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. 2020 Apr 16;21(8):2773. doi: 10.3390/ijms21082773

Figure 1.

Figure 1

Chemotherapeutic agents in CRC. (A) 5-FU activates p38α and β isoforms leading to cell death, and the p38δ MAPK isoform, though MKK3 activation, leading to cell survival. Depletion of p38δ MAPK by RNA interference (siRNA) exerts antitumor effects. (B) Oxaliplatin induces apoptosis in CRC through p38 MAPK signaling pathway activation. The hyperactivation of p38 MAPK signaling supports oxaliplatin-resistance in CRC. Pharmacological p38 MAPK inhibition (SB 202190) re-sensitizes CRC cells to drug response. (C) Irinotecan (CPT-11) induces p38 MAPK activation dose dependently exerting different therapeutic outcomes in CRC: high dosage CPT-11 induces acute and short-lasting p38 MAPK activation leading to apoptosis; low dosage CPT-11 activates p38 MAPK in a delayed but sustained manner promoting cell-survival. Up arrows show levels of p38 activation via phosphorylation; down arrows show workflow of cell signaling; T bars represent inhibitory actions via siRNAs or chemicals.