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MOMORDIN IC TRIGGERS MITOCHONDRIA-MEDIATED APOPTOSIS OF CHOLANGIOCARCINOMA CELLS AND ENHANCES THE EFFICACY OF CONVENTIONAL CHEMOTHERAPEUTIC DRUGS

PREEYAKAN MALIKRONG 1, AUEMDUAN PRAWAN 1,2, SARINYA KONGPETCH 1,2, LADDAWAN SENGGUNPRAI 1,2*

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Novel treatment strategies are of great interest in cholangiocarcinoma (CCA) treatment due to the low response rate and increasing drug resistance with conventional chemotherapy based on gemcitabine and cisplatin. The current study evaluated the apoptosis-inducing effect of the phytochemical momordin Ic on CCA cells, as well as its underlying mechanisms. According to the findings, momordin Ic potently inhibited KKU-213 CCA cell viability by inducing apoptotic cell death. Molecular analyses demonstrated that the compound activated initiator caspase-9 activity caused mitochondrial depolarization, upregulated cleaved-caspase-9, cytochrome C and pro-apoptotic protein BAX expression. These findings suggested that momordin Ic’s apoptosis-inducing activity in CCA cells was mediated by a mitochondrial-dependent pathway. This study also investigated whether momordin Ic improves the therapeutic efficacy of conventional chemotherapeutic drugs for the CCA treatment. The results revealed the synergistic effects of momordin Ic, gemcitabine and cisplatin on KKU-213 CCA cells. Momordin Ic as a whole may be a promising candidate with chemotherapeutic potential for the CCA therapy.