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Acetylshikonin Inhibits Human Pancreatic PANC-1 Cancer Cell Proliferation by Suppressing the NF-κB Activity.

Cho SC, Choi BY - Biomol Ther (Seoul) (2015)

Bottom Line: Proteome cytokine array and real-time RT-PCR results illustrated that acetylshikonin inhibition of PMA-induced production of cytokines was mediated at the transcriptional level and it was associated with suppression of NF-κB activity and matrix metalloprotenases.Finally, we observed that an exposure of acetylshikonin significantly inhibited the anchorage-independent growth of PANC-1 cells.Together, our results indicate that acetylshikonin could serve as a promising therapeutic agent for future treatment of pancreatic cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of Food Science & Engineering, Seowon University, Cheongju 361-742, Republic of Korea.

ABSTRACT
Acetylshikonin, a natural naphthoquinone derivative compound, has been used for treatment of inflammation and cancer. In the present study, we have investigated whether acetylshikonin could regulate the NF-κB signaling pathway, thereby leading to suppression of tumorigenesis. We observed that acetylshikonin significantly reduced proliferation of several cancer cell lines, including human pancreatic PANC-1 cancer cells. In addition, acetylshikonin inhibited phorbol 12-myristate 13-acetate (PMA) or tumor necrosis-α (TNF-α)-induced NF-κB reporter activity. Proteome cytokine array and real-time RT-PCR results illustrated that acetylshikonin inhibition of PMA-induced production of cytokines was mediated at the transcriptional level and it was associated with suppression of NF-κB activity and matrix metalloprotenases. Finally, we observed that an exposure of acetylshikonin significantly inhibited the anchorage-independent growth of PANC-1 cells. Together, our results indicate that acetylshikonin could serve as a promising therapeutic agent for future treatment of pancreatic cancer.

No MeSH data available.


Related in: MedlinePlus

Levels of human cytokines released in the medium of PMA-treated HEK293 cells. HEK293 cells were exposed to PMA (10 ng/ml) alone or in combination with acetylshikonin and the media was collected to examine the level of released cytokines, using the human proteome cytokine array kit. The intensity were determined by pixel densities using myECL imager analysis software (Themo Fisher Scientific, Waltham, MA) (Membrane spot No : 1.C5/C5a., 2. CD40 Ligand., 3. IL-13., 4. MIF., 5. IL-23., 6. IL-8., R. Reference).
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f3-bt-23-428: Levels of human cytokines released in the medium of PMA-treated HEK293 cells. HEK293 cells were exposed to PMA (10 ng/ml) alone or in combination with acetylshikonin and the media was collected to examine the level of released cytokines, using the human proteome cytokine array kit. The intensity were determined by pixel densities using myECL imager analysis software (Themo Fisher Scientific, Waltham, MA) (Membrane spot No : 1.C5/C5a., 2. CD40 Ligand., 3. IL-13., 4. MIF., 5. IL-23., 6. IL-8., R. Reference).

Mentions: A previous study illustrated that the activation of NF-κB signaling pathway by PMA is responsible for the production of a variety of cellular cytokines (Im et al., 2014). By conducting the human proteome cytokine array, we observed that that PMA increased the production of a number of cytokines, such as C5/C5a, CD40 ligand, IL-13, MIF, IL-23 and IL-8 and that acetylshikonin inhibited PMA-induced production of these cytokines in HEK293 cells (Fig. 3). To examine whether acetylshikonin suppression of PMA-induced production of these cytokines could be transcriptionally regulated, we conducted both conventional and real-time reverse transcription-polymerase chain reaction (RT-PCR). As a result, we observed that an exposure of acetylshikonin to PANC-1 cells suppressed PMA-induced production of a number of cytokine mRNAs (IL-2, IL-4, IL-8, IL-12, IL-13 and TNF-α) (Fig. 4). Together, these results illustrate that acetylshikonin inhibition of PMA-induced production of cytokines is mediated by modulating the transcription.


Acetylshikonin Inhibits Human Pancreatic PANC-1 Cancer Cell Proliferation by Suppressing the NF-κB Activity.

Cho SC, Choi BY - Biomol Ther (Seoul) (2015)

Levels of human cytokines released in the medium of PMA-treated HEK293 cells. HEK293 cells were exposed to PMA (10 ng/ml) alone or in combination with acetylshikonin and the media was collected to examine the level of released cytokines, using the human proteome cytokine array kit. The intensity were determined by pixel densities using myECL imager analysis software (Themo Fisher Scientific, Waltham, MA) (Membrane spot No : 1.C5/C5a., 2. CD40 Ligand., 3. IL-13., 4. MIF., 5. IL-23., 6. IL-8., R. Reference).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4556202&req=5

f3-bt-23-428: Levels of human cytokines released in the medium of PMA-treated HEK293 cells. HEK293 cells were exposed to PMA (10 ng/ml) alone or in combination with acetylshikonin and the media was collected to examine the level of released cytokines, using the human proteome cytokine array kit. The intensity were determined by pixel densities using myECL imager analysis software (Themo Fisher Scientific, Waltham, MA) (Membrane spot No : 1.C5/C5a., 2. CD40 Ligand., 3. IL-13., 4. MIF., 5. IL-23., 6. IL-8., R. Reference).
Mentions: A previous study illustrated that the activation of NF-κB signaling pathway by PMA is responsible for the production of a variety of cellular cytokines (Im et al., 2014). By conducting the human proteome cytokine array, we observed that that PMA increased the production of a number of cytokines, such as C5/C5a, CD40 ligand, IL-13, MIF, IL-23 and IL-8 and that acetylshikonin inhibited PMA-induced production of these cytokines in HEK293 cells (Fig. 3). To examine whether acetylshikonin suppression of PMA-induced production of these cytokines could be transcriptionally regulated, we conducted both conventional and real-time reverse transcription-polymerase chain reaction (RT-PCR). As a result, we observed that an exposure of acetylshikonin to PANC-1 cells suppressed PMA-induced production of a number of cytokine mRNAs (IL-2, IL-4, IL-8, IL-12, IL-13 and TNF-α) (Fig. 4). Together, these results illustrate that acetylshikonin inhibition of PMA-induced production of cytokines is mediated by modulating the transcription.

Bottom Line: Proteome cytokine array and real-time RT-PCR results illustrated that acetylshikonin inhibition of PMA-induced production of cytokines was mediated at the transcriptional level and it was associated with suppression of NF-κB activity and matrix metalloprotenases.Finally, we observed that an exposure of acetylshikonin significantly inhibited the anchorage-independent growth of PANC-1 cells.Together, our results indicate that acetylshikonin could serve as a promising therapeutic agent for future treatment of pancreatic cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of Food Science & Engineering, Seowon University, Cheongju 361-742, Republic of Korea.

ABSTRACT
Acetylshikonin, a natural naphthoquinone derivative compound, has been used for treatment of inflammation and cancer. In the present study, we have investigated whether acetylshikonin could regulate the NF-κB signaling pathway, thereby leading to suppression of tumorigenesis. We observed that acetylshikonin significantly reduced proliferation of several cancer cell lines, including human pancreatic PANC-1 cancer cells. In addition, acetylshikonin inhibited phorbol 12-myristate 13-acetate (PMA) or tumor necrosis-α (TNF-α)-induced NF-κB reporter activity. Proteome cytokine array and real-time RT-PCR results illustrated that acetylshikonin inhibition of PMA-induced production of cytokines was mediated at the transcriptional level and it was associated with suppression of NF-κB activity and matrix metalloprotenases. Finally, we observed that an exposure of acetylshikonin significantly inhibited the anchorage-independent growth of PANC-1 cells. Together, our results indicate that acetylshikonin could serve as a promising therapeutic agent for future treatment of pancreatic cancer.

No MeSH data available.


Related in: MedlinePlus