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. 2020 Oct 14;22(6):5095–5104. doi: 10.3892/mmr.2020.11601

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Copyright: © Yang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 6. — Upregulation of RAC1 reverses the anti-apoptotic and anti-inflammatory effects of HULC knockdown in HMEC-1 cells. (A) The protein expression of RAC1 in HMEC-1 cells treated with LPS or DMSO (control). (B) RAC1 protein expression in HMEC-1 cells transfected with an empty vector or a RAC1-overexpression vector. (C-F) HMEC-1 cells treated with LPS were transfected with si-NC, si-HULC, si-HULC + vector or si-HULC + RAC1. (C) Apoptotic rate of transfected HMEC-1 cells. (D) Protein expression levels of cleaved-cas3 and cleaved-cas9 in transfected HMEC-1 cells. The (E) mRNA and (F) protein expression levels of IL-6, TNF-α, ICAM1 and VCAM1 in transfected HMEC-1 cells. *P<0.05, **P<0.01. HULC, highly upregulated in liver cancer; siRNA, small interfering RNA; NC, negative control; LPS, lipopolysaccharide; RAC1, Rac family small GTPase 1; ICAM1, intercellular adhesion molecule; VCAM1, vascular cell adhesion molecule; HMEC-1, human dermal microvascular endothelial cells; DMSO, dimethyl sulfoxide.