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Research Paper Volume 11, Issue 18 pp 7678—7693
Long noncoding RNA TTN-AS1 enhances the malignant characteristics of osteosarcoma by acting as a competing endogenous RNA on microRNA-376a thereby upregulating dickkopf-1
Figure 7. TTN-AS1 enhances HOS and MG-63 cell proliferation, migration, and invasion and inhibits their apoptosis, via the miR-376a–DKK1 axis. (A) Either antagomir-376a or antagomir-NC was introduced into HOS and MG-63 cells. The transfection efficiency was assessed through RT-qPCR. *P < 0.05 vs. the antagomir-NC group. (B, C) Si-TTN-AS1 in combination with either antagomir-376a or antagomir-NC was transfected into HOS and MG-63 cells. After 48 h transfection, expression levels of the DKK1 protein and miR-376a were determined respectively by western blotting and RT-qPCR. *P < 0.05 vs. group si-NC. #P < 0.05 vs. group si-TTN-AS1+antagomir-NC. (D) The CCK-8 assay was conducted to evaluate the proliferative ability of HOS and MG-63 cells after cotransfection with si-TTN-AS1 and either antagomir-376a or antagomir-NC. *P < 0.05 vs. the si-NC group. #P < 0.05 vs. group si-TTN-AS1+antagomir-NC. (E) The proportion of apoptotic HOS or MG-63 cells that were cotransfected with either antagomir-376a or antagomir-NC and si-TTN-AS1 was determined via flow cytometry. *P < 0.05 vs. the si-NC group. #P < 0.05 vs. group si-TTN-AS1+antagomir-NC. (F, G) Transwell migration and invasion assays were conducted to evaluate the migratory and invasive abilities of HOS and MG-63 cells treated as described above. *P < 0.05 vs. the si-NC group. #P < 0.05 vs. group si-TTN-AS1+antagomir-NC.