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Apoptosis-Inducing Activity of Marine Sponge Haliclona sp. Extracts Collected from Kosrae in Nonsmall Cell Lung Cancer A549 Cells.

Bae W, Lim HK, Kim KM, Cho H, Lee SY, Jeong CS, Lee HS, Jung J - Evid Based Complement Alternat Med (2015)

Bottom Line: Further, methanol extracts of Haliclona sp. significantly inhibited cell proliferation and cell viability.A549 cells treated with Haliclona sp. demonstrated induced expression of c-Jun N-terminal kinase (JNK), p53, p21, caspase-8, and caspase-3.The percentage of apoptotic cells significantly increased in A549 cultures treated with Haliclona sp.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Duksung Women's University, Seoul 132-714, Republic of Korea.

ABSTRACT
Although various anticancer drugs have been developed for the treatment of nonsmall cell lung cancer, chemotherapeutic efficacy is still limited. Natural products such as phytochemicals have been screened as novel alternative materials, but alternative funds such as marine bioresources remain largely untapped. Of these resources, marine sponges have undergone the most scrutiny for their biological activities, including antiinflammatory, antiviral, and anticancer properties. However, the biological mechanisms of the activities of these marine sponges are still unclear. We investigated the anticancer activity of marine sponges collected from Kosrae in Micronesia and examined their mechanisms of action using nonsmall cell lung cancer A549 cells as a model system. Of 20 specimens, the Haliclona sp. (KO1304-328) showed both dose- and time-dependent cytotoxicity. Further, methanol extracts of Haliclona sp. significantly inhibited cell proliferation and cell viability. A549 cells treated with Haliclona sp. demonstrated induced expression of c-Jun N-terminal kinase (JNK), p53, p21, caspase-8, and caspase-3. The percentage of apoptotic cells significantly increased in A549 cultures treated with Haliclona sp. These results indicate that Haliclona sp. induces apoptosis via the JNK-p53 pathway and caspase-8, suggesting that this marine sponge is a good resource for the development of drugs for treatment of nonsmall cell lung cancer.

No MeSH data available.


Related in: MedlinePlus

Haliclona sp. extract inhibits cell viability in A549 cells. (a) A549 cells were treated with Haliclona sp. extract for 24 h or 48 h. (b) Haliclona sp. extract (100 μg/mL) was added to the medium. Cells were observed by microscopy (40x magnifications).
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fig2: Haliclona sp. extract inhibits cell viability in A549 cells. (a) A549 cells were treated with Haliclona sp. extract for 24 h or 48 h. (b) Haliclona sp. extract (100 μg/mL) was added to the medium. Cells were observed by microscopy (40x magnifications).

Mentions: To evaluate cytotoxicity, Haliclona sp. extract was serially diluted and applied to A549 cells for 24 h or 48 h. As shown in Figure 2(a), cell viability of A549 cells decreased in a dose- and time-dependent fashion. At 24 h, cytotoxicity was statistically significant for extracts of 50 and 100 μg/mL, but maximal cell viability inhibition was only 27.5 ± 2%. In A549 cells treated with Haliclona sp. extract for 48 h, a significant difference in cell viability was shown at 12.5, 25, 50, and 100 μg/mL (Figure 2(a)). Further, the maximum dose (100 μg/mL) inhibited cell viability by 51.6 ± 4.7%. Concurrently, we treated A549 cells with a control or Haliclona sp. extract and observed the decrease of cell density at 24 or 48 h (Figure 2(b)). Furthermore, the cytotoxicity of Haliclona sp. extract showed only in A549 cells, but not in RAW264.7 cells as noncancerous cell line (see Supplemental Data 1 in the Supplementary Material available online at http://dx.doi.org/10.1155/2015/717959). This data suggests that Haliclona sp. extract exerts an anticancer effect in a dose- and time-dependent manner.


Apoptosis-Inducing Activity of Marine Sponge Haliclona sp. Extracts Collected from Kosrae in Nonsmall Cell Lung Cancer A549 Cells.

Bae W, Lim HK, Kim KM, Cho H, Lee SY, Jeong CS, Lee HS, Jung J - Evid Based Complement Alternat Med (2015)

Haliclona sp. extract inhibits cell viability in A549 cells. (a) A549 cells were treated with Haliclona sp. extract for 24 h or 48 h. (b) Haliclona sp. extract (100 μg/mL) was added to the medium. Cells were observed by microscopy (40x magnifications).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4508479&req=5

fig2: Haliclona sp. extract inhibits cell viability in A549 cells. (a) A549 cells were treated with Haliclona sp. extract for 24 h or 48 h. (b) Haliclona sp. extract (100 μg/mL) was added to the medium. Cells were observed by microscopy (40x magnifications).
Mentions: To evaluate cytotoxicity, Haliclona sp. extract was serially diluted and applied to A549 cells for 24 h or 48 h. As shown in Figure 2(a), cell viability of A549 cells decreased in a dose- and time-dependent fashion. At 24 h, cytotoxicity was statistically significant for extracts of 50 and 100 μg/mL, but maximal cell viability inhibition was only 27.5 ± 2%. In A549 cells treated with Haliclona sp. extract for 48 h, a significant difference in cell viability was shown at 12.5, 25, 50, and 100 μg/mL (Figure 2(a)). Further, the maximum dose (100 μg/mL) inhibited cell viability by 51.6 ± 4.7%. Concurrently, we treated A549 cells with a control or Haliclona sp. extract and observed the decrease of cell density at 24 or 48 h (Figure 2(b)). Furthermore, the cytotoxicity of Haliclona sp. extract showed only in A549 cells, but not in RAW264.7 cells as noncancerous cell line (see Supplemental Data 1 in the Supplementary Material available online at http://dx.doi.org/10.1155/2015/717959). This data suggests that Haliclona sp. extract exerts an anticancer effect in a dose- and time-dependent manner.

Bottom Line: Further, methanol extracts of Haliclona sp. significantly inhibited cell proliferation and cell viability.A549 cells treated with Haliclona sp. demonstrated induced expression of c-Jun N-terminal kinase (JNK), p53, p21, caspase-8, and caspase-3.The percentage of apoptotic cells significantly increased in A549 cultures treated with Haliclona sp.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Duksung Women's University, Seoul 132-714, Republic of Korea.

ABSTRACT
Although various anticancer drugs have been developed for the treatment of nonsmall cell lung cancer, chemotherapeutic efficacy is still limited. Natural products such as phytochemicals have been screened as novel alternative materials, but alternative funds such as marine bioresources remain largely untapped. Of these resources, marine sponges have undergone the most scrutiny for their biological activities, including antiinflammatory, antiviral, and anticancer properties. However, the biological mechanisms of the activities of these marine sponges are still unclear. We investigated the anticancer activity of marine sponges collected from Kosrae in Micronesia and examined their mechanisms of action using nonsmall cell lung cancer A549 cells as a model system. Of 20 specimens, the Haliclona sp. (KO1304-328) showed both dose- and time-dependent cytotoxicity. Further, methanol extracts of Haliclona sp. significantly inhibited cell proliferation and cell viability. A549 cells treated with Haliclona sp. demonstrated induced expression of c-Jun N-terminal kinase (JNK), p53, p21, caspase-8, and caspase-3. The percentage of apoptotic cells significantly increased in A549 cultures treated with Haliclona sp. These results indicate that Haliclona sp. induces apoptosis via the JNK-p53 pathway and caspase-8, suggesting that this marine sponge is a good resource for the development of drugs for treatment of nonsmall cell lung cancer.

No MeSH data available.


Related in: MedlinePlus