that , in response to mitomycin C and doxorubicin , human hepatocellular carcinoma cells generate conflicting signals , mediated by cyclin E and p21WAF1/CIP1 , which respectively accelerates and represses cell cycle transition .
Mitomycin C and doxorubicin elicit conflicting signals by causing accumulation             of cyclin E prior to p21WAF1/CIP1 elevation in human hepatocellular carcinoma             cells. Proteins involved in the G1 phase of the cell cycle are aberrantly expressed,             sometimes in mutated forms, in human cancers including human hepatocellular carcinoma.             Upon attack by a DNA-damaging anticancer drug, a cell arrests at the G1 phase;             this is a safety feature prohibiting entry of DNA-damaged cells into S-phase.             p21WAF1/CIP1 prevents damaged cells from progressing to the next cell cycle. Here,             we show that , in response to mitomycin C and doxorubicin , human hepatocellular carcinoma cells generate conflicting signals , mediated by cyclin E and p21WAF1/CIP1 , which respectively accelerates and represses cell cycle transition . Exposure to             these anticancer drugs led to rapid accumulation of cyclin E in both p53-proficient             HepG2 and p53-deficient Hep3B cells. Such anticancer drug-induced cyclin E accumulation             influenced the G1-S-phase transition, but not DNA fragmentation-mediated death.             In p53-proficient HepG2 cells, accumulation of cyclin E was followed by an increase             in the level of p53-dependent p21WAF1/CIP1, thereby inhibiting further the G1-S-phase             transition. Sublethal drug concentrations also induced rapid accumulation of cyclin             E, but p21WAF1/CIP1 accumulation was delayed, further facilitating the G1-S-phase             transition. Eventually, most cells arrested in G2/M. Thus, mitomycin C- or doxorubicin-induced             conflicting signals, mediated by cyclin E and p21WAF1/CIP1, are in play in human             hepatocellular carcinoma cells. Damaged G1 cells either immediately enter S-phase,             or do not do so at all, depending on the extent of DNA damage.
### Instruction:
            Given the context about compound efficacy for the given treatment mentioned within the input, mentioned the compounds 
            that can co-occur for the mentioned treatment

            ### Input:
            Mitomycin C and doxorubicin elicit conflicting signals by causing accumulation             of cyclin E prior to p21WAF1/CIP1 elevation in human hepatocellular carcinoma             cells. Proteins involved in the G1 phase of the cell cycle are aberrantly expressed,             sometimes in mutated forms, in human cancers including human hepatocellular carcinoma.             Upon attack by a DNA-damaging anticancer drug, a cell arrests at the G1 phase;             this is a safety feature prohibiting entry of DNA-damaged cells into S-phase.             p21WAF1/CIP1 prevents damaged cells from progressing to the next cell cycle. Here,             we show that , in response to mitomycin C and doxorubicin , human hepatocellular carcinoma cells generate conflicting signals , mediated by cyclin E and p21WAF1/CIP1 , which respectively accelerates and represses cell cycle transition . Exposure to             these anticancer drugs led to rapid accumulation of cyclin E in both p53-proficient             HepG2 and p53-deficient Hep3B cells. Such anticancer drug-induced cyclin E accumulation             influenced the G1-S-phase transition, but not DNA fragmentation-mediated death.             In p53-proficient HepG2 cells, accumulation of cyclin E was followed by an increase             in the level of p53-dependent p21WAF1/CIP1, thereby inhibiting further the G1-S-phase             transition. Sublethal drug concentrations also induced rapid accumulation of cyclin             E, but p21WAF1/CIP1 accumulation was delayed, further facilitating the G1-S-phase             transition. Eventually, most cells arrested in G2/M. Thus, mitomycin C- or doxorubicin-induced             conflicting signals, mediated by cyclin E and p21WAF1/CIP1, are in play in human             hepatocellular carcinoma cells. Damaged G1 cells either immediately enter S-phase,             or do not do so at all, depending on the extent of DNA damage.

            ### Response:
            mitomycin, doxorubicin
            