Jumonji domain containing 2A predicts prognosis and regulates cell growth in lung cancer depending on miR-150.
نویسندگان
چکیده
Lung cancer has become the most common cancer worldwide, of which non-small cell lung cancer (NSCLC) accounts for over 80%. Previous studies have shown that the Jumonji domain containing 2A (JMJD2A) was aberrantly expressed in various tumors and involved in the regulation of tumor progression, but the role of JMJD2A on the tumorigenesis in NSCLC and the underlying mechanisms are still unclear. In the present study, we first identified the expression of JMJD2A in NSCLC tissues and cell lines through quantitative RT-PCR (qRT-PCR) and western blotting. Next, the effects of JMJD2A on the progression of NSCLC were analyzed. MTT assay was performed to measure the cell numbers and fluorescence-activated cell sorting (FACS) was adopted to evaluate cell apoptosis. Finally, the relationship between JMJD2A and miR-150 involved in NSCLC was studied. Our results suggested that JMJD2A was significantly overexpressed in NSCLC samples and cell lines. Kaplan-Meier analysis showed that high level of JMJD2A predicted a poor prognosis. Knockdown of JMJD2A inhibited tumor growth and promoted cell apoptosis in NSCLC cells. Additionally, miR-150 was upregulated in NSCLC tissues and positively related with JMJD2A expression. Significant downregulation of miR-150 was observed with JMJD2A knockdown. Furthermore, JMJD2A knockdown inhibited NSCLC cell proliferation while the silencing of miR-150 attenuated the inhibition effect on cell proliferation, suggesting that the effect of JMJD2A on NSCLC cell growth was dependent on miR-150. Thus, our findings identified that JMJD2A played an oncogenic role in NSCLC via regulating miR-150. JMJD2A could possibly serve as a prognostic factor and potential target for NSCLC therapy.
منابع مشابه
Jumonji domain-containing protein 1A promotes cell growth and progression via transactivation of c-Myc expression and predicts a poor prognosis in cervical cancer
Jumonji domain-containing protein 1A (JMJD1A) plays a key role in the development and progression of several cancers. Here, we showed that the expression of JMJD1A is increased in cervical cancer cells and tissues, and that suppression of JMJD1A inhibits proliferation, migration, and invasion of cervical cancer cells. JMJD1A induced transcription of c-Myc, which is essential for cervical cancer...
متن کاملPCAF-mediated acetylation of transcriptional factor HOXB9 suppresses lung adenocarcinoma progression by targeting oncogenic protein JMJD6
HOXB9 is a homeobox domain-containing transcription factor, playing an important role in embryonic development and cancer progression. However, the precise post-translational modifications (PTMs) of HOXB9 and the corresponding roles are unclear. Here, we report that acetyltransferase p300/CBP-associated factor (PCAF) interacts with and acetylates HOXB9 both in vivo and in vitro Conversely, the ...
متن کاملMiR-134/487b/655 cluster regulates TGF-β-induced epithelial-mesenchymal transition and drug resistance to gefitinib by targeting MAGI2 in lung adenocarcinoma cells.
Epithelial-mesenchymal transition (EMT) has recently been recognized as a key element of cell invasion, migration, metastasis, and drug resistance in several types of cancer, including non-small cell lung cancer (NSCLC). Our aim was to clarify microRNA (miRNA)-related mechanisms underlying EMT followed by acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TK...
متن کاملCancer Biology and Signal Transduction MiR-134/487b/655 Cluster Regulates TGF-b–Induced Epithelial–Mesenchymal Transition and Drug Resistance to Gefitinib by Targeting MAGI2 in Lung Adenocarcinoma Cells
Epithelial–mesenchymal transition (EMT) has recently been recognized as a key element of cell invasion, migration, metastasis, and drug resistance in several types of cancer, including non–small cell lung cancer (NSCLC). Our aim was to clarify microRNA (miRNA)-related mechanisms underlying EMT followed by acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TK...
متن کاملMiR-134/487b/655 Cluster Regulates TGF-b–Induced Epithelial–Mesenchymal Transition and Drug Resistance to Gefitinib by Targeting MAGI2 in Lung Adenocarcinoma Cells
Epithelial–mesenchymal transition (EMT) has recently been recognized as a key element of cell invasion, migration, metastasis, and drug resistance in several types of cancer, including non–small cell lung cancer (NSCLC). Our aim was to clarify microRNA (miRNA)-related mechanisms underlying EMT followed by acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TK...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Oncology reports
دوره 35 1 شماره
صفحات -
تاریخ انتشار 2016