Fig 1: MIR210HG facilitated the proliferative, migratory, and invasive capacities of LCa by downregulating SH3GL3. (A) Analysis of the mRNA and protein expression levels of SH3GL3 after transfection of the LCa cell lines with sh‐MIR210HG alone or sh‐MIR210HG plus sh‐SH3GL3. (B–E) Measurements of the viability, proliferation, migration, and invasion in A549, and NCI‐H1299 cells after transfection with sh‐MIR210HG alone or in combination with sh‐SH3GL3 using the MTT, colony formation, wound healing, and transwell assays. The experimental data are shown as mean ± SD. N = 3. *p < 0.05, **p < 0.01, ***p < 0.001.
Fig 2: Overexpression of SH3GL3 suppressed LCa cell growth and metastasis in vitro. (A) Measurements of the transfection efficiencies of oe‐SH3GL3 and sh‐SH3GL3. (B) The cell activities were detected using the MTT assay after transfection with the control, oe‐NC, oe‐SH3GL3, sh‐NC, or sh‐SH3GL3. (C–E) Analysis of the proliferation, migration, and invasion of LCa cells in response to transfection with oe‐NC, oe‐SH3GL3, sh‐NC, or sh‐SH3GL3. The experimental data are shown as the mean ± SD. N = 3. *p < 0.05, **p < 0.01, ***p < 0.001.
Fig 3: SH3GL3 was downregulated in the LCa tissues and cells. (A) The expression analysis of SH3GL3 in LCa tissues and control samples in the TCGA‐PRAD provisional data. (B) Relative levels of SH3GL3 in LCa tissues. (C) Correlation between the expression of MIR210H and SH3GL3 in LCa tissues. N = 38. (D and E) The relative mRNA and protein levels of SH3GL3 in the LCa cell lines. The experimental data are shown as the mean ± SD. N = 3. *p < 0.05, **p < 0.01, ***p < 0.001.
Fig 4: MIR210HG inhibited the transcription of SH3GL3 by recruiting DNMT1. (A) The localization of MIR210HG was analyzed using the FISH assay. (B) The overexpression efficiency of oe‐MIR210HG in A549 and NCI‐H1299 cells. (C) Analysis of the mRNA and protein levels of SH3GL3 after MIR210HG overexpression. (D) MS‐PCR was used to measure the effects of oe‐MIR210HG or sh‐DNMT1 transfection on the promoter methylation of SH3GL3. (E) Analysis of the CpG islands in the SH3GL3 promoter region. (F) RIP analysis of the interaction between MIR210HG and DNMT1. (G) The binding of DNMT1 to the SH3GL3 promoter region was analyzed in response to the overexpression of MIR210HG in LCa cell lines using the ChIP assay. (H) Colocalization of MIR210HG and DNMT1 using FISH and IF double staining. The experimental data are shown as the mean ± SD. N = 3. *p < 0.05, **p < 0.01, ***p < 0.001.
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