Fig. 1: IL-16 suppresses tumor development and correlates with favorable survival in cancer patients. | Nature Communications

Fig. 1: IL-16 suppresses tumor development and correlates with favorable survival in cancer patients.

From: Interleukin-16 enhances anti-tumor immune responses by establishing a Th1 cell-macrophage crosstalk through reprogramming glutamine metabolism in mice

Fig. 1

a Serum levels of IL-16 in cancer patients were measured by ELISA. H, healthy control (n = 28); BC, breast cancer (n = 20); LC, lung cancer (n = 20). b The expression of IL-16 in tumor and corresponding normal tissues was analyzed using the integrated TCGA and the Genotype-Tissue Expression (GTEx) databases by Mann–Whitney U-test. BRCA = breast cancer, LUAD = lung adenocarcinoma. c, d Tumor tissues and the corresponding normal tissues from breast cancer patients (n = 6) were subjected to scRNA-seq and major cell clusters, and the cell-specific expression of IL16 was shown. Epic = epithelial cells, Mac = macrophages, Mono = monocytes, B = B cells, MC = mast cells, FB = fibroblasts, EC = endothelial cells (c); the levels of IL16 in various cell clusters were compared between tumor (T) and normal (N) tissues (d, left), the relative expression of IL16 (T/N) was calculated (d, right). e The correlations between IL16 expression and patient overall survival (OS) were analyzed in TCGA BRCA and LUAD cohorts. Patients were divided into IL16high and IL16low groups based on the optimal cut-off values. HR = hazard ratio. f, g E0071 cells were inoculated into the mammary fat pad of mice. When tumors were palpable, mice were intraperitoneally (i.p.) injected with PBS or IL-16 (1 μg/mouse, twice a week, n = 6/group). Tumor growth was monitored (f); tumors were weighed on day 22 (g). (h, i) LLC cells were subcutaneously (s.c.) inoculated into mice. When tumors were palpable, mice were i.p. injected with PBS or IL-16 (1 μg/mouse, twice a week, n = 5/group). Tumor growth was monitored (h); tumors were weighed on day 21 (i). j, k MMTV-PyMT spontaneous breast cancer mice were i.p. injected with PBS or IL-16 when tumors were palpable (n = 8/group). Tumor growth was monitored (j); tumors were weighed four weeks after IL-16 treatment (k). l E0071-bearing mice were administered with anti-IL-16 (αIL-16, 150 μg/mouse, twice a week, n = 4/group) or control IgG, tumor growth was monitored. Unpaired, two-tailed Student’s t-test (a, d, f–l), Mann–Whitney U-test (b), and log-rank test (e) were used. Data are presented as mean ± standard deviation (SD).

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