Abstract
Lung cancer is the most commonly diagnosed type of cancer worldwide. Although TRIM65 is an important protein involved in white matter lesion, the role of TRIM65 in human cancer remains less understood. Here, we reported that TRIM65 was significantly overexpressed in lung cancer tissues compared with adjacent normal lung tissues. Furthermore, TRIM65 expression was closely related to overall survival of patients with lung cancer. Knock down of TRIM65 in two lung cancer cell lines, SPC-A-1 and NCI-H358, resulted in a significant reduction in cell proliferation, migration, invasion and adhesion and a dramatic increase in G0-G1 phase arrest and apoptosis. In vivo tumorigenesis experiment also revealed that depletion of TRIM65 expression inhibited NCI-H358 cell growth. Moreover, based on gene set enrichment analysis (GSEA) with The Cancer Genome Atlas (TCGA) dataset, we found that TRIM65 was positive related to cell cycle, metastasis up and RHOA-REG pathways, which was further validated by RT-PCR and Western blot in TRIM65 knockdown lung cancer cells and indicated a possible mechanism underlying its effects on lung cancer. In summary, our study suggests that TRIM65 may work as an oncogene and a new effective therapeutic target for lung cancer treatment.
Highlights
Malignant tumor cells use their inherent ability of migration, invasion of adjacent tissue and blood vessels, and to metastasize [1]
Based on gene set enrichment analysis (GSEA) with The Cancer Genome Atlas (TCGA) dataset, we found that TRIM65 was positive related to cell cycle, metastasis up and Ras Homolog Family Member A (RHOA)-REG pathways, which was further validated by Real-time PCR (RT-PCR) and Western blot in TRIM65 knockdown lung cancer cells and indicated a possible mechanism underlying its effects on lung cancer
We demonstrated that up-regulation of TRIM65 is closely related to human lung cancer tumorigenesis, and knockdown of TRIM65 reduces the cell growth, invasion, migration and adhesion, and arrests cell cycle and promotes apoptosis of human lung cancer cells
Summary
Malignant tumor cells use their inherent ability of migration, invasion of adjacent tissue and blood vessels, and to metastasize [1]. Metastasis, the most critical prognostic factor, is composed of multiple steps as follows: attachment of tumor cells to the extracellular matrix (ECM), secretion of matrix-degrading enzymes, migration of tumor cells through the degraded matrix, invasion of blood vessels and circulation, and implantation into other distant organs [2]. Understanding the underlying mechanisms of cell migration is necessary for our understanding of the development and progression of the disease. Radiation therapy has been established as a standard treatment for lung cancer and has improved survival of the patients [5], the major health threat for lung cancer is death due to metastasis. For developing more effective therapies, a better understanding of the molecular biology of lung cancer is important to obtain
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