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.

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.

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.

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.