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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

Effect of acetylshikonin on PMA-induced mRNA expression. PANC-1 cells were exposed to PMA alone or in combination with acetylshikonin for 24 h. The mRNA levels of amplified genes by RT-PCR were determined on 1 % agarose gel, in which GAPDH was used as a control for normalization (Left panel). Real-time RT-PCR data are depicted as means ± standard deviation (SD) of three independent experiments (Right panel). The asterisk(s) indicate a significant statistical significance (**p<0.01).
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f4-bt-23-428: Effect of acetylshikonin on PMA-induced mRNA expression. PANC-1 cells were exposed to PMA alone or in combination with acetylshikonin for 24 h. The mRNA levels of amplified genes by RT-PCR were determined on 1 % agarose gel, in which GAPDH was used as a control for normalization (Left panel). Real-time RT-PCR data are depicted as means ± standard deviation (SD) of three independent experiments (Right panel). The asterisk(s) indicate a significant statistical significance (**p<0.01).

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)

Effect of acetylshikonin on PMA-induced mRNA expression. PANC-1 cells were exposed to PMA alone or in combination with acetylshikonin for 24 h. The mRNA levels of amplified genes by RT-PCR were determined on 1 % agarose gel, in which GAPDH was used as a control for normalization (Left panel). Real-time RT-PCR data are depicted as means ± standard deviation (SD) of three independent experiments (Right panel). The asterisk(s) indicate a significant statistical significance (**p<0.01).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4-bt-23-428: Effect of acetylshikonin on PMA-induced mRNA expression. PANC-1 cells were exposed to PMA alone or in combination with acetylshikonin for 24 h. The mRNA levels of amplified genes by RT-PCR were determined on 1 % agarose gel, in which GAPDH was used as a control for normalization (Left panel). Real-time RT-PCR data are depicted as means ± standard deviation (SD) of three independent experiments (Right panel). The asterisk(s) indicate a significant statistical significance (**p<0.01).
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