Erratum: Targeting cysteine-rich angiogenic inducer-61 by antibody immunotherapy suppresses growth and migration of non-small cell lung cancer.

[This corrects the article DOI: 10.3892/etm.2018.6274.].

Potential of curcumin and resveratrol as biochemical and biophysical modulators during lung cancer in rats.

The present study explored chemopreventive aspects of curcumin and resveratrol in the experimental model of lung carcinogenesis in rats. The main aim was to establish efficacy of combined phytochemicals treatment over individual treatments in rat cancer model. The study was performed in terms of both biophysical and biochemical parameters. The rats were segregated into five groups, which included normal control, benzo[a]pyrene (BP) treated, BP + curcumin treated, BP + resveratrol treated, and BP + curcumin + resveratrol treated groups. The results confirmed significant changes in the biochemical indices of the BP treated rats. Further, radiorespirometric studies showed significant rise in the 14C-glucose turnover and uptakes in BP treated rats. Also, a significant increase in the cell proliferation was noticed indirectly by recording uptakes of 3H-thymidine in the lung slices of BP treated rats. On the other hand, supplementation with curcumin and resveratrol in combination to BP treated rats significantly modulated both biophysical and biochemical indices. The histopathological studies also supported the efficacy of combined treatment of phytochemicals during lung carcinogenesis. The present study concluded that the combination of curcumin and resveratrol efficiently modulated lung carcinogenesis in rats.

Targeting cysteine-rich angiogenic inducer-61 by antibody immunotherapy suppresses growth and migration of non-small cell lung cancer.

Non-small cell lung cancer (NSCLC) is the most frequent type of human lung cancer; lung cancer is responsible for the highest rates of cancer-associated mortality in the world. Cysteine-rich angiogenic inducer-61 (CYR-61) has been identified as a tumorigenesis-, development- and metastasis-related gene, and is reported to enhance proliferation, migration and invasion through hepatocyte growth factor (HGF)-induced scattering and the metastasis-inducing HGF/Met signaling pathway in tumor cells and xenograft models. CYR-61 is a protein that promotes human lung cancer cell metastasis and is closely related to the patient's prognosis in NSCLC. The purpose of the present study was to investigate whether CYR-61 may serve as a dual potential target for gene therapy of human NSCLC. In the present study, an antibody targeted against CYR-61 (anti-CYR-61) was constructed and the therapeutic effects and underlying mechanism of this antibody in NSCLC cells and mice with NSCLC was investigated. It was observed that NSCLC cell viability, migration and invasion were inhibited while cell apoptosis was induced by the neutralization of CYR-61 protein by anti-CYR-61. Western blotting demonstrated that extracellular signal-regulated kinase (ERK) and protein kinase B (AKT) expression levels in NSCLC cells were decreased following treatment with anti-CYR-61. In addition, it was observed that inhibition of NSCLC cell viability was achieved by the suppression of the epithelial-mesenchymal transition signaling pathway. ERK and AKT phosphorylation levels were downregulated in NSCLC cells and tumors following anti-CYR-61 treatment. Analysis of a murine model indicated that tumor growth was inhibited and tumor metastasis was significantly suppressed (P<0.01) following anti-CYR-61 treatment for CYR-61. In conclusion, CYR-61 may serve as a potential target for gene therapy for the treatment of human NSCLC.

TASK-1 induces gefitinib resistance by promoting cancer initiating cell formation and epithelial-mesenchymal transition in lung cancer.

Cancer initiating cell (CIC) formation and epithelial-mesenchymal transition (EMT) are pivotal events in lung cancer cell invasion and metastasis. They have been shown to occur in gefitinib resistance. Studying the molecular mechanisms of CICs, EMT and acquired gefitinib resistance will enhance the understanding of the pathogenesis and progression of the disease and offer novel targets for effective therapies. TWIK-related acid-sensitive K(+) (TASK-1) is expressed in a subset of non-small-cell lung cancer (NSCLC) cell lines, where it promotes cell proliferation while inhibiting apoptosis. In the present study, TASK-1 was demonstrated to induce gefitinib resistance in the A549 NSCLC cell line. Overexpression of TASK-1 promoted the acquisition of CIC-like traits by A549 cells. CD133, octamer-binding transcription factor 4 (OCT-4) and Nanog have been suggested to be markers of CICs in lung cancer. It was demonstrated that overexpression of TASK-1 promoted CD133, OCT-4 and Nanog protein expression in A549 cells. Increased formation of stem cell-like populations results in EMT of cancer cells. The present study found that overexpression of TASK-1 promoted EMT of A549 cells. Thus, downregulation of TASK-1 may represent a novel strategy for EMT reversal, decreasing CIC-like traits and increasing gefitinib sensitivity of NSCLCs.