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SUPPLEMENTARY FIGURES
EGFR signaling pathways are wired differently in normal 184A1L5 human mammary
epithelial and MDA-MB-231 breast cancer cells
Zachary Speth, Tanzila Islam, Kasturi Banerjee, Haluk Resat
SUPPLEMENTARY FIGURE 1. Statistical distribution of the interactions regulating the Akt
activity, i.e., Akt←Erk, Akt←p38, Akt←JNK, and Akt←STAT3 interactions in HME cells.
Distributions for the Akt←Erk, Akt←p38, and Akt←STAT3 interactions were bi-modal. The
horizontal axis shows the interaction strength r. The vertical axis reports the probability of
observing the interaction at a particular strength, and it is in arbitrary units. Area under each
curve totals to 100%.
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SUPPLEMENTARY FIGURE 2. Comparison of the strengths of the Akt←Erk, Akt←p38,
and Akt←STAT3 interactions in HME cells showing the strong correlation between obtained
interaction strength values. Horizontal and vertical axes show the interaction strengths r. (A)
rakt,p38 (y-axis) vs rakt,erk (x-axis); (B) rakt,stat3 (y-axis) vs rakt,erk (x-axis); and (C) rakt,stat3 (y-axis) vs
rakt,p38 (x-axis). The R2 values for linear correlation fits are reported in the plots.
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SUPPLEMENTARY FIGURE 3. Statistical distribution of the interaction strengths for the
p38←Erk and p38←JNK regulatory interactions in MDA-MB-231 breast cancer cells. The
horizontal axis shows the interaction strength r. The vertical axis reports the probability of
observing the interaction at a particular strength, and it is in arbitrary units. Area under each
curve totals to 100%.
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SUPPLEMENTARY FIGURE 4. Statistical distribution of the interactions regulating the
STAT3 activity in MDA-MB-231 breast cancer cells. Distributions for the STAT3←Erk (blue)
and STAT3←JNK (purple) interactions were slightly bi-modal. The horizontal axis shows the
interaction strength r. The vertical axis reports the probability of observing the interaction at a
particular strength, and it is in arbitrary units. Area under each curve totals to 100%.
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SUPPLEMENTARY FIGURE 5. Expanded and simplified version of Figure 3 in the main
text. Cellular proliferation of HME (dashed lines; N) and MDA-MB-231 (solid lines; C) cells
when STAT3 was inhibited with chemical inhibitors. The vertical axis shows the cell counts
normalized with respect to the starting seeding.
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SUPPLEMENTARY FIGURE 6. Figure 4 from the main text but without error bars showing
the effect of various inhibitors on the cellular proliferation of (A) MDA-MB-231 and (B)
184A1L5 cells over 7-day duration. Plots show the proliferation profiles when no protein was
inhibited (solid line), single proteins were inhibited (long dashed lines), two proteins were
inhibited simultaneously (short dashed lines), and three proteins were inhibited (dotted line). The
vertical axis shows cell counts normalized with respect to the starting seeding.
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SUPPLEMENTARY FIGURE 7. Figure 5 from the main text but without error bars. Cellular
proliferation of (A) MDA-MB-231 and (B) 184A1L5 cells over 7-day duration when Akt was
inhibited alone or together with other proteins. Plots show the proliferation profiles when no
protein was inhibited (solid black line), Akt was inhibited alone (solid red line), Akt and another
protein (listed in the legends) were inhibited (dashed lines), and Akt, p38 and JNK were
inhibited simultaneously (dotted line). The vertical axis shows cell counts normalized with
respect to the starting seeding.
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SUPPLEMENTARY FIGURE 8. Figure 6 from the main text but without error bars. Cellular
proliferation of MDA-MB-231 (solid lines; C) and 184A1L5 (dashed lines; N) cells when no
protein was inhibited (black), STAT3 was inhibited (red), p38 and JNK were inhibited (blue),
and Erk and JNK were inhibited (green). Dual inhibition of p38 and JNK or Erk and JNK cause
death of MDA-MB-231 cells but not of 184A1L5 HME cells. The vertical axis shows cell counts
normalized with respect to the starting seeding.
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