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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

Cell apoptosis. Following 72 h of exposure to X-ray radiation at various doses, the U87 glioma cells were assessed by Annexin V-fluorescein isothiocyanate/propidium iodide double staining.
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f2-ol-08-06-2601: Cell apoptosis. Following 72 h of exposure to X-ray radiation at various doses, the U87 glioma cells were assessed by Annexin V-fluorescein isothiocyanate/propidium iodide double staining.

Mentions: To evaluate whether the cellular proliferation inhibition of U87 cells in response to X-ray radiation is associated with apoptosis or senescence, U87 cells were treated with X-ray radiation at 1, 2, 4.6 and 8 Gy. Following 72 h of exposure to radiation, no significant apoptosis was identified in any of the groups (Fig. 2). Using SA-β-Gal staining, it was observed that senescence had occurred in all treatment groups in a dose-dependent manner (Fig. 3B). Under phase-contrast microscopy, the senescent morphology of a large and flattened shape was observed (Fig. 3A). These morphological changes were more evident in the cells that were exposed to radiation doses of ≥6 Gy.


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)

Cell apoptosis. Following 72 h of exposure to X-ray radiation at various doses, the U87 glioma cells were assessed by Annexin V-fluorescein isothiocyanate/propidium iodide double staining.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f2-ol-08-06-2601: Cell apoptosis. Following 72 h of exposure to X-ray radiation at various doses, the U87 glioma cells were assessed by Annexin V-fluorescein isothiocyanate/propidium iodide double staining.
Mentions: To evaluate whether the cellular proliferation inhibition of U87 cells in response to X-ray radiation is associated with apoptosis or senescence, U87 cells were treated with X-ray radiation at 1, 2, 4.6 and 8 Gy. Following 72 h of exposure to radiation, no significant apoptosis was identified in any of the groups (Fig. 2). Using SA-β-Gal staining, it was observed that senescence had occurred in all treatment groups in a dose-dependent manner (Fig. 3B). Under phase-contrast microscopy, the senescent morphology of a large and flattened shape was observed (Fig. 3A). These morphological changes were more evident in the cells that were exposed to radiation doses of ≥6 Gy.

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