Knockdown of POLDIP2 suppresses tumor growth and invasion capacity and is linked to unfavorable transformation ability and metastatic feature in non-small cell lung cancer
- Division of Pulmonary and Critical Care, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC (China)
- Teaching and Research Office, Tri-Service General Hospital Songshan Branch, National Defense Medical Center, Taipei, Taiwan, ROC (China)
- Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University Hospital, Taipei, Taiwan, ROC (China)
- Division of Gastroenterology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC (China)
- Department and Graduate Institute of Microbiology and Immunology, National Defense Medical Center, Taipei, Taiwan, ROC (China)
- Department of Obstetrics and Gynecology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC (China)
Highlights: • Overexpression of POLDIP2 promoters transformation ability in H1299 cells. • Knockdown of POLDIP2 inhibits tumorigenicity and metastasis in vitro and in vivo. • Knockdown of POLDIP2 reduces cyclin D1, CDH2, Slug, and Twist expression. The main problem in the treatment of non-small cell lung cancer (NSCLC) is metastasis. Epithelial–mesenchymal transition (EMT) is known as the critical signaling in tumor progression, metastasis, and also the drug resistance. In this study, we reported a novel gene Polymerase delta-interacting protein 2 (POLDIP2) was downregulated in NSCLC tissues and first demonstrated that overexpression of POLDIP2 increased the anchorage-independent growth (AIG) and invasiveness of H1299 cells. In addition, we examined that knockdown of POLDIP2 in H1299 and A549 cells reduced tumorigenicity and metastatic capacity in vitro and also in vivo. Moreover, downregulation of the cell proliferation marker cyclin D1 and EMT markers CDH2, Slug, and Twist was showed in H1299 cells by POLDIP2 knockdown, suggesting that the inhibition of malignancy was affected by modulating key genes for tumor growth and invasiveness. Taken together, our study is the first study that demonstrated that POLDIP2 gene was function as an oncogene in NSCLC and implied the oncogenic ability might be through promoting cell proliferation or EMT.
- OSTI ID:
- 23082725
- Journal Information:
- Experimental Cell Research, Vol. 368, Issue 1; Other Information: Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
- Country of Publication:
- United States
- Language:
- English
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