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. Author manuscript; available in PMC: 2022 Dec 15.
Published in final edited form as: Cancer Res. 2022 Jun 15;82(12):2254–2268. doi: 10.1158/0008-5472.CAN-21-3230

Figure 4. MCU promotes cell migration / invasion, metabolic stress resistance and PDAC metastasis through activation of Nrf2.

Figure 4.

A-D, the effects of Nrf2 knockdown on cell migration (A), invasion (B), wound closure (C) and glucose deprivation-induced cell death (D) by in AsPC-1 and SW1990 cells, as determined using transwell assays (A and B), wound healing assays (C) and PI staining (D).

E, the effects of Keap1 knockdown on Nrf2 protein levels in control or MCU KO PDAC cells (AsPC1 and MiaPaCa-2).

F-I, the effects of Keap1 knockdown on cell migration (F), invasion (G), wound closure (H) and glucose deprivation-induced cell death (I) by in AsPC-1 and MiaPaCa-2 cells, as determined using transwell assays (F and G), wound healing assays (H) and PI staining (I).

J-M, the effects of MCU OE and Nrf2 knockdown on SW1990 tumor growth and metastasis in a orthotopic xenograft model. J and M, images of harvested tumor (J) and quantitation of tumor weight (M) at the end of the experiment. L, representative images showing metastatic lesions (red arrow)in the peritoneal cavity and liver in mice implanted with control of MCU OE SW1990 cells with or without Nrf2 knockdown. M, quantitation of the numbers of metastatic lesions observed in L.

Data in A-D, F-I were presented as mean ± SD from three biological replicates and analyzed using two-tailed, two sample unpaired Student’s t-test. *, **, *** and **** indicated p<0.05, 0.01, 0.001 and 0.0001, respectively.