LncRNA LINC-PINT Inhibits Malignant Behaviors of Laryngeal Squamous Cell Carcinoma Cells via Inhibiting ZEB1

• Published in: Pathology oncology research Vol. 27; p. 584466
• Main Authors: Yang, Xianguang, Miao, Susheng, Mao, Xionghui, Xiu, Cheng, Sun, Ji, Pei, Rong, Jia, Shenshan
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media SA 01-04-2021; Frontiers Media S.A
• Subjects: Antibodies; Cell Line, Tumor; Cell Movement; Cell Proliferation; Chemotherapy; Enhancer of Zeste Homolog 2 Protein - genetics; Enhancer of Zeste Homolog 2 Protein - metabolism; Esophageal cancer; Female; Gene Expression Regulation, Neoplastic; Genes; Head & neck cancer; Humans; Laryngeal cancer; Laryngeal Neoplasms - genetics; Laryngeal Neoplasms - pathology; Male; Melanoma; Middle Aged; Prognosis; Proteins; Proto-Oncogene Proteins c-akt - metabolism; Radiation therapy; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Signal Transduction; Society Journal Archive; Squamous cell carcinoma; Squamous Cell Carcinoma of Head and Neck - genetics; Squamous Cell Carcinoma of Head and Neck - pathology; TOR Serine-Threonine Kinases; Zinc Finger E-box-Binding Homeobox 1 - genetics; Zinc Finger E-box-Binding Homeobox 1 - metabolism; United Kingdom > UK; United States > US; China; migration; ZEB1; LINC-PINT; invasion; laryngeal squamous cell carcinoma; EZH2
• ISSN: 1532-2807; 1219-4956; 1532-2807
• DOI: 10.3389/pore.2021.584466

Laryngeal squamous cell carcinoma (LSCC) belongs to head and neck squamous cell carcinoma (HNSCC), with dismal prognosis. Here, this study aims to disclose the role of LINC-PINT in cancer development, which may contribute to improving the clinical outcomes of LSCC treatment.
LINC-PINT expression in LSCC tissues and in TU-177 and Hep-2 cells was quantified, and subsequently, the association between LINC-PINT and LSCC malignancies was analyzed. pcDNA3.1-LINC-PINT or pcDNA3.1-EZH2 was introduced into Hep-2 and TU-177 cells. qRT-PCR and Western blot analyses examined the levels of proteins related to the AKT/mTOR pathway and their phosphorylated proteins in Hep-2 and TU-177 cells. The viability as well as migration and invasion abilities of Hep-2 and TU-177 cells were determined. Also, the distribution of LINC-PINT in Hep-2 cells was investigated as well as the interplay between LINC-PINT and EZH2. The downstream genes that might interact with EZH2 were screened.
LINC-PINT expression was inhibited in LSCC tissues and in Hep-2 and TU-177 cells, whose downregulation was associated with unsatisfactory prognosis. LINC-PINT overexpression suppressed the proliferative, migratory and invasive capacities of Hep-2 and TU-177 cells. LINC-PINT, mainly expressing in nuclei, could enrich EZH2 to silence ZEB1. In Hep-2 and TU-177 cells, the inhibition of LINC-PINT or overexpression of ZEB1 could enhance cell proliferation, migration and invasion. The phosphorylated levels of proteins related to the AKT/mTOR pathway were declined in cells with LINC-PINT overexpression, and the levels of these phosphorylated proteins were increased in cells with LINC-PINT inhibition.
LINC-PINT enriches EZH2 to silence ZEB1 and thus inhibits the proliferative, migratory, and invasive capacities of Hep-2 and TU-177 cells. In addition, LINC-PINT might exert its biological function through the AKT/mTOR pathway.