Figures & data
Figure 1. Cobalt chloride (CoCl2) induced hypoxia injury. (A) Cell viability, (B) cell apoptosis, (C) cell apoptotic proteins p53, Bcl-2, Bax and cleaved-Caspase-3 were detected using cell counting kit-8 assay, flow cytometry and western blot, respectively. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05, **p < .01 and ***p < .001 were all significant difference.
![Figure 1. Cobalt chloride (CoCl2) induced hypoxia injury. (A) Cell viability, (B) cell apoptosis, (C) cell apoptotic proteins p53, Bcl-2, Bax and cleaved-Caspase-3 were detected using cell counting kit-8 assay, flow cytometry and western blot, respectively. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05, **p < .01 and ***p < .001 were all significant difference.](/cms/asset/2d46ab01-f940-44c7-a9a0-68ddd2cba90f/ianb_a_1620759_f0001_b.jpg)
Figure 2. Cobalt chloride (CoCl2) induced expression of lncRNA regulator of reprogramming (ROR). The expression of ROR was detected using qRT-PCR. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05 indicated significant difference.
![Figure 2. Cobalt chloride (CoCl2) induced expression of lncRNA regulator of reprogramming (ROR). The expression of ROR was detected using qRT-PCR. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05 indicated significant difference.](/cms/asset/cdc0ae8d-0e1e-433d-90df-5418558fa60f/ianb_a_1620759_f0002_b.jpg)
Figure 3. Overexpression of regulator of reprogramming (ROR) promoted cobalt chloride (CoCl2) treated HK-2 cell growth. (A) The alter expression of ROR was via transfection and expression of ROR was determined using qRT-PCR. (B) Cell viability, (C) cell apoptosis, (D,E) cell apoptosis-related proteins and (F) HIF-α expression were analyzed using cell counting kit-8 assay, flow cytometry and western blot, respectively. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05, **p < .01 and ***p < .001 were all significant difference.
![Figure 3. Overexpression of regulator of reprogramming (ROR) promoted cobalt chloride (CoCl2) treated HK-2 cell growth. (A) The alter expression of ROR was via transfection and expression of ROR was determined using qRT-PCR. (B) Cell viability, (C) cell apoptosis, (D,E) cell apoptosis-related proteins and (F) HIF-α expression were analyzed using cell counting kit-8 assay, flow cytometry and western blot, respectively. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05, **p < .01 and ***p < .001 were all significant difference.](/cms/asset/fa4090c8-ae1e-4e32-a8e7-b9f7c1d72b56/ianb_a_1620759_f0003_b.jpg)
Figure 4. Silence of regulator of reprogramming (ROR) inhibited cobalt chloride (CoCl2) treated HK-2 cell growth. (A) The alter expression of ROR was via transfection and expression of ROR was determined using qRT-PCR. (B) Cell viability, (C) cell apoptosis, (D,E) cell apoptosis-related proteins and (F) hypoxia-inducible factor (HIF)-α expression were analyzed using cell counting kit-8 assay, flow cytometry and western blot, respectively. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05, **p < .01 and ***p < .001 were all significant difference.
![Figure 4. Silence of regulator of reprogramming (ROR) inhibited cobalt chloride (CoCl2) treated HK-2 cell growth. (A) The alter expression of ROR was via transfection and expression of ROR was determined using qRT-PCR. (B) Cell viability, (C) cell apoptosis, (D,E) cell apoptosis-related proteins and (F) hypoxia-inducible factor (HIF)-α expression were analyzed using cell counting kit-8 assay, flow cytometry and western blot, respectively. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05, **p < .01 and ***p < .001 were all significant difference.](/cms/asset/23b054c8-c8f1-4924-ac2c-11bad9a136ce/ianb_a_1620759_f0004_b.jpg)
Figure 5. Regulator of reprogramming (ROR) decreased the expression of miR-145 in cobalt chloride (CoCl2) treated cells. The expression of miR-145 was detected using qRT-PCR. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05 and **p < .01 were both significant difference.
![Figure 5. Regulator of reprogramming (ROR) decreased the expression of miR-145 in cobalt chloride (CoCl2) treated cells. The expression of miR-145 was detected using qRT-PCR. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05 and **p < .01 were both significant difference.](/cms/asset/56ef79a0-1e09-481f-927f-38dd8c5fbfe3/ianb_a_1620759_f0005_b.jpg)
Figure 6. Overexpression of regulator of reprogramming (ROR) promoted cobalt chloride (CoCl2) treated HK-2 cell growth through downregulation of miR-145. (A) The alter expression of miR-145 was via transfection and expression of miR-145 was determined using qRT-PCR. (B) Cell viability, (C) cell apoptosis, (D,E) cell apoptosis-related proteins and (F) hypoxia-inducible factor (HIF)-α expression were analyzed using cell counting kit-8 assay, flow cytometry and western blot, respectively. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05, **p < .01 and ***p < .001 were all significant difference.
![Figure 6. Overexpression of regulator of reprogramming (ROR) promoted cobalt chloride (CoCl2) treated HK-2 cell growth through downregulation of miR-145. (A) The alter expression of miR-145 was via transfection and expression of miR-145 was determined using qRT-PCR. (B) Cell viability, (C) cell apoptosis, (D,E) cell apoptosis-related proteins and (F) hypoxia-inducible factor (HIF)-α expression were analyzed using cell counting kit-8 assay, flow cytometry and western blot, respectively. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05, **p < .01 and ***p < .001 were all significant difference.](/cms/asset/6939f094-068e-494d-aa0f-e7db6b01b55b/ianb_a_1620759_f0006_b.jpg)
Figure 7. Regulator of reprogramming (ROR) activated ERK and inactivated MAPK pathway. (A) The phosphorylation of ERK and (B) MAPK was determined through western blot. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05 and **p < .01 were both significant difference.
![Figure 7. Regulator of reprogramming (ROR) activated ERK and inactivated MAPK pathway. (A) The phosphorylation of ERK and (B) MAPK was determined through western blot. All data demonstrated as mean + standard deviation (SD) of three replicates. *p < .05 and **p < .01 were both significant difference.](/cms/asset/9d8c89d1-531e-43b6-8102-f93c88335f1c/ianb_a_1620759_f0007_b.jpg)