Abstract:
:The evading apoptosis of tumor cells may result in chemotherapy resistance. Therefore, investigating what molecular events contribute to drug-induced apoptosis, and how tumors evade apoptotic death, provides a paradigm to explain the relationship between cancer genetics and treatment sensitivity. In this study, we focused on the role of RMP/URI both in cisplatin-induced endogenous apoptosis and in TRAIL-induced exogenous apoptosis in HCC cells. Although flow cytometric analysis indicated that RMP overexpression reduced the apoptosis rate of HCC cells treated with both cisplatin and TRAIL, there was a difference in mechanism between the two treatments. Western blot showed that in intrinsic apoptosis induced by cisplatin, the overexpression of RMP promoted the Bcl-xl expression both in vitro and in vivo. Besides, RMP activated NF-κB/p65(rel) through the phosphorylation of ATM. However, in TRAIL-induced extrinsic apoptosis, RMP significantly suppressed the transcription and expression of P53. Moreover, the forced expression of P53 could offset this inhibitory effect. In conclusion, we presumed that RMP inhibited both intrinsic and extrinsic apoptosis through different signaling pathways. NF-κB was distinctively involved in the RMP circumvention of intrinsic apoptosis, but not in the extrinsic apoptosis of HCC cells. RMP might play an important role in defects of apoptosis, hence the chemotherapeutic resistance in hepatocellular carcinoma. These studies are promising to shed light on a more rational approach to clinical anticancer drug design and therapy.
journal_name
Int J Biol Scijournal_title
International journal of biological sciencesauthors
Ji Y,Shen J,Li M,Zhu X,Wang Y,Ding J,Jiang S,Chen L,Wei Wdoi
10.7150/ijbs.36829subject
Has Abstractpub_date
2019-10-15 00:00:00pages
2692-2706issue
12issn
1449-2288pii
ijbsv15p2692journal_volume
15pub_type
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