lncRNA metastasis-associated lung adencarcinoma transcript 1 (MALAT1) plays an important role in the metastasis of lung cancer. Yet, its role in bone metastasis and the related mechanism remain unknown. The present study aimed to investigate the role of lncRNA MALAT1 in the bone metastasis of non-small cell lung cancer (NSCLC), including the expression pattern in tumor tissues, and the effect on the apoptosis, proliferation, migration and invasion of NSCLC cells. The expression level of MALAT1 in NSCLC tissues with/without bone metastasis and in NSCLC cell lines with (ACC-LC-319/bone2)/without (SPC‑A1) bone metastatic ability was determined with qRT-PCR and compared with t-test. si-MALAT1 was used to downregulate the expression of MALAT1 in ACC-LC-319/bone2 cells. The proliferation ability was assessed by MTT assay, and the apoptosis, migration, invasion and tumorigenesis in vivo were also assessed to detect the effect of MALAT1 expression on NSCLC cells. In conclusion, the present study found that MALAT1 was significantly highly expressed in NSCLC tissues with bone metastasis and in NSCLC cell lines with high bone metastatic ability (P<0.0001). Downregulation of MALAT1 expression significantly inhibited proliferation and induced cell apoptosis in comparing with the negative controls. Our results also revealed that MALAT1 significantly increased the migration, invasion and tumorigenesis in vivo, which suggests its important role in the bone metastasis of NSCLC.

Background Uremic tumoral calcinosis (UTC) is a rare complication in hemodialysis patients, whose mechanism remains incompletely understood. We report two cases with UTC who experienced completely different patterns of regression following parathyroidectomy, although there were no significant differences in serum calcium levels, parathyroid hormone, or phosphorus production between the two patients. Case presentation Case 1 had a substantial improvement in soft tissue calcification. However, in Case 2, one calcified mass was partially absorbed, while the others were aggravated with severe microvascular calcification and subcutaneous extravascular calcification. Whole-exome sequencing data revealed five mutation sites associated with atherosclerosis. Conclusion The different outcomes in UTC patients after PTX are rare. Further studies are required to elucidate the mechanism of paradoxical changes occurring in patients with UTC after parathyroidectomy.