Research Paper Volume 15, Issue 11 pp 4949—4962

PZR promotes tumorigenicity of lung cancer cells by regulating cell migration and invasion via modulating oxidative stress and cell adhesion

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Figure 5. PZR knockout reduced tumor-forming ability of SPC-A1 cells in immunodeficient NYG mice. NYG mice (7-week male, 5 in each group) were subcutaneously engrafted with wild- type or PZR-KO SPC-A1 cells. (A) Tumor volumes were measured every four days from day 5. Tumor sizes are expressed as mean ± SD. (n = 5). ***P < 0.001 versus control group after day 9. (BD) Size and weight of tumor tissues excised from NYG mice after 24 days of implantation. Error bars denote standard deviation (n = 5). ***P < 0.001, ****P < 0.0001. (EG) Histochemical staining of paraffin-embedded tissue sections of tumors revealed that PZR-KO SPC-A1 cells displayed an absence of PZR expression in tumor cells (E), increased necrosis (green arrow) and lack of blood vessels (red arrows) (F), and reduced number of Ki-67-positive cells with PZR-KO SPC-A1 cells (G), (magnification, ×200).