Panoply™ Human TNFRSF9 Over-expressing Stable Cell Line

Breast cancer is the most common cancer in women worldwide. Endocrine therapy is effective in 85% of breast cancer patients, but 15% are left with chemotherapy and surgery, which carries a poor prognosis. Immunotherapy is a novel treatment option for breast cancer, with PD-1 and CTLA-4 antibodies demonstrating immunomodulatory effects in breast cancer drug trials. Here, researchers discovered that TNFRSF9 regulates breast cancer cell proliferation, invasion, and apoptosis by regulating p38 phosphorylation, which in turn regulates PAX6 expression. TNFRSF9 levels were significantly reduced in breast cancer tissues and cell lines, and knockdown of TNFRSF9 promoted breast cancer cell development and progression. Furthermore, researchers found that downregulating TNFRSF9 upregulated phosphorylated p38 (p-p38) and PAX6 expression. A p38 phosphorylation inhibitor reversed PAX6 upregulation, inhibiting breast cancer cell proliferation and invasion and promoting apoptosis. This study proposes a novel TNFRSF9/p38/PAX6 axis that contributes to tumor suppression, suggesting a potential immunotherapy target for breast cancer.

Here, researchers investigated the role of TNFRSF9 gene deregulation in tumor development. Transwell assays were used to assess cell invasion (Figures 1a and b). Compared with the negative control, the TNFRSF9 knockdown in both MCF-7 and ZR-75-30 cell lines enhanced cell invasion, whereas the TNFRSF9 overexpression in both MCF-7 and ZR-75-30 cell lines inhibited cell invasion. Flow cytometry was used to assess apoptosis in both cell lines (Figures 1c and d). In the TNFRSF9 overexpressing cell lines, the apoptosis rate was reduced. These results suggest that TNFRSF9 is a suppressor of breast cancer malignancy and that activation of TNFRSF9 can inhibit breast cancer progression.

Figure 1 (a, b). Transwell assays were used to assess cell invasion. (Liu X, et al., 2022)

Figure 1 (c-d). The cell apoptosis was examined through flow cytometry in both cell lines. (Liu X, et al., 2022)