LncRNA ADPGK-AS1 regulated cell proliferation, invasion, migration and apoptosis via targeting miR-542-3p in osteosarcoma
EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES
Authors: Luo, X-F; Wu, X-J; Wei, X.; Wang, A-G; Wang, S-H; Wang, J-L
Abstract
OBJECTIVE: The functions of lncRNAs have been verified to be important biomarkers and regulators for diagnosis and treatment of human diseases. In osteosarcoma (OS), emerging evidence determined that lncRNA was associated with cell progression. However, due to the high incidence and recurrence rate of osteosarcoma, it is important to find an effective treatment for osteosarcoma. PATIENTS AND METHODS: QRT-PCR was used to detect the expression of ADPGK-AS1 and miR-542-3p in tissues and cells. Western blot was applied to measure the protein expression of CDK4, Cyclin D1, Bcl-2, Bax, Cleaved caspase-3, MMP-2, and MMP-9. MTT assay and flow cytometry were used to measure cell proliferation and apoptosis. Cell invasion and migration were determined using the transwell assay. Moreover, luciferase reporter assay was used to ensure the relation between ADPGK-AS1 and miR-542-3p. RESULTS: LncRNA ADPGK-AS1 expression was induced while miR-542-3p expression was reduced in OS tissues and cells. Functional experiments showed that inhibition of ADPGK-AS1 could decrease cell proliferation, migration, and invasion, as well as promoted cell apoptosis in OS cells. Also, miR-542-3p has been verified to be a target miRNA of ADPGK-AS1 and miR-542-3p could reverse the effects of ADPGK-AS1 on cell proliferation, apoptosis, migration, and invasion in OS cells. CONCLUSIONS: ADPGK-AS1 affected cell proliferation. invasion, migration, and apoptosis via targeting miR-542-3p in OS, providing a theoretical basis and a new therapeutic target for the diagnosis and treatment of OS.
High expression of ADPGK increases the sensitivity of gastric cancer to chemotherapy
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
Authors: Hu, Wenhua; Hua, Ye
Abstract
Objective: To verify that high expression of LNCRNA ADPGK-AS1 can increase the sensitivity of gastric cancer (GC) to chemotherapy. Methods: The expression of ADPGK-AS1 in MKN-45, MKN-28, MGC-803, AZ521 and HFE-145 cell lines was detected by qRT-PCR. In addition, si-LncRNA ADPGK-AS1, sh-LncRNA ADPGK-AS1 and Si-NC sequences were transfected into MKN-45 and AZ521 cells. QRT-PCR was employed to detect the ADPGK-AS1 expression in si-LncRNA ADPGK-AS1 and sh-LncRNA groups. MTT, Transwell and flow cytometry (FC) were adopted to test the proliferation, invasion and apoptosis of transfected cells, while Western blot (WB) was utilized to examine the expression of Bax and Bcl-2 in MKN-45 and AZ521 cells. What's more, the cells were respectively subjected to cisplatin (4, 8, 16 and 32 mu mol/L) treatment at different concentrations, and the cell survival was measured 24 hours later. Results: The ADPGK-AS1 level in HFE-145 was significantly higher than that in MKN-45, MKN-28, MGC803 and AZ521 (P<0.05). After transfection, the ADPGK-AS1 level in the MKN-45 and AZ521 cells in the Si-RNA group was significantly lower than that in the Sh-RNA and Si-NC groups (P<0.05). Compared with the Sh-RNA group, the proliferation of MKN-45 and AZ521 in the Si-RNA group was remarkably higher (P<0.05), the invasion capacity was evidently higher (P<0.05) and the apoptosis rate was lower (P<0.05). The Bax protein was reduced statistically in MKN-45 and AZ521 cells in the Si-RNA group (P<0.05), while Bcl-2 protein was increased significantly (P<0.05). At the concentration of 16 mu mol/L and 32 mu mol/L, the survival rate of cells in the Si-RNA group was dramatically higher than that in the other two groups (P<0.05). Conclusion: Highly expressed LncRNA ADPGK-AS1 can inhibit the proliferation and invasion of GC cells and promote apoptosis, and can increase the sensitivity of GC to chemotherapy.