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. Author manuscript; available in PMC: 2023 Oct 10.
Published in final edited form as: Cancer Cell. 2022 Sep 22;40(10):1128–1144.e8. doi: 10.1016/j.ccell.2022.08.015

Figure 3. MPS1 inhibition induces micronuclei formation and subsequent STING activation in KL cells.

Figure 3.

(A) Representative confocal microscope images of DAPI staining in H1944 cells treated with 200 nM CFI-402257, 5 nM docetaxel, or 200 nM barasertib. Arrows indicate micronuclei. Inset highlights micronucleus. Scale bars, 10 μm.

(B) Number of micronuclei in H1944 cells treated with the indicated DNA-damaging agents (n = 3).

(C) Relative messenger RNA (mRNA) expression of CXCL10 (y axis) versus number of micronucleus (x axis) in H1944 cells treated with the indicated DNA-damaging agents. R2 values and p values for the correlation (Pearson’s r correlation) are shown.

(D) Quantification of cell cycle analysis through propidium iodide staining for the cells after treatment with 200 nM CFI-402257 (CFI), 2.5 μM cisplatin (CDDP), 5 μM etoposide (ETP), 500 nM pemetrexed (PEM), or 50 μM hydroxyurea (HU) for 48 h.

(E and F) Enzyme-linked immunosorbent assay (ELISA) of human CXCL10 or IFN-β levels in CM (E), or immunoblot (IB) of the indicated proteins (F) in H1944 cells treated with 200 nM CFI-402257 (n = 4). GM, growth medium.

(G and H) ELISA of human CXCL10 in CM (G), or IB of the indicated proteins (H) in H1944 or THP1 cells treated with 200 nM CFI-402257, or 10 μM ADU-S100 for 24 h (n = 4). THP1 cells were differentiated to macrophages in the presence of 25 nM phorbol 12-myristate13-acetate (PMA) for 48 h.

All quantitative data are represented as mean ± standard deviation; p values were calculated by one-way analysis of variance followed by Tukey’s post hoc test (E and G), **p < 0.01. See also Figure S3.