Quinalizarin enhances radiosensitivity of nasopharyngeal carcinoma cells partially by suppressing SHP-1 expression

Abstract

The purpose of this study was to investigate the influence of quinalizarin on the radiosensitivity of nasopharyngeal carcinoma (NPC) cells and the relevant underlying mechanisms. Human NPC cell lines CNE-1, CNE-2 and 5-8F were treated with quinalizarin and then irradiated with different X-rays doses. Cell viability, survival, DNA double-strand breaks (DSB), apoptosis, cell cycle distribution, expression of SHP-1 and other related proteins were detected with MTT assay, colony formation assay, immunofluorescent assay, flow cytometry and western blot analysis, respectively. We also examined how the effects of quinalizarin were affected by SHP-1-overexpression by lentivirus transfection. Quinalizarin at 25 µM enhanced radiosensitivity of NPC cells. This increased radiosensitivity was due to inhibition of cell viability, which delayed DSB repair as seen by significantly increased γ-H2AX foci, promoting apoptosis by 34% in CNE-1 and 9% in CNE-2 cells compared to controls and changing cell cycle distribution in CNE-1, but not CNE-2 cells. Quinalizarin treatment obviously decreased SHP-1 protein expression. Overexpressing SHP-1 partially reversed the radiosensitive effect of quinalizarin. Quinalizarin inhibited binding of p65 and the promoter of SHP-1, and decreased the activities of SHP-1 promoter and SHP-1. Quinalizarin enhanced radiosensitivity of NPC cells partially by suppressing SHP-1 expression.

Involvement of endothelial CK2 in the radiation induced perivascular resistant niche (PVRN) and the induction of radioresistance for non-small cell lung cancer (NSCLC) cells

“…The inhibition of CK2 in lung cancer cells effectively suppresses the proliferation of tumor cells [24, 30–33]. Down regulation of CK2 is also reported to enhance the radiosensitivity of nasopharyngeal carcinoma cells [34]. In addition, in our previous study we verified that CK2 inhibition could radiosensitize lung cancer cells [22].…”

Association of protein kinase CK2 inhibition with cellular radiosensitivity of non-small cell lung cancer

“…We also tried si-CK2α to exclude the nonspecific effects of the inhibitor. The data showed that the inhibition of CK2 enhanced the radiosensitivity of nasopharyngeal carcinoma cells 21 , but failed to radiosensitize malignant glioma cells 22 . Our results showed that pretreatment with Quinalizarin before IR decreased SF 2 in A549 and H460 cells, revealing that Quinalizarin enhanced the radiosensitivity (Fig.…”

“…Our results are in agreement with Xiaofen Pan, et al . and Felix Zwicker, et al ., who found that the inhibition of CK2 increases the number of IR-induced γ-H2AX foci and delays their removal of it in human nasopharyngeal carcinoma cells 21 and colon carcinoma cells 28 . 53BP1 is a P53 binding protein, which also participants in the early repair of IR-induced DSBs 29 , 30 .…”

Quinalizarin Induces Apoptosis through Reactive Oxygen Species (ROS)-Mediated Mitogen-Activated Protein Kinase (MAPK) and Signal Transducer and Activator of Transcription 3 (STAT3) Signaling Pathways in Colorectal Cancer Cells

“…Quinalizarin (1,2,5,8-tetrahydroxyanthraquinone) has been regarded as a highly selective cell-permeable compound [ 5 ]. Many studies have shown that quinalizarin can regulate proliferation, migration, and apoptosis in various cancer cell lines [ 6 , 7 ]; however, the mode of action of quinalizarin as an anticancer drug needs further investigation and its potential signaling pathways need to be identified.…”