Methylation of RILP in lung cancer promotes tumor cell proliferation and invasion
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Methylation of RILP in lung cancer promotes tumor cell proliferation and invasion Jianbo Lin1 · Yi Zhuo1 · Yinhe Yin1 · Linbin Qiu1 · Xu Li1 · Fancai Lai1 Received: 15 July 2020 / Accepted: 14 October 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Rab-interacting lysosomal protein (RILP) has been suggested to perform as a tumor suppressor in breast and prostate cancer cell lines. However, its expression profile and functional role in lung cancer have never been investigated. We applied the well-established cancer genomic database-The Cancer Genome Atlas to compare the RILP expression and methylation between lung cancer tissues and normal tissues. The potential correlation of RILP with clinical characteristics of lung cancer patients (e.g., stages, smoking, TP53, and methylation) was also be explored. Our results showed that the downregulation of RILP and upregulation of RILP methylation were identified in lung cancer tissues compared to normal healthy tissues. Downregulation of RILP was positively associated with lung cancer later stage (N3), smoking history, TP53 mutation, and poor prognosis, as well as inversely correlated with DNA (cytosine-5)-methyltransferase 1 (DNMT1) expression. Demethylation treatment enhanced RILP expression in lung cancer cells, suggesting hypermethylation is responsible for RILP silencing in lung cancer. We further found that RILP depletion promoted lung cancer cell proliferation, migration, and invasion. We concluded that RILP acts as a tumor suppressor in lung cancer cells. Our results provided the theoretical basis for developing RILP-targeting or demethylating agents for lung cancer treatment. Keywords DNMT1 · Prognosis marker · Lung adenocarcinoma · Squamous cell carcinoma · 5-aza
Introduction Lung cancer is one of the most common cancers and the main cause of cancer mortality in the world. It is estimated approximately 2.1 million newly diagnosed cases of lung cancer and 1.8 million lung cancer-related death globally [1]. Many factors acting solely or jointly contribute to lung carcinogenesis, including the use of tobacco products, air pollution exposures, chronic inflammation or infections, and gene mutations [2, 3]. Based on the lung cancer pathological examination of the size of the tumor cells and the difference Jianbo Lin and Yi Zhuo have contributed equally to this work. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11010-020-03950-0) contains supplementary material, which is available to authorized users. * Fancai Lai [email protected] 1
Department of Thoracic Surgery, the First Affiliated Hospital of Fujian Medical University, No. 20 Chazhong Road, Fuzhou 350005, Fujian, China
of tumor growth and spreading criterion, lung cancer can be generally classified into two histologic classes: small-cell lung carcinomas (SCLC) and non-small cell lung carcinomas (NSCLC) [4]. About 15% of lung cancer are SCLC, and SCLC cancer cells usually grow faster and spread quicker than NSCLC. It i
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