STK3 Suppresses Ovarian Cancer Progression by Activating NF-κB Signaling to Recruit CD8⁺ T-Cells

Figure 5

STK3 promoted release of CXCL16 and CX3CL1, migration of CD8+ T-cell, and activation of NF-κB signaling. (a) Chemokine array of the conditional medium (CM) from vector and lenti-STK3 OVCAR8 cells. A. Table summarizing the relative signal intensity of indicated chemokines is presented in the lower left corner. (b) Real-time qPCR analysis of the effect of STK3 overexpression on the CXCL16 and CX3CL1 mRNA level in OVCAR3 and OVCAR8 cells (two-tailed Student’s -test, ; ). (c) ELISA analysis of the CXCL16 and CX3CL1 level in the CM from vector and lenti-STK3 OVCAR3 and OVCAR8 cells (two-tailed Student’s -test, ; ). (d) Effects of rCXCL16 and rCX3CL1 on the migratory ability of human CD8+ T-cells. The number of cells was counted by Cellometer (two-tailed Student’s -test, ; ; ). (e) Ovarian cancer cell culture supernatants were neutralized with anti-CXCL16 antibody and anti-CX3CL1 antibody and the migratory ability of CD8+ T-cells. The number of cells was counted by Cellometer (two-tailed Student’s -test, ; ; ). (f) Correlation between STK3 and NFKB1 in the TCGA database. (g) Correlation between NFKB1 and CXCL16 or CX3CL1 in the TCGA database. (h) Western blot analysis of the effect of the STK3 overexpression on the NF-κB pathway activity.

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