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. 2021 Jun 4;11:649029. doi: 10.3389/fonc.2021.649029

Figure 8.

Figure 8

The molecular mechanisms of FHL3-mediated EMT and chemotherapy resistance. (1) Ubiquitin inhibitor bortezomib was added into the medium of FHL3-NC and SH1 to observe the regulation of Slug; it might reverse the FHL3-downregulation-induced decrease of Slug (A, B); (2) 293T cell was transfected with Slug-plasmid and/or RNF146-plasmid and FHL3-plasmid, and the basic expression of those protein was detected by western blot (C, E); Co-IP assay was used to detect the interaction between FHL3, Slug, and RNF146, and the result suggested that RNF146-myc can interact with FHL3-HA and Slug-Flag (C); (3) The levels of HIF-1α, cleaved-caspase-3 and MDR1 were investigated in OHP-resistance FHL3-NC/SH1cells (D, F); (4) The relationship of FHL3 and MDR1was investigated in GC cell line and slices; IHC showed that advanced GC with chemotherapy resistance has higher level of FHL3 and MDR1 (200× magnification) (G, H). (5) Mechanism scheme: FHL3 leads to EMT via competitively bonding the ubiquitin complex with Slug, and multi-pathway activation contributes to chemotherapy resistance (I).