Abstract
Lung cancer is the second most common cancer among others. In most people, lung cancer is related to cigarette smoking. However, there exist the other factors that may cause this disease. We will investigate lysine specific demethylase 1 (LSD1) that has been identified and biochemically characterized in epigenetics. Lysine-specific demethylase 1 (LSD1), catalysing demethylation of mono- and di-methylated histone H3-K4 or K9, exhibits diverse transcriptional activities by mediating chromatin reconfiguration. The telomerase reverse transcriptase (hTERT) gene, encoding an essential component for telomerase activity that is involved in cellular immortalization and transformation, is silent in most normal human cells while activated in up to 90% of human cancers. It remains to be defined how exactly the transcriptional activation of thehTERT gene occurs during the oncogenic process. Cancer-related genes show racial differences. Therefore, identification and characterization of DNA copy number alteration regions in different racial groups helps to dissect the mechanism of tumorigenesis. TAL1/SCL is a hematopoietic specific oncogene and its activity is regulated by associated transcriptional coactivators and corepressors. Dysregulation of TAL1 activity has been associated with T cell leukemogenesis. However, it remains unclear how the interactions between TAL1 and corepressors versus coactivators are properly regulated.
Key words: Disease, genetic polymorphisms, smoking.
Introduction
Lung cancer is one of the leading causes of cancer death worldwide. The 5-year survival rate for lung cancer remains poor. In order to develop more effective therapies, it is important to obtain a better understanding of the molecular biology of lung cancer. Genetic alterations are a hallmark of human cancer. In recent years, the cancer genomics field has made significant advances in identifying genetic lesions in cancer.
The aim of this study is to evaluate the prognostic significance of LSD1 expression in patients with non-small cell lung cancer (NSCLC) and to define its exact role in lung cancer proliferation, migration and invasion. Over-expression of LSD1 was associated with poor prognosis in NSCLC, and promoted tumor cell proliferation, migration and invasion. These results suggest that LSD1 is a tumor-promoting factor with promising therapeutic potential for NSCLC. Since MCM7 expression was generally low in a number of normal tissues we examined, MCM7 has the characteristics of an ideal candidate for molecular targeted cancer therapy in various tumors and also as a good prognostic biomarker for NSCLC patients. Our study provides an invaluable database revealing common and differential imbalance regions at specific chromosomes among Asian and Caucasian lung cancer patients. LSD1 represses hTERT transcription via demethylating H3-K4 in normal and cancerous cells, and together with HDACs, participates in the establishment of a stable repression state of the hTERT gene in normal or differentiated malignant cells. The findings contribute to better understandings of hTERT/telomerase regulation, which may be implicated in the development of therapeutic strategies for telomerase dysregulation-associated human diseases including cancers.
Evidence of Carcinogenesis from lsd1. Risk Factors for lsd1. Biotransformation lsd1. Student’s t-test and ANOVA were used to investigate the associations between LSD1 expression and clinical factors (age, sex, smoking, tumor stage, histology, tumor size, nodal status, and overall survival). Pearson’s …