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. Author manuscript; available in PMC: 2021 Mar 22.
Published in final edited form as: Oncogene. 2020 Sep 22;39(43):6719–6732. doi: 10.1038/s41388-020-01463-0

Figure 6. MBIP drives the JNK/c-JUN/MMP axis in vivo.

Figure 6.

Representative IHC staining images from (A) Primary tumors or (B) metastatic lung lesions, from mice injected with MBIP-overexpressing (393-mCherry control and 393P-MBIP) and MBIP knockdown (344SQ-Scramble control and 344SQ-ShMBIP#5) cells, analyzed with antibodies against MBIP, p-JNK, p-c-Jun and MMP7. Scale bar = 50 μm. (C) Immunoblot analysis to determine expression levels of MBIP, p-JNK, total JNK, p-c-Jun, total c-Jun and MMP-7, in primary tumors formed by flank injection of MBIP-overexpressing (393-mCherry control and 393P-MBIP) and MBIP knockdown (344SQ-Scramble control and 344SQ-ShMBIP#5) cells as indicated. β-Actin was used as an internal loading control. (D) Schematic model: MBIP amplification leads to phosphorylation of JNK. Phosphorylated JNK actives c-JUN and AP-1 promoter which results into the transcription of MMPs, which is necessary for the increase in migration, invasion and metastasis.