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Specificity protein 1 is a novel target of 2,4-bis (p-hydroxyphenyl)-2-butenal for the suppression of human oral squamous cell carcinoma cell growth.

Chae JI, Lee R, Cho J, Hong J, Shim JH - J. Biomed. Sci. (2014)

Bottom Line: The Maillard reaction is a chemical reaction occurring between a reducing sugar and an amino acid, generally requiring thermal processing.HPB242 treatment dramatically reduced the cell growth rate and apoptotic cell morphologies.Sp1 was significantly inhibited by HPB242 in a dose-dependent manner.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pharmacy, College of Pharmacy, Mokpo National University, 1666 Youngsan-ro, Muan-gun, Jeonnam 534-729, Republic of Korea. s1004jh@gmail.com.

ABSTRACT

Background: The Maillard reaction is a chemical reaction occurring between a reducing sugar and an amino acid, generally requiring thermal processing. Maillard reaction products (MRPs) have antioxidant, antimutagenic, and antibacterial effects though 2,4-bis (p-hydroxyphenyl)-2-butenal (HPB242), a fructose-tyrosine MRP, appears to inhibit proliferation of cancer cells, its mechanism of action has not been studied in detail. The purpose of this study was to investigate the anti-proliferative effects of 2,4-bis (p-hydroxyphenyl)-2-butenal (HPB242) on two oral squamous cell carcinoma (OSCC) cell lines, HN22 and HSC4, through regulation of specificity protein 1 (Sp1).

Results: HPB242 treatment dramatically reduced the cell growth rate and apoptotic cell morphologies. Sp1 was significantly inhibited by HPB242 in a dose-dependent manner. Furthermore, cell cycle regulating proteins and anti-apoptotic proteins, which are known as Sp1 target genes, were altered at the molecular levels. The key important regulators in the cell cycle such as p27 were increased, whereas cell proliferation- and survival-related proteins such as cyclin D1, myeloid leukemia sequence 1 (Mcl-1) and survivin were significantly decreased by HPB242 or suppressed Sp1 levels, however pro-apoptotic proteins caspase3 and PARP were cleaved in HN22 and HSC4.

Conclusions: HPB242 may be useful as a chemotherapeutic agent for OSCC for the purpose of treatment and prevention of oral cancer and for the improvement of clinical outcomes.

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Related in: MedlinePlus

The apoptotic effect induced by HPB242 in HN22 and HSC4 cells. Cells were incubated with HPB242 (5, 10, and 20 μg/ml) and untreated for 48 hours. The cells were harvested and prepared for DAPI staining and PI staining as described in the Methods section. (A) Analysis of DNA fragmentation and nuclear condensation by fluorescence microscopy (magnification ×600) after HPB242 treatment in HN22 and HSC4 cells. (B) DNA fragmentation and nuclear condensation were quantified, and the results in triplicate are expressed as the mean ± SD. (C and D) Representative histograms of Sub-G1 population. HPB242-treated cells were compared with untreated cells, and data are shown as the average of triplicate samples from three independent experiments. The asterisks (*) indicates p < 0.05 versus control cells.
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Figure 2: The apoptotic effect induced by HPB242 in HN22 and HSC4 cells. Cells were incubated with HPB242 (5, 10, and 20 μg/ml) and untreated for 48 hours. The cells were harvested and prepared for DAPI staining and PI staining as described in the Methods section. (A) Analysis of DNA fragmentation and nuclear condensation by fluorescence microscopy (magnification ×600) after HPB242 treatment in HN22 and HSC4 cells. (B) DNA fragmentation and nuclear condensation were quantified, and the results in triplicate are expressed as the mean ± SD. (C and D) Representative histograms of Sub-G1 population. HPB242-treated cells were compared with untreated cells, and data are shown as the average of triplicate samples from three independent experiments. The asterisks (*) indicates p < 0.05 versus control cells.

Mentions: The effect of HPB242 treatment on initiation was due to the induction of apoptotic cell death by nuclear morphology using DAPI staining, which allowed visualization of nuclear shrinkage and fragmentation. HPB242 treatment of HN22 and HSC4 cells led to an increase in nuclear condensation and fragmentation compared to the control group (Figure 2A, B). In order to determine whether Sub-G1 population induction by HPB242 is related to apoptosis, HPB242 treated cells were marked with PI staining. When HN22 and HSC4 cells were treated with HPB242, an increased number of cells in the Sub-G1 population was observed in 3.6 - 34% of HPB242-treated HN22 cells and in 5.6 – 30.4% of HPB242-treated HSC4 cells (Figure 2C, D).


Specificity protein 1 is a novel target of 2,4-bis (p-hydroxyphenyl)-2-butenal for the suppression of human oral squamous cell carcinoma cell growth.

Chae JI, Lee R, Cho J, Hong J, Shim JH - J. Biomed. Sci. (2014)

The apoptotic effect induced by HPB242 in HN22 and HSC4 cells. Cells were incubated with HPB242 (5, 10, and 20 μg/ml) and untreated for 48 hours. The cells were harvested and prepared for DAPI staining and PI staining as described in the Methods section. (A) Analysis of DNA fragmentation and nuclear condensation by fluorescence microscopy (magnification ×600) after HPB242 treatment in HN22 and HSC4 cells. (B) DNA fragmentation and nuclear condensation were quantified, and the results in triplicate are expressed as the mean ± SD. (C and D) Representative histograms of Sub-G1 population. HPB242-treated cells were compared with untreated cells, and data are shown as the average of triplicate samples from three independent experiments. The asterisks (*) indicates p < 0.05 versus control cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3928619&req=5

Figure 2: The apoptotic effect induced by HPB242 in HN22 and HSC4 cells. Cells were incubated with HPB242 (5, 10, and 20 μg/ml) and untreated for 48 hours. The cells were harvested and prepared for DAPI staining and PI staining as described in the Methods section. (A) Analysis of DNA fragmentation and nuclear condensation by fluorescence microscopy (magnification ×600) after HPB242 treatment in HN22 and HSC4 cells. (B) DNA fragmentation and nuclear condensation were quantified, and the results in triplicate are expressed as the mean ± SD. (C and D) Representative histograms of Sub-G1 population. HPB242-treated cells were compared with untreated cells, and data are shown as the average of triplicate samples from three independent experiments. The asterisks (*) indicates p < 0.05 versus control cells.
Mentions: The effect of HPB242 treatment on initiation was due to the induction of apoptotic cell death by nuclear morphology using DAPI staining, which allowed visualization of nuclear shrinkage and fragmentation. HPB242 treatment of HN22 and HSC4 cells led to an increase in nuclear condensation and fragmentation compared to the control group (Figure 2A, B). In order to determine whether Sub-G1 population induction by HPB242 is related to apoptosis, HPB242 treated cells were marked with PI staining. When HN22 and HSC4 cells were treated with HPB242, an increased number of cells in the Sub-G1 population was observed in 3.6 - 34% of HPB242-treated HN22 cells and in 5.6 – 30.4% of HPB242-treated HSC4 cells (Figure 2C, D).

Bottom Line: The Maillard reaction is a chemical reaction occurring between a reducing sugar and an amino acid, generally requiring thermal processing.HPB242 treatment dramatically reduced the cell growth rate and apoptotic cell morphologies.Sp1 was significantly inhibited by HPB242 in a dose-dependent manner.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pharmacy, College of Pharmacy, Mokpo National University, 1666 Youngsan-ro, Muan-gun, Jeonnam 534-729, Republic of Korea. s1004jh@gmail.com.

ABSTRACT

Background: The Maillard reaction is a chemical reaction occurring between a reducing sugar and an amino acid, generally requiring thermal processing. Maillard reaction products (MRPs) have antioxidant, antimutagenic, and antibacterial effects though 2,4-bis (p-hydroxyphenyl)-2-butenal (HPB242), a fructose-tyrosine MRP, appears to inhibit proliferation of cancer cells, its mechanism of action has not been studied in detail. The purpose of this study was to investigate the anti-proliferative effects of 2,4-bis (p-hydroxyphenyl)-2-butenal (HPB242) on two oral squamous cell carcinoma (OSCC) cell lines, HN22 and HSC4, through regulation of specificity protein 1 (Sp1).

Results: HPB242 treatment dramatically reduced the cell growth rate and apoptotic cell morphologies. Sp1 was significantly inhibited by HPB242 in a dose-dependent manner. Furthermore, cell cycle regulating proteins and anti-apoptotic proteins, which are known as Sp1 target genes, were altered at the molecular levels. The key important regulators in the cell cycle such as p27 were increased, whereas cell proliferation- and survival-related proteins such as cyclin D1, myeloid leukemia sequence 1 (Mcl-1) and survivin were significantly decreased by HPB242 or suppressed Sp1 levels, however pro-apoptotic proteins caspase3 and PARP were cleaved in HN22 and HSC4.

Conclusions: HPB242 may be useful as a chemotherapeutic agent for OSCC for the purpose of treatment and prevention of oral cancer and for the improvement of clinical outcomes.

Show MeSH
Related in: MedlinePlus