Endocan Promotes Pro-Tumorigenic Signaling in Lung Cancer Cells: Modulation of Cell Proliferation, Migration and lncRNAs H19 and HULC Expression

• Published in: International journal of molecular sciences 2023-05, Vol.24 (9), p.8178
• Main Authors: Aliquò, Federica, Minuti, Aurelio, Avenoso, Angela, Mandraffino, Giuseppe, Campo, Giuseppe Maurizio, Campo, Salvatore, D'Ascola, Angela, Scuruchi, Michele
• Format: Article
• Language: English
• Subjects: AKT protein; Analysis; Angiogenesis; Biomarkers; Carcinoma, Non-Small-Cell Lung - genetics; Cell activation; Cell growth; Cell Line, Tumor; Cell Movement - genetics; Cell proliferation; Cell Proliferation - genetics; Development and progression; endocan; Humans; Hypoxia-inducible factor 1a; Kinases; long non-coding RNAs; Lung cancer; Lung cancer, Non-small cell; Lung carcinoma; Lung Neoplasms - metabolism; Non-coding RNA; Non-small cell lung carcinoma; NSCLC; Phenotypes; Prognosis; Proteoglycans; Proto-Oncogene Proteins c-akt - metabolism; RNA; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; siRNA; tumors; Vascular endothelial growth factor; Vascular Endothelial Growth Factor A - genetics; Vascular Endothelial Growth Factor Receptor-2; Vascular endothelial growth factor receptors
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms24098178

Endocan is a circulating proteoglycan secreted by several cell lines and identified as a potential biomarker of inflammation and angiogenesis. Endocan-increased expression has been found in a broad spectrum of human tumors, including lung cancer, and is associated with a poor prognosis. To elucidate the possible mechanism, this study aimed to investigate the role of endocan in non-small-cell lung carcinoma (NSCLC) using an in vitro model of cultured cells. Endocan expression was knocked down by using a specific small interfering RNA. The effects of endocan knockdown have been evaluated on VEGF-A, VEGFR-2, HIF-1α, the long non-coding RNAs H19 and HULC expression, and AKT and ERK 1/2 degree of activation. Cell migration and proliferation have been studied as well. VEGF-A, VEGFR-2, HIF-1α, and the long non-coding RNAs H19 and HULC expression were significantly affected by endocan knockdown. These effects correlated with a reduction of cell migration and proliferation and of AKT and ERK 1/2 activation. Our findings suggest that endocan promotes a more aggressive cancer cell phenotype in NSCLC.