Background Long-chain non-coding RNA (LncRNA) plays a key role in the biological processes of tumors. LncRNA-FTX has been the invasion of tumors. However, its function and mechanism in osteosarcoma have not been studied. Methods qRT-PCR was measured the expression levels of FTX and miR-214-5p in osteosarcoma. The protein levels of SRY-related HMG box transcription factor 4 (SOX4) were detected by Western Blot. Cholecystokinin (CCK-8) assay, cell colony formation and Transwell assay, Annexin V-FITC/PI assay were analyzed the effects of FTX and miR-214-5p on cell proliferation, cell invasion and apoptosis. The relationship between FTX, miR-214-5p and SOX4 was analyzed by bioinformatics analysis and Luciferase. The tumor changes in mice were detected by vivo experiments in nude mice. Results The expression levels of FTX were increased in osteosarcoma tissues and cell lines and negatively correlated with the expression levels of miR-214-5p. FTX could modulate the expression of miR-214-5p in osteosarcoma cell lines. sh-FTX inhibited the growth and metastasis of osteosarcoma. FTX could regulate the growth of osteosarcoma through miR-214-5p. The knockdown of miR-214-5p reversed the inhibitory effect of sh-FTX on osteosarcoma cell proliferation and growth in mice. Furthermore, FTX regulated the expression of SOX4 by acting as a sponge of miR-214-5p in osteosarcoma. Conclusion FTX could promote proliferation, invasion and inhibited apoptosis by regulating miR-214-5p/SOX4 axis in osteosarcoma, suggesting that FTX might be a potential target for osteosarcoma treatment.

Doxorubicin (DOX) has been widely used to treat cancers as a first-line antitumor drug. However, it causes severe, irreversible, dose-dependent cardiotoxicity. To evaluate the protective effects of naringin (NRG) on cardiotoxicity, the authors investigated the molecular mechanism of the p38MAPK signaling pathway. H9c2 cells were treated for 24 h by using 5 µmol/l DOX without or with being pretreated by 1 µM NRG for 150 min or by 3 µM SB203580 for 60 min. Cell viability was detected by cell counting kit-8 assay. Intracellular reactive oxygen species (ROS) levels were detected based on the oxidative conversion of 2′,7′-dichlorfluorescein-diacetate (cell-permeable) to dichlorofluorescein (fluorescent). The expression of p38MAPK was determined by western blotting. The expression level of p-p38MAPK in H9c2 cells, which was significantly increased by exposure to 5 µM DOX for 60 min (P<0.01), was significantly decreased by pretreatment with 1 µM NRG for 150 min beforehand (P<0.01). The viability of H9c2 cells pretreated for 150 min with 1 µM NRG was significantly enhanced compared with that using DOX directly (P<0.01). Intracellular ROS levels were significantly reduced by being pretreated with 1 µM NRG for 150 min or with 3 µM SB203580 for 60 min before the cells were exposed to 5 µM DOX. Collectively, NRG protected H9c2 cells against the cardiotoxicity induced by DOX through suppressing the expression and activity of the p38MAPK pathway. The findings provided valuable evidence for the possible use of NRG to relieve DOX-induced cardiotoxicity.

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