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. 2020 Feb 17;38(3):266–274. doi: 10.1002/cbf.3473

Figure 5.

Figure 5

LINC00341 interacts with HMGB2 and suppress it into the nucleus. A, RNA pulldowns were performed with SW620 cells using full‐length LINC00341 transcript sense and antisense. HMGB2 was confirmed by immunoblotting. B, Interaction of LINC00341 with HMGB2 was verified by an RNA immunoprecipitation (RIP) assay. C,D, The expression of HMGB2 in nucleus and cytoplasm of LINC00341 overexpressing HCT116 cells and LINC00341‐knockdown SW620 cells were demonstrated by Western blot. The immunosignal was quantified using the quantity one software. Nuclear segregation is assayed by Histone H3. Cytoplasmic segregation is assayed by Actin. E, Real‐time PCR analysis of epithelial to mesenchymal transition (EMT) markers expression infected with LINC00341 lentivirus or control lentivirus and transfection of HMGB2 vector and empty vector. F, Western blot analysis was performed to detect EMT markers. G, A hypothetical model illustrating that LINC00341 suppresses colorectal cancer progression through nucleocytoplasmic shuttling of HMGB2. Error bars represent mean ± SD based on three independent experiments. Results are shown as means ± SD by two‐tailed Student's t test. *P < .001. **P < .01. ***P < .001