Skip to main content
. 2019 Mar 4;20(4):e47638. doi: 10.15252/embr.201847638

Figure 1. Fusobacterium nucleatum preferentially binds, invades, and stimulates the growth of cancerous colorectal cells via Annexin A1.

Figure 1

  1. Lung cancer cells PC‐9, prostate cancer cells 22RV1, bladder cancer cells UMUC3, breast cancer cells MCF‐7, colonic adenoma‐derived non‐cancerous cells AA/C1 (aka C1) and AA/C1/SB (aka SB), or cancerous cells AA/C1/SB/10C (aka 10C) were incubated with wild‐type F. nucleatum 12230 (Fn), the fadA‐deletion mutant US1 (US1), or E. coli DH5α (E. coli) at multiplicity of infection (MOI) of 1,000:1. Cell numbers are mean values ± SEM. The experiment was performed in triplicates and repeated three times. *P < 0.05, **P < 0.01, ***P < 0.001, compared to untreated controls; # P < 0.05, ### P < 0.001, compared to US1‐treated cells (two‐way ANOVA).
  2. Attachment (left panel) and invasion (right panel) of wild‐type F. nucleatum 12230 (Fn) to the non‐cancerous SB cells, either untreated or transfected with antisense or sense ANXA1, and to the cancerous 10C cells, either untreated or transfected with control or ANXA1‐ or CDH1‐specific siRNA or both (MOI 50:1). F. nucleatum attachment and invasion to the untreated SB cells were designated as 100%, respectively; all other values were expressed as relative to those obtained with untreated SB. Data are mean values ± SEM. The experiment was performed in triplicates and repeated four times. *P < 0.05, **P < 0.01, and ***P < 0.001 (one‐way ANOVA).
  3. Left panel: qPCR analysis of Villin 1 (VIL1) mRNA levels in 10C cells treated with control siRNA or VIL1‐specific siRNA, demonstrating knockdown of Villin 1. Right panel: Attachment of F. nucleatum 12230 to 10C cells treated with control siRNA or VIL1‐specific siRNA. Data are mean values ± SD. The experiment was performed in triplicates and repeated twice. *P < 0.05 (Student's t‐test).