J Cancer 2019; 10(23):5714-5721. doi:10.7150/jca.28887 This issue
1. Department of Ultrasonics, the Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China;
2. Department of Pathophysiology, the Institute of Basic Medicine, Guizhou Medical University, Guiyang 550004, China;
3. Department of General Surgery, Wujiang NO.1 People's Hospital, Suzhou 215200, China;
4. Department of acute infectious disease Prevention, Jiangsu Provincial Center for Disease Control and Prevention, Nanjing 210009, China;
5. Central Laboratory, the Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China;
6. Department of Endocrinology, the Hospital Affiliated to Guizhou Medical University, Guiyang 550004, China;
7. College of Medicine, Henan University of Science and Technology, Luoyang 471023, China
8. Department of Thyroid Surgery, the Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China;
9. Department of Public Health Sciences, University of North Carolina Charlotte, Charlotte, NC 28223, USA.
*These authors contributed equally to this article.
Background: Long noncoding RNA MALAT1 has been previously reported in the carcinogenesis of several tumors, and its potential functional polymorphisms have also been investigated in various diseases. However, the relationship between these polymorphisms and the susceptibility of thyroid cancer has still been largely unknown. In the present study, we aimed to explore the association between MALAT1 polymorphisms and thyroid cancer (TC) susceptibility, as well as potential biological function in TC.
Methods: We conducted a case-control study with 1134 papillary thyroid cancer (PTC) patients and 1228 controls to evaluate the potential correlation between MALAT1 genetic variations (single nucleotide polymorphism, SNP) and the risk of PTC. More detailed molecular mechanisms were explored by luciferase assay, cell counting kit-8 (CCK-8), and flow cytometry.
Results: MALAT1 SNP rs619586 was identified as a significantly protective factor of PTC susceptibility (P = 0.017, OR= 0.76, 95%CI = 0.60-0.95). Further functional experiments of rs619586 indicated that G allele of rs619586 could significantly decrease MALAT1expression, reduce PTC proliferation, and directly increase PTC apoptosis.
Conclusions: Our findings suggested that MALAT1 SNP rs619586 could serve as a potential indicator for PTC susceptibility and pathogenesis.
Keywords: thyroid cancer, long noncoding RNA, MALAT1, polymorphism, susceptibility.