Bmi-1 induces radioresistance by suppressing senescence in human U87 glioma cells
Radiotherapy is the main locoregional control modality for a number of types of malignant tumors, including glioblastoma. However, radiotherapy fails to prevent recurrence in numerous patients due to the intrinsic radioresistance of cancer cells. Cell senescence is significant in tumor suppressor me...
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| Published in | Oncology letters Vol. 8; no. 6; pp. 2601 - 2606 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Greece
D.A. Spandidos
01.12.2014
Spandidos Publications Spandidos Publications UK Ltd |
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| Abstract | Radiotherapy is the main locoregional control modality for a number of types of malignant tumors, including glioblastoma. However, radiotherapy fails to prevent recurrence in numerous patients due to the intrinsic radioresistance of cancer cells. Cell senescence is significant in tumor suppressor mechanisms and is closely associated with the radioresistance of cancer cells. Bmi-1 has been proposed to be an oncogene that can induce anti-senescence in tumor cells. The present study investigated the response of U87 glioma cells to radiation exposure and the role of Bmi-1 in the response following radiotherapy. Cell apoptosis and cell cycle distribution were assessed using flow cytometry, and a SA-β-Gal stain was used to observe the senescence ratio of U87 cells following radiation. The expression of Bmi-1 in U87 cells exposed to different doses of radiation was evaluated by western blot analysis. X-ray radiation was found to inhibit U87 cell proliferation through the induction of senescence rather than apoptosis. Following exposure to radiation, the cell cycle distribution was dysregulated, with an increased number of cells in the G2/M phase, and the expression of Bmi-1 was upregulated, particularly when a dose of ≥6 Gy was administered. The results indicated that senescence is the main mechanism by which U87 cell growth is inhibited following radiation. In addition, Bmi-1 may be significant in increasing the radioresistance of glioma cells by enabling cell senescence. |
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| AbstractList | Radiotherapy is the main locoregional control modality for a number of types of malignant tumors, including glioblastoma. However, radiotherapy fails to prevent recurrence in numerous patients due to the intrinsic radioresistance of cancer cells. Cell senescence is significant in tumor suppressor mechanisms and is closely associated with the radioresistance of cancer cells. Bmi-1 has been proposed to be an oncogene that can induce anti-senescence in tumor cells. The present study investigated the response of U87 glioma cells to radiation exposure and the role of Bmi-1 in the response following radiotherapy. Cell apoptosis and cell cycle distribution were assessed using flow cytometry, and a SA-β-Gal stain was used to observe the senescence ratio of U87 cells following radiation. The expression of Bmi-1 in U87 cells exposed to different doses of radiation was evaluated by western blot analysis. X-ray radiation was found to inhibit U87 cell proliferation through the induction of senescence rather than apoptosis. Following exposure to radiation, the cell cycle distribution was dysregulated, with an increased number of cells in the G2/M phase, and the expression of Bmi-1 was upregulated, particularly when a dose of ≥6 Gy was administered. The results indicated that senescence is the main mechanism by which U87 cell growth is inhibited following radiation. In addition, Bmi-1 may be significant in increasing the radioresistance of glioma cells by enabling cell senescence. Radiotherapy is the main locoregional control modality for a number of types of malignant tumors, including glioblastoma. However, radiotherapy fails to prevent recurrence in numerous patients due to the intrinsic radioresistance of cancer cells. Cell senescence is significant in tumor suppressor mechanisms and is closely associated with the radioresistance of cancer cells. Bmi-1 has been proposed to be an oncogene that can induce anti-senescence in tumor cells. The present study investigated the response of U87 glioma cells to radiation exposure and the role of Bmi-1 in the response following radiotherapy. Cell apoptosis and cell cycle distribution were assessed using flow cytometry, and a SA-β-Gal stain was used to observe the senescence ratio of U87 cells following radiation. The expression of Bmi-1 in U87 cells exposed to different doses of radiation was evaluated by western blot analysis. X-ray radiation was found to inhibit U87 cell proliferation through the induction of senescence rather than apoptosis. Following exposure to radiation, the cell cycle distribution was dysregulated, with an increased number of cells in the [G.sub.2]/M phase, and the expression of Bmi-1 was upregulated, particularly when a dose of ≥ 6 Gy was administered. The results indicated that senescence is the main mechanism by which U87 cell growth is inhibited following radiation. In addition, Bmi-1 may be significant in increasing the radioresistance of glioma cells by enabling cell senescence. Radiotherapy is the main locoregional control modality for a number of types of malignant tumors, including glioblastoma. However, radiotherapy fails to prevent recurrence in numerous patients due to the intrinsic radioresistance of cancer cells. Cell senescence is significant in tumor suppressor mechanisms and is closely associated with the radioresistance of cancer cells. Bmi-1 has been proposed to be an oncogene that can induce anti-senescence in tumor cells. The present study investigated the response of U87 glioma cells to radiation exposure and the role of Bmi-1 in the response following radiotherapy. Cell apoptosis and cell cycle distribution were assessed using flow cytometry, and a SA-β-Gal stain was used to observe the senescence ratio of U87 cells following radiation. The expression of Bmi-1 in U87 cells exposed to different doses of radiation was evaluated by western blot analysis. X-ray radiation was found to inhibit U87 cell proliferation through the induction of senescence rather than apoptosis. Following exposure to radiation, the cell cycle distribution was dysregulated, with an increased number of cells in the G 2 /M phase, and the expression of Bmi-1 was upregulated, particularly when a dose of ≥6 Gy was administered. The results indicated that senescence is the main mechanism by which U87 cell growth is inhibited following radiation. In addition, Bmi-1 may be significant in increasing the radioresistance of glioma cells by enabling cell senescence. Radiotherapy is the main locoregional control modality for a number of types of malignant tumors, including glioblastoma. However, radiotherapy fails to prevent recurrence in numerous patients due to the intrinsic radioresistance of cancer cells. Cell senescence is significant in tumor suppressor mechanisms and is closely associated with the radioresistance of cancer cells. Bmi-1 has been proposed to be an oncogene that can induce anti-senescence in tumor cells. The present study investigated the response of U87 glioma cells to radiation exposure and the role of Bmi-1 in the response following radiotherapy. Cell apoptosis and cell cycle distribution were assessed using flow cytometry, and a SA-β-Gal stain was used to observe the senescence ratio of U87 cells following radiation. The expression of Bmi-1 in U87 cells exposed to different doses of radiation was evaluated by western blot analysis. X-ray radiation was found to inhibit U87 cell proliferation through the induction of senescence rather than apoptosis. Following exposure to radiation, the cell cycle distribution was dysregulated, with an increased number of cells in the [G.sub.2]/M phase, and the expression of Bmi-1 was upregulated, particularly when a dose of ≥ 6 Gy was administered. The results indicated that senescence is the main mechanism by which U87 cell growth is inhibited following radiation. In addition, Bmi-1 may be significant in increasing the radioresistance of glioma cells by enabling cell senescence. Key words: glioma, Bmi-1, senescence, radiation Radiotherapy is the main locoregional control modality for a number of types of malignant tumors, including glioblastoma. However, radiotherapy fails to prevent recurrence in numerous patients due to the intrinsic radioresistance of cancer cells. Cell senescence is significant in tumor suppressor mechanisms and is closely associated with the radioresistance of cancer cells. Bmi-1 has been proposed to be an oncogene that can induce anti-senescence in tumor cells. The present study investigated the response of U87 glioma cells to radiation exposure and the role of Bmi-1 in the response following radiotherapy. Cell apoptosis and cell cycle distribution were assessed using flow cytometry, and a SA-β-Gal stain was used to observe the senescence ratio of U87 cells following radiation. The expression of Bmi-1 in U87 cells exposed to different doses of radiation was evaluated by western blot analysis. X-ray radiation was found to inhibit U87 cell proliferation through the induction of senescence rather than apoptosis. Following exposure to radiation, the cell cycle distribution was dysregulated, with an increased number of cells in the G /M phase, and the expression of Bmi-1 was upregulated, particularly when a dose of ≥6 Gy was administered. The results indicated that senescence is the main mechanism by which U87 cell growth is inhibited following radiation. In addition, Bmi-1 may be significant in increasing the radioresistance of glioma cells by enabling cell senescence. |
| Audience | Academic |
| Author | HU, LIKUAN LIU, PING ZHANG, ZAIYUN WANG, CUIHONG WEI, WEI DU, BIN LI, XIAOMEI YU, GUANYING YU, XIAOMING JIANG, YUHUA CHENG, JIAN YE, LAN SUN, DIANSHUI |
| AuthorAffiliation | 1 Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China 2 Jinan Central Hospital, Jinan, Shandong 250014, P.R. China 3 Department of Radiotherapy, Qilu Hospital, Shandong University, Jinan, Shandong 250012, P.R. China |
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| Author_xml | – sequence: 1 givenname: LAN surname: YE fullname: YE, LAN organization: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China – sequence: 2 givenname: CUIHONG surname: WANG fullname: WANG, CUIHONG organization: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China – sequence: 3 givenname: GUANYING surname: YU fullname: YU, GUANYING organization: Jinan Central Hospital, Jinan, Shandong 250014, P.R. China – sequence: 4 givenname: YUHUA surname: JIANG fullname: JIANG, YUHUA organization: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China – sequence: 5 givenname: DIANSHUI surname: SUN fullname: SUN, DIANSHUI organization: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China – sequence: 6 givenname: ZAIYUN surname: ZHANG fullname: ZHANG, ZAIYUN organization: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China – sequence: 7 givenname: XIAOMING surname: YU fullname: YU, XIAOMING organization: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China – sequence: 8 givenname: XIAOMEI surname: LI fullname: LI, XIAOMEI organization: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China – sequence: 9 givenname: WEI surname: WEI fullname: WEI, WEI organization: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China – sequence: 10 givenname: PING surname: LIU fullname: LIU, PING organization: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China – sequence: 11 givenname: JIAN surname: CHENG fullname: CHENG, JIAN organization: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China – sequence: 12 givenname: BIN surname: DU fullname: DU, BIN organization: Jinan Central Hospital, Jinan, Shandong 250014, P.R. China – sequence: 13 givenname: LIKUAN surname: HU fullname: HU, LIKUAN organization: Department of Radiotherapy, Qilu Hospital, Shandong University, Jinan, Shandong 250012, P.R. China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25364434$$D View this record in MEDLINE/PubMed |
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| Keywords | senescence glioma radiation Bmi-1 |
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176 Zhang (key20180108104847_b11-ol-08-06-2601) 2008; 65 Liu (key20180108104847_b24-ol-08-06-2601) 2013; 5 Roninson (key20180108104847_b29-ol-08-06-2601) 2003; 63 (key20180108104847_b3-ol-08-06-2601) 2008; 455 Taylor (key20180108104847_b19-ol-08-06-2601) 2010; 75 Ohgaki (key20180108104847_b2-ol-08-06-2601) 2004; 64 Dewey (key20180108104847_b27-ol-08-06-2601) 1995; 33 Hara (key20180108104847_b33-ol-08-06-2601) 1996; 16 Xie (key20180108104847_b23-ol-08-06-2601) 2014; 445 Bruggeman (key20180108104847_b15-ol-08-06-2601) 2007; 12 Jacobs (key20180108104847_b31-ol-08-06-2601) 1999; 397 Chowdhury (key20180108104847_b9-ol-08-06-2601) 2007; 21 Dhawan (key20180108104847_b14-ol-08-06-2601) 2009; 23 Vonlanthen (key20180108104847_b10-ol-08-06-2601) 2001; 84 |
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