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Bmi-1 induces radioresistance by suppressing senescence in human U87 glioma cells.

Ye L, Wang C, Yu G, Jiang Y, Sun D, Zhang Z, Yu X, Li X, Wei W, Liu P, Cheng J, DU B, Hu L - Oncol Lett (2014)

Bottom Line: 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.In addition, Bmi-1 may be significant in increasing the radioresistance of glioma cells by enabling cell senescence.

View Article: PubMed Central - PubMed

Affiliation: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.

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.

No MeSH data available.


Related in: MedlinePlus

Western blot analysis demonstrating that ionizing radiation increased Bmi-1 expression. β-actin was used as a loading control.
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f5-ol-08-06-2601: Western blot analysis demonstrating that ionizing radiation increased Bmi-1 expression. β-actin was used as a loading control.

Mentions: To observe whether the expression of Bmi-1 was associated with exposure to X-ray radiation, U87 cells were exposed to X-ray radiation in doses of 1, 2, 4.6 and 8 Gy. Following 72 h of exposure to radiation, the expression of Bmi-1 was determined (Fig. 5). Bmi-1 expression was increased in the 6 Gy and 8 Gy groups (P<0.05). No significant difference in Bmi-1 expression was observed between the 1, 2 and 4 Gy and control groups.


Bmi-1 induces radioresistance by suppressing senescence in human U87 glioma cells.

Ye L, Wang C, Yu G, Jiang Y, Sun D, Zhang Z, Yu X, Li X, Wei W, Liu P, Cheng J, DU B, Hu L - Oncol Lett (2014)

Western blot analysis demonstrating that ionizing radiation increased Bmi-1 expression. β-actin was used as a loading control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4214493&req=5

f5-ol-08-06-2601: Western blot analysis demonstrating that ionizing radiation increased Bmi-1 expression. β-actin was used as a loading control.
Mentions: To observe whether the expression of Bmi-1 was associated with exposure to X-ray radiation, U87 cells were exposed to X-ray radiation in doses of 1, 2, 4.6 and 8 Gy. Following 72 h of exposure to radiation, the expression of Bmi-1 was determined (Fig. 5). Bmi-1 expression was increased in the 6 Gy and 8 Gy groups (P<0.05). No significant difference in Bmi-1 expression was observed between the 1, 2 and 4 Gy and control groups.

Bottom Line: 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.In addition, Bmi-1 may be significant in increasing the radioresistance of glioma cells by enabling cell senescence.

View Article: PubMed Central - PubMed

Affiliation: Cancer Center, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.

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.

No MeSH data available.


Related in: MedlinePlus