SHP-1 overexpression increases the radioresistance of NPC cells by enhancing DSB repair, increasing S phase arrest and decreasing cell apoptosis

Pan, Xia; Mou, Jingjing; Li, Sha; Sun, Ziyi; Meng, Rui; Zhou, Zhenwei; Wu, Gang; Peng, Gang

doi:10.3892/or.2015.3939

Cited by 10 publications

(4 citation statements)

References 34 publications

(37 reference statements)

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“…Chk2, an important signal transduction protein in the DNA damage pathway, activates a variety of downstream DNA repair genes by phosphorylation. Studies have shown that the increased activation of ATM/Chk2 leads to the enhancement of DNA repair, resulting in radioresistance 58 . Activated ATM can increase the levels of activated p53 protein and the ability for DNA repair.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA PVT1 predicts poor prognosis and induces radioresistance by regulating DNA repair and cell apoptosis in nasopharyngeal carcinoma

et al. 2018

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The long non-coding RNA, plasmacytoma variant translocation 1 (PVT1), is highly expressed in a variety of tumors, and is believed to be a potential oncogene. However, the role and mechanism of action of PVT1 in the carcinogenesis and progression of nasopharyngeal carcinomas (NPCs) remains unclear. In this study, for the first time, we have discovered that PVT1 shows higher expression in NPCs than in normal nasopharyngeal epithelial tissue, and patients with NPCs who show higher expression of PVT1 have worse progression-free and overall survivals. Additionally, we observed that the proliferation of NPC cells decreased, and their rate of apoptosis increased; these results indicated that the knockdown of PVT1 expression in the NPC cells induced radiosensitivity. Further, we have shown that the knockdown of PVT1 expression can induce apoptosis in the NPC cells by influencing the DNA damage repair pathway after radiotherapy. In general, our study shows that PVT1 may be a novel biomarker for prognosis and a new target for the treatment of NPCs. Additionally, targeting PVT1 may be a potential strategy for the clinical management of NPC and for the improvement of the curative effect of radiation in NPCs.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA PVT1 predicts poor prognosis and induces radioresistance by regulating DNA repair and cell apoptosis in nasopharyngeal carcinoma

et al. 2018

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“…Our previous investigation found that SHP-1 was highly expressed in NPC tissues in contrast to normal nasopharyngeal mucosa and was associated with local recurrence and metastasis after radiotherapy in NPC patients (27). Further research showed that SHP-1 overexpression increased the radioresistance of NPC cells by enhancing DSB repair, increasing S phase arrest and decreasing cell apoptosis (34). To assess whether quinalizarin has an influence on SHP-1 expression, we treated NPC cells with quinalizarin and detected the expression of SHP-1.…”

Section: Discussionmentioning

confidence: 97%

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

Pan

Meng

Zhong

et al. 2016

International Journal of Oncology

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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.

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“…P53, a transcription factor that can activate the inhibitor of the cell cycle and participate in DNA damage response and transcription of apoptosis [ 43 ], may also play a role in premature aging by causing reactive damage to DNA [ 44 ]. p53 is associated with the two key kinases of ataxia telangiectasia and rad3-related protein-checkpoint kinase 1 pathway [ 45 ] that induce the transcription of cell cycle suppressor p21 gene and delay damaged G1 cells from entering S phase, preventing new start events at the beginning of the duplication process and slowing down the branching processes of reproduction of UV-irradiated cells in the S phase. Thus, p53 transiently suppresses DNA synthesis in UV-damaged cells [ 46 ].…”

Section: Role Of Ros In Uv-induced Photodamage Of the Skinmentioning

confidence: 99%

Role of reactive oxygen species in ultraviolet-induced photodamage of the skin

Wei,

He,

Liu

et al. 2024

Cell Div

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Reactive oxygen species (ROS), such as superoxides (O2 •−) and hydroxyl groups (OH·), are short-lived molecules containing unpaired electrons. Intracellular ROS are believed to be mainly produced by the mitochondria and NADPH oxidase (NOX) and can be associated with various physiological processes, such as proliferation, cell signaling, and oxygen homeostasis. In recent years, many studies have indicated that ROS play crucial roles in regulating ultraviolet (UV)-induced photodamage of the skin, including exogenous aging, which accounts for 80% of aging. However, to the best of our knowledge, the detailed signaling pathways, especially those related to the mechanisms underlying apoptosis in which ROS are involved have not been reviewed previously. In this review, we elaborate on the biological characteristics of ROS and its role in regulating UV-induced photodamage of the skin.

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SHP-1 overexpression increases the radioresistance of NPC cells by enhancing DSB repair, increasing S phase arrest and decreasing cell apoptosis

Cited by 10 publications

References 34 publications

Long non-coding RNA PVT1 predicts poor prognosis and induces radioresistance by regulating DNA repair and cell apoptosis in nasopharyngeal carcinoma

Long non-coding RNA PVT1 predicts poor prognosis and induces radioresistance by regulating DNA repair and cell apoptosis in nasopharyngeal carcinoma

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

Role of reactive oxygen species in ultraviolet-induced photodamage of the skin

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