Section 80
Chapter 79,648

T63 induces apoptosis in nasopharyngeal carcinoma cells through mitochondrial dysfunction and inhibition of PI3K/Akt signaling pathway

Liu, Q.; Chen, W.; Yang, H.

Translational Cancer Research 9(8): 4635-4645


ISSN/ISBN: 2219-6803
PMID: 35117827
Accession: 079647559

Nasopharyngeal carcinoma (NPC) is a common malignant tumor in china. T63 is one of novel curcumin analogues, which reduces the tumorigenic potential effectively. We investigated the mechanism of anti-cancer activity on NPC cells treatment with T63 for the first time. Cell viability was monitored using the method of MTT and colony formation assay. Morphological changes observed by fluorescence microscope with Hoechst33342 staining. The cell cycle, the rates of cell apoptotic and mitochondrial membrane potential were identified by flow cytometry, and apoptotic proteins were identified by western blot analysis. In our study, we found a significant decrease in the number of viable cells and in colony formation abilities of NPC cells (CNE2 and CNE2R) after 24, 48 and 72 h treatment with T63. T63 promoted morphologic changes of apoptosis and increased apoptotic rate. T63 promoted also cell cycle arrest of G2/M phases followed by decreased cell viability in CNE2 and CNE2R after 48 h. Then the loss of the mitochondrial membrane potential and release of cytochrome-c were demonstrated. Western blotting analysis found a decrease in Bcl-2/Bax ratio and activation of caspase-8, -9, -3 and PARP. And the changes of PTEN and p-Aktp473 suggested PTEN/PI3K/Akt might be an important signaling pathway in the anticancer role of T63. T63 definitely induced apoptosis in radiosensitive and radioresistant NPC cell lines. But the apoptotic effect was stronger on radioresistant cells than that on radiosensitive cells through activation of mitochondria-mediated apoptotic pathway.

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