Overexpression of HN1L promotes cell malignant proliferation in non-small cell lung cancer
| Autor: | Ying Hui Zhu, Ting Ting Zeng, Xin Yuan Guan, Lei Li, Bao Zhu Zhang, Yan Li |
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| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine Oncology MAPK/ERK pathway Cancer Research medicine.medical_specialty Lung Neoplasms Cell cycle checkpoint Cell Mice Nude Cell Cycle Proteins Nerve Tissue Proteins Biology Transfection Small hairpin RNA Mice 03 medical and health sciences Downregulation and upregulation Carcinoma Non-Small-Cell Lung Cell Line Tumor Internal medicine medicine Animals Humans Lung cancer Cell Proliferation Pharmacology Oncogene Cell growth Nuclear Proteins medicine.disease Up-Regulation 030104 developmental biology medicine.anatomical_structure Gene Knockdown Techniques Cancer research Heterografts Molecular Medicine Female Microtubule-Associated Proteins Research Paper |
| Zdroj: | Cancer Biology & Therapy. 18:904-915 |
| ISSN: | 1555-8576 1538-4047 |
| DOI: | 10.1080/15384047.2017.1385678 |
| Popis: | Non-small cell lung cancer (NSCLC) is a progressive malignant disease, involving the activation of oncogenes and inactivation of tumor suppressors. In this study, we identified and characterized a novel oncogene hematopoietic- and neurologic-expressed sequence 1-like (HN1L) in human NSCLC. Overexpression of HN1L was frequently detected in primary NSCLC compared with their non-tumor counterparts (P < 0.001), which was significantly associated with tumor size (P = 0.022). In addition, Kaplan–Meier analysis showed that upregulation of HN1L correlated with worse overall survival (P = 0.029) and disease-free survival (P = 0.011) for NSCLC patients. Both in vitro and in vivo studies demonstrated that inhibition of HN1L expression with shRNA dramatically inhibited cell growth, adherent and non-adherent colony formation, and tumorigenicity in nude mice. The positive correlation of HN1L expression and Ki67 level in a large NSCLC samples further suggested the key role of HN1L in the regulation of cell growth. Further study showed that knockdown of HN1L resulted in dramatic cell cycle arrest by interfering with MAPK pathway via interacting with RASA4 protein. In conclusion, HN1L plays a crucial role in the progression of NSCLC by contributing to malignant proliferation, with possible use as a new intervention point for therapeutic strategies. |
| Databáze: | OpenAIRE |
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