effects of lenvatinib in combination with rAd-p53 for the treatment of non-small cell lung cancer.

The aim of the present study was to analyze the effects of the combined treatment of lenvatinib and adenoviral delivered p53 gene (rAd-p53) on non-small cell lung cancer (NSCLC) cells and a total of 120 patients with NSCLC. The therapeutic effects of gene therapy of rAd-p53 and target therapy of Lenvatinib were investigated in NSCLC patients. The anti-tumor effects of combined treatment of llenvatinib and rAd-p53 was administered orally once-daily in NSCLC patients. Patients with NSCLC were divided into three groups and received lenvatinib (n=40), rAd-p53 (n=40) or combined treatment of lenvatinib and rAd-p53 (n=40) for a total of 30 days. Results showed that p53 was down-regulated and VEGFR, FGFR and PDGFR-ß were up-regulated in NSCLC tissues compared to adjacent normal tissues. Combined treatment of Lenvatinib and rAd-p53 markedly inhibited NSCLC cell growth, migration and invasion, and promoted apoptosis compared to either lenvatinib or rAd-p53 alone. The most common treatment-related adverse events included hypertension, diarrhea, nausea, proteinuria and body weight loss. Outcomes indicated that combined treatment of lenvatinib and rAd-p53 markedly inhibited tumor growth compared to lenvatinib and rAd-p53 alone for NSCLC patients. Combined treatment of lenvatinib and rAd-p53 did not exhibit drug accumulation after 30-day treatment. In conclusion, these outcomes indicate that combined treatment of lenvatinib and rAd-p53 may be an efficient therapeutic schedule for the treatment of NSCLC patients.

Kruppel-like factor 4 inhibits non-small cell lung cancer cell growth and aggressiveness by stimulating transforming growth factor-ß1-meidated ERK/JNK/NF-κB signaling pathways.

Non-small cell lung cancer is one of the most common epithelial tumors that cause the most common cancer-related mortality due to invasive ability. Research has found that Kruppel-like factor 4, a zinc-finger transcription factor, plays a critical role in the tumor evolution and progression. However, the molecular signal pathways mediated by Kruppel-like factor 4 in the progression of non-small cell lung cancer cells have not been well understood yet. In this study, we investigated the possible role and potential mechanism of Kruppel-like factor 4 in growth and aggressiveness of non-small cell lung cancer cells. Results showed that Kruppel-like factor 4 is downregulated in non-small cell lung cancer cells. Here, we found that Kruppel-like factor 4 knockdown promoted growth and aggressiveness of non-small cell lung cancer cells, as well as enhanced apoptotic resistance induced by tunicamycin. We also found that Kruppel-like factor 4 overexpression significantly suppressed growth and aggressiveness of non-small cell lung cancer cells. Apoptosis rate of non-small cell lung cancer cells induced by tunicamycin was promoted by Kruppel-like factor 4 overexpression. Kruppel-like factor 4 overexpression inhibited transforming growth factor-ß1, extracellular signal-regulated protein kinase, C-jun N-terminal kinase, and nuclear factor-κB expression levels in non-small cell lung cancer cells. Mechanistically, Kruppel-like factor 4-mediated tumorigenesis involved suppression of a transforming growth factor-ß1-meidated extracellular signal-regulated protein kinase/C-jun N-terminal kinase/nuclear factor-κB transcriptional program in non-small cell lung cancer cells. Our results revealed that Kruppel-like factor 4 overexpression non-small cell lung cancer cell reduces tumor growth in experimental mice. Overall, these data indicate the inhibitory role of Kruppel-like factor 4 in non-small cell lung cancer cells and elaborate a potential molecular signal pathway involving in growth and aggressiveness. Findings identify Kruppel-like factor 4 can be regarded as a possible new molecular agent for designing novel therapeutic protein drug for lung cancer treatment to control non-small cell lung cancer growth.