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. Author manuscript; available in PMC: 2016 Apr 26.
Published in final edited form as: Cell Rep. 2015 Dec 31;14(2):282–297. doi: 10.1016/j.celrep.2015.12.029

Figure 4. STING signal defect leads colon cancer cells more susceptible to DNA virus infection.

Figure 4

(A) Cells (same as in figure 1) were infected with HSV1γ34.5 at M.O.I. 5 for 1 hour and human IFNB induction was analyzed by qPCR 3 hours post infection. (B) Normal human hTERT cells and selected human colon cancer cell lines (cGAS positive: SW1116, HT29; cGAS negative: SW480, HT116) were infected with HSV1γ34.5 at indicated M.O.I. for 1 hour, and titration of HSV1γ34.5 was analyzed by standard plaque assay in Vero cells 24 hours later. (C) Cells (same as in B) were infected with HSV1γ34.5 at M.O.I. 1 for 1 hour, and cell viability was analyzed by trypan blue staining 24 hours and 48 hours later. (D) Cells (same as in A) were infected with HSV1-Luc at indicated M.O.I. for 1 hour, and luciferase activity was analyzed 24 hours later. (E) Colon Cancer cells were infected with Vaccinia Virus at M.O.I. 100 and analyzed by qPCR for IFNB expression 3 hours post infection. (F) Cells same as E were analyzed by qPCR for CXCL10 expression. Data is representative of at least two independent experiments. Error bars indicate s.d. *, p<0.05; **, p<0.01; Student’s t-test. See also Figure S2.