SOD3/EC-SOD Antibody (4GG11G6) NBP1-22417 from Novus Biologicals, a Bio-Techne Brand

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Breast cancer research : BCR
October 30 2014

Fig 1: Restoration of Sod3 in 66 cl4-VEGF-C KD cells partially rescues resistance to oxidative stress and tumor progression. (A) Expression of Sod3 in 66 cl4-VEGF-C KD cells (KD2 in Figure 5). Empty vector was also introduced into 66 cl4-scram and 66 cl4-VEGF-C KD2 cells as a control. Sod3 expression was assessed in each cell line using a real-time PCR SYBR Green assay (top). Expression of secreted Sod3 in the media of 66 cl4-scram, 66 cl4-VEGF-C KD and 66 cl4-VEGF-C KD + Sod3 cells was measured by Western blot analysis (bottom). (B) Flow cytometry was performed to measure cell death induced by H2O2 under each condition shown. Three independent experiments were performed, and the data were combined for quantitation. (C) Cells from the 66 cl4-scram, VEGF-C KD and VEGF-C KD + Sod3 lines were injected into the fourth mammary fat pad of female BALB/c mice. Tumor growth in the mice was measured using calipers and calculated using the formula V = 1/2(W)(W)(L) (top). A representative picture of tumors from each group shows that restoration of Sod3 in VEGF-C KD cells partially rescues the size of tumors compared to scramble control tumors (bottom). (D) Representative in vivo image of 66 cl4-scram, VEGF-C KD and VEGF-C KD + Sod3 groups at day 60 after injection (top). Quantitation of bioluminescence imaging (in photons per second) emanating from the region surrounding the lungs (bottom). Mice that did not develop primary tumors were excluded from the quantitation. (E) Incidence of tumor formation and metastasis in the groups of mice injected with 66 cl4-scram, VEGF-C KD or VEGF-C KD + Sod3 cells. Restoration of Sod3 expression in the VEGF-C KD cells increased the number of mice that developed primary tumors and metastases, although not to the levels observed in the scramble control group. Fisher's exact test (two-sided) results indicated a significant increase in the number of mice that developed metastases when Sod3 expression was restored in the VEGF-C KD tumors.
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Breast cancer research : BCR
October 30 2014

Fig 2: Expression of VEGFC and SOD3 in human cancers. (A) VEGFC and SOD3 expression values were retrieved from an Oncomine microarray data set [43] (as indicated in the figure) and were plotted by expression value. Statistical analysis was performed using Pearson r correlation (two-tailed). (B) Proposed model for the function of vascular endothelial growth factor C (VEGF-C) in breast cancer progression. Expression of VEGF-C in a subset of tumor cells confers the ability to resist oxidative stress generated during tumor growth, and this ability is partially mediated by Sod3. However, VEGF-C mediates other pathways that are important in conferring resistance to chemotherapies, thus contributing to tumor recurrence. Blocking VEGF-C signaling would therefore be expected to sensitize breast cancers to chemotherapies that induce oxidative stress, to contribute to a reduction in tumor-initiating cells (TICs) and to decrease lymphangiogenesis, thus likely improving survival and prevent recurrence.
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Breast cancer research : BCR
October 30 2014

Fig 3: Vascular endothelial growth factor C regulates Sod3 expression in 66 cl4 mammary carcinoma cells. (A) Total RNA from 66 cl4-scramble and 66 cl4-VEGF-C KD2 cells was converted to cDNA and used to perform a mouse oxidative stress PCR array. Nine candidate genes of the eighty-four examined were identified in the PCR array with more than a twofold change in response to VEGF-C KD. (B) Sod3 mRNA expression was determined using a real-time PCR SYBR Green assay on 66 cl4-scram and 66 cl4-VEGF-C KD1 and KD2 cells (top). Western blot analysis of Sod3 expression in 66 cl4-scram and VEGF-C KD1 and KD2 cells (bottom). (C) Sod3 mRNA expression was determined by real-time PCR SYBR Green assay on three pairs of 66 cl4-scram and VEGF-C KD1 or KD2 tumors (each pair was derived from the same animal).
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Breast cancer research : BCR
October 30 2014

Fig 4: Neuropilin 2-knockdown in 66 cl4 mouse mammary carcinoma cells decreases superoxide dismutase 3 expression and sensitizes cells to oxidative stress. (A) NRP2 and VEGFR3 mRNA expression in human breast cancer cell lines. Box plots of NRP2 (left) or VEGFR3 (FLT4) (right) gene expression across 51 previously reported breast cancer cell lines grouped into basal A, basal B and luminal subgroups. NRP2 and VEGFR3 gene expression in human breast cancer cell lines was assessed using GOBO [21]. (B) Two different short-hairpin RNAs (shRNAs 1 and 2) were used to knock down neuropilin 2 (Nrp2) in 66 cl4 cells. Expression of Nrp2 in 66 cl4-scram and 66 cl4-Nrp2 knockdown (KD) cells was determined by Western blot analysis (left). Decreased expression of superoxide dismutase 3 (Sod3) was observed in 66 cl4-Nrp2 KD cells compared to 66 cl4-scram cells (right). Whole-cell lysates (top) or media (bottom) from 66 cl4-scram and 66 cl4-Nrp2 KD cells were collected for the detection of Sod3 by Western blotting. (C) Viability of 66 cl4-scram and 66 cl4-Nrp2 KD cells treated with increasing doses of H2O2. A CellTiter-Glo assay was used to measure viable cells. Three independent experiments were performed and combined for quantification.