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Influence of P53 on the radiotherapy response of hepatocellular carcinoma.

Gomes AR, Abrantes AM, Brito AF, Laranjo M, Casalta-Lopes JE, Gonçalves AC, Sarmento-Ribeiro AB, Botelho MF, Tralhão JG - Clin Mol Hepatol (2015)

Bottom Line: Flow cytometry was carried out to examine the effects of iodine-131 on cell death, oxidative stress, reduced intracellular glutathione expression, the mitochondrial membrane potential, and the cell cycle.Irradiation induced a decrease in cell survival and led to a decrease in cell viability in all of the cell lines studied, accompanied by cell death via late apoptosis/necrosis and necrosis.Irradiation with 131-iodine induced mostly cell-cycle arrest in the G0/G1 phase.

View Article: PubMed Central - PubMed

Affiliation: Biophysics Unit, Faculty of Medicine of University of Coimbra, Coimbra, Portugal.

ABSTRACT

Background/aims: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, and it has a poor prognosis and few therapeutic options. Radiotherapy is one of the most effective forms of cancer treatment, and P53 protein is one of the key molecules determining how a cell responds to radiotherapy. The aim of this study was to determine the therapeutic efficacy of iodine-131 in three human HCC cell lines.

Methods: Western blotting was used to measure P53 expression. The effects of radiotherapy with iodine-131 were assessed by using the clonogenic assay to evaluate cell survival. Flow cytometry was carried out to examine the effects of iodine-131 on cell death, oxidative stress, reduced intracellular glutathione expression, the mitochondrial membrane potential, and the cell cycle.

Results: The P53 protein was not expressed in Hep3B2.1-7 cells, was expressed at normal levels in HepG2 cells, and was overexpressed in HuH7 cells. P53 expression in the HuH7 and HepG2 cell lines increased after internal and external irradiation with iodine-131. Irradiation induced a decrease in cell survival and led to a decrease in cell viability in all of the cell lines studied, accompanied by cell death via late apoptosis/necrosis and necrosis. Irradiation with 131-iodine induced mostly cell-cycle arrest in the G0/G1 phase.

Conclusions: These results suggest that P53 plays a key role in the radiotherapy response of HCC.

No MeSH data available.


Related in: MedlinePlus

(a) Flow cytometry analysis of the production of intracellular peroxides and superoxide radicals, and of reduced intracellular glutathione expression and the mitochondrial membrane potential. Data are mean and SE values (n=8). Asterisks and hashes respectively indicate statistically significant differences compared to controls and between IR and ER (P<0.05). (b) Cell-cycle analysis in the HepG2, HuH7, and Hep3B2.1-7 cell lines by flow cytometry at 24 h after IR and ER exposure to iodine-131 at 1 to 20 Gy. Data are mean and SE values (n=8).
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Figure 6: (a) Flow cytometry analysis of the production of intracellular peroxides and superoxide radicals, and of reduced intracellular glutathione expression and the mitochondrial membrane potential. Data are mean and SE values (n=8). Asterisks and hashes respectively indicate statistically significant differences compared to controls and between IR and ER (P<0.05). (b) Cell-cycle analysis in the HepG2, HuH7, and Hep3B2.1-7 cell lines by flow cytometry at 24 h after IR and ER exposure to iodine-131 at 1 to 20 Gy. Data are mean and SE values (n=8).

Mentions: Regarding to the intracellular peroxide concentrations in cells exposed to internal 1 Gy irradiation was observed an increase in intracellular peroxide concentration in Hep3B2.1-7 cell line (P=0.015), relative to control cell population (Fig. 6A). Similarly, in the external irradiation, it was observed, for the same irradiation dose, an increase in intracellular peroxide concentration in HuH7 cells (P=0.013) as well as for 20 Gy (P=0.016), in comparison to control. The intracellular reduced glutathione concentration exposed to 1Gy external irradiation, increased in Hep3B2.1-7 cells (P=0.016), in comparison to control.


Influence of P53 on the radiotherapy response of hepatocellular carcinoma.

Gomes AR, Abrantes AM, Brito AF, Laranjo M, Casalta-Lopes JE, Gonçalves AC, Sarmento-Ribeiro AB, Botelho MF, Tralhão JG - Clin Mol Hepatol (2015)

(a) Flow cytometry analysis of the production of intracellular peroxides and superoxide radicals, and of reduced intracellular glutathione expression and the mitochondrial membrane potential. Data are mean and SE values (n=8). Asterisks and hashes respectively indicate statistically significant differences compared to controls and between IR and ER (P<0.05). (b) Cell-cycle analysis in the HepG2, HuH7, and Hep3B2.1-7 cell lines by flow cytometry at 24 h after IR and ER exposure to iodine-131 at 1 to 20 Gy. Data are mean and SE values (n=8).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4612287&req=5

Figure 6: (a) Flow cytometry analysis of the production of intracellular peroxides and superoxide radicals, and of reduced intracellular glutathione expression and the mitochondrial membrane potential. Data are mean and SE values (n=8). Asterisks and hashes respectively indicate statistically significant differences compared to controls and between IR and ER (P<0.05). (b) Cell-cycle analysis in the HepG2, HuH7, and Hep3B2.1-7 cell lines by flow cytometry at 24 h after IR and ER exposure to iodine-131 at 1 to 20 Gy. Data are mean and SE values (n=8).
Mentions: Regarding to the intracellular peroxide concentrations in cells exposed to internal 1 Gy irradiation was observed an increase in intracellular peroxide concentration in Hep3B2.1-7 cell line (P=0.015), relative to control cell population (Fig. 6A). Similarly, in the external irradiation, it was observed, for the same irradiation dose, an increase in intracellular peroxide concentration in HuH7 cells (P=0.013) as well as for 20 Gy (P=0.016), in comparison to control. The intracellular reduced glutathione concentration exposed to 1Gy external irradiation, increased in Hep3B2.1-7 cells (P=0.016), in comparison to control.

Bottom Line: Flow cytometry was carried out to examine the effects of iodine-131 on cell death, oxidative stress, reduced intracellular glutathione expression, the mitochondrial membrane potential, and the cell cycle.Irradiation induced a decrease in cell survival and led to a decrease in cell viability in all of the cell lines studied, accompanied by cell death via late apoptosis/necrosis and necrosis.Irradiation with 131-iodine induced mostly cell-cycle arrest in the G0/G1 phase.

View Article: PubMed Central - PubMed

Affiliation: Biophysics Unit, Faculty of Medicine of University of Coimbra, Coimbra, Portugal.

ABSTRACT

Background/aims: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, and it has a poor prognosis and few therapeutic options. Radiotherapy is one of the most effective forms of cancer treatment, and P53 protein is one of the key molecules determining how a cell responds to radiotherapy. The aim of this study was to determine the therapeutic efficacy of iodine-131 in three human HCC cell lines.

Methods: Western blotting was used to measure P53 expression. The effects of radiotherapy with iodine-131 were assessed by using the clonogenic assay to evaluate cell survival. Flow cytometry was carried out to examine the effects of iodine-131 on cell death, oxidative stress, reduced intracellular glutathione expression, the mitochondrial membrane potential, and the cell cycle.

Results: The P53 protein was not expressed in Hep3B2.1-7 cells, was expressed at normal levels in HepG2 cells, and was overexpressed in HuH7 cells. P53 expression in the HuH7 and HepG2 cell lines increased after internal and external irradiation with iodine-131. Irradiation induced a decrease in cell survival and led to a decrease in cell viability in all of the cell lines studied, accompanied by cell death via late apoptosis/necrosis and necrosis. Irradiation with 131-iodine induced mostly cell-cycle arrest in the G0/G1 phase.

Conclusions: These results suggest that P53 plays a key role in the radiotherapy response of HCC.

No MeSH data available.


Related in: MedlinePlus