Overexpression of heat-shock protein 25 augments radiation-induced cell-cycle arrest in murine L929 cells

Cho, H.-N.; Lee, S.-J.; Park, S.-H.; Lee, Y. J.; Cho, C.-K.; Lee, Y.-S.

doi:10.1080/09553000010001024

Cited by 12 publications

(7 citation statements)

References 34 publications

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“…4A and B), which was consistent with previous reports. 46,47 However, the IR-induced G 2 /M arrest was not correlated with IR-induced miR-34 expression (Fig. 2B), suggesting that miR-34a may not play a role in IR-induced G 2 /M arrest in HMEC cells.…”

Section: Mir-34a Does Not Correlate To Ir-induced Transient G 2 /M Armentioning

confidence: 87%

“…46,47 Considering the well-documented role of miR-34a in cell cycle control, 43 we wondered whether it too could mediate IR-induced cell cycle arrest. The cell cycle analysis showed a rapid and transient G 2 /M arrest in HMEC cells exposed to both low-dose/low-energy and high-dose/high-energy X-rays ( Fig.…”

Section: Mir-34a Does Not Correlate To Ir-induced Transient G 2 /M Armentioning

confidence: 99%

See 1 more Smart Citation

p53 Ser15 phosphorylation and histone modifications contribute to IR-induced miR-34a transcription in mammary epithelial cells

Wang

Li²,

Kovalchuk³

2013

Cell Cycle

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Section: Mir-34a Does Not Correlate To Ir-induced Transient G 2 /M Armentioning

confidence: 87%

Section: Mir-34a Does Not Correlate To Ir-induced Transient G 2 /M Armentioning

confidence: 99%

p53 Ser15 phosphorylation and histone modifications contribute to IR-induced miR-34a transcription in mammary epithelial cells

Wang

Li²,

Kovalchuk³

2013

Cell Cycle

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“…L929 transformant clones were obtained from stable transfection with phsp6 (containing the complete genomic sequence for murine hsp25) and pBC vector (Stratagene, La Jolla, CA, USA). 3,24 Hsp25 transfectants were subsequently transfected with plasmids containing antisense hsp25 cDNA which was kindly provided by Dr Davidson, 25 and stable transfectants were selected with 6 mg/ml puromycin for approximately 2 weeks, followed by continued growth in the presence of 4 mg/ml puromycin. Clones with downregulated HSP25 protein detected by Western blotting, were selected.…”

Section: Cell Culturementioning

confidence: 99%

Downregulation of ERK2 is essential for the inhibition of radiation-induced cell death in HSP25 overexpressed L929 cells

Hn¹,

Ck³

et al. 2002

Cell Death Differ

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We previously reported that overexpression of HSP25 delayed cell growth, increased the level of p21 waf , reduced the levels of cyclin D1, cyclin A and cdc2, and induced radioresistance in L929 cells. In this study, we demonstrated that HSP25 inducedradioresistance was abolished by transfection with plasmids containing antisense hsp25 cDNA. Extracellular regulated kinase (ERK) and MAP kinase/ERK kinase (MEK) expressions as well as their activation (phospho-forms) were inhibited by hsp25 overexpression. Furthermore, when control vector transfected cells were treated with PD98059, MEK inhibitor, they became resistant to radiation, suggesting that inhibition of ERK1/2 activities was essential for radioresistance in L929 cells. To confirm the relationship between ERK1/2 and hsp25-mediated radioresistance, ERK1 or ERK2 cDNA was transiently transfected into the hsp25 overexpressed cells and their radioresistance was examined. HSP25-mediated radioresistance was abolished by overexpression of ERK2, but not by overexpression of ERK1. Alteration of cell cycle distribution and cell cycle related protein expressions (cyclin D, cyclin A and cdc2) by hsp25 overexpression were also recovered by ERK2 cDNA transfection. Increase in Bcl-2 protein by hsp25 gene transfection was also reduced by subsequent ERK2 cDNA-transfection. Taken together, these results suggest that downregulation of ERK2 is essential for the inhibition of radiation-induced cell death in HSP25 overexpressed cells.

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“…Previous studies proposed that heat-shock protein 25 (HSP25) was one of the important proteins that affected radiation-induced cell death via regulation of cell cycle arrest (Cho et al, 2001). Overexpression of HSP25 delayed cell growth and reduced the levels of cyclin D1, cyclin A and cdc2, the key proteins involved in cell cycle arrest (G 1 arrest) and thus inhibited radiation-induced cell death.…”

Section: Discussionmentioning

confidence: 99%

“…HSP25 is another important defense protein against the effects of γ-irradiation. Cho et al reported the protective effect of heat-shock protein 25 (HSP25) against γ-irradiation, which might be associated with HSP25-induced cell-cycle delay (Cho et al, 2001). HSP25-overexpressing cells also showed reduction of cyclin D1.…”

Section: Polyamine-mediated Regulation Of Hsp25 and Cyclin D1mentioning

confidence: 99%

Polyamine depletion partially reduces the radiation-induced cell death via cell cycle delay mediated by thioredoxin

Moon

Kim

et al. 2006

Cell Biol Toxicol

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In previous studies, polyamine depletion by DFMO (alpha-difluoromethylornithine)-treatment reduced H(2)O(2)-induced apoptotic cell death by reduction of ferric ion uptake. In the present study, we analyzed the reduction of radiation-induced cell death by polyamine depletion. Exposure of HT29 cells to radiation induced severe cell death, but when cells were pretreated with DFMO, a specific inhibitor of polyamine biosynthesis, radiation-induced cell death was reduced to 50-60% of control. Cell cycle analysis showed that, in these cells, the time to reach the G(2)/M phase arrest was delayed for 20-24 h compared to the control cells, at which stage the fate of cells exposed to ionizing radiation is determined. DFMO-treated cells also showed a low level of thioredoxin, which is a high-level determinant of the cellular fate. To investigate the relationship between the G(2)/M phase arrest and the reduction of thioredoxin caused by polyamine depletion, we also analyzed thioredoxin-antisensed (asTRX) HT29 cells as for DFMO-treated cells. In asTRX-transfected cells, the gamma-irradiation-induced G(2)/M phase arrest was also significantly delayed and radiation-induced cell death was profoundly reduced, as in the DFMO-treated cells. Both sets of cells showed a decrease of cyclin D1 and an increment of HSP25, which are involved in radiation-induced cell cycle progress. Overall, these results suggest that polyamines are essential for normal cell death of HT29 cells triggered by gamma-radiation and that this is partially mediated by the regulation of thioredoxin expression.

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Overexpression of heat-shock protein 25 augments radiation-induced cell-cycle arrest in murine L929 cells

Abstract: HSP25 augmented radiation-induced cell-cycle arrest (G1, S, and G2/M phase) may be caused by the HSP25-mediated cell-growth delay and is associated with radioresistance.

Cited by 12 publications

References 34 publications

p53 Ser15 phosphorylation and histone modifications contribute to IR-induced miR-34a transcription in mammary epithelial cells

p53 Ser15 phosphorylation and histone modifications contribute to IR-induced miR-34a transcription in mammary epithelial cells

Downregulation of ERK2 is essential for the inhibition of radiation-induced cell death in HSP25 overexpressed L929 cells

Polyamine depletion partially reduces the radiation-induced cell death via cell cycle delay mediated by thioredoxin

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