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Aqueous Extract of Solanum nigrum Leaf Activates Autophagic Cell Death and Enhances Docetaxel-Induced Cytotoxicity in Human Endometrial Carcinoma Cells.

Tai CJ, Wang CK, Chang YJ, Lin CS, Tai CJ - Evid Based Complement Alternat Med (2012)

Bottom Line: An effective complementary ingredient can be helpful in improving the clinical outcome.Aqueous extract of Solanum nigrum leaf (AE-SN) is a principal ingredient for treating cancer patients in traditional Chinese medicinal practice but lacks sufficient evidence to verify its tumor suppression efficacy.The activation of apoptotic markers, caspase-3 and poly-ADP-ribose polymerase, and autophagic marker, microtubule-associated protein 1 light chain 3 A/B, wAS determined to clarify the cell death pathways responsible for AE-SN induced tumor cell death.

View Article: PubMed Central - PubMed

Affiliation: Division of Hematology and Oncology, Department of Internal Medicine, Taipei Medical University Hospital, Taipei 110, Taiwan ; Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.

ABSTRACT
Chemotherapy is the main approach in dealing with advanced and recurrent endometrial cancer. An effective complementary ingredient can be helpful in improving the clinical outcome. Aqueous extract of Solanum nigrum leaf (AE-SN) is a principal ingredient for treating cancer patients in traditional Chinese medicinal practice but lacks sufficient evidence to verify its tumor suppression efficacy. This study evaluated the antitumor effects of AE-SN and also assessed the synergistic effects of AE-SN with docetaxel On the human endometrial cancer cell lines, HEC1A, HEC1B, and KLE. The activation of apoptotic markers, caspase-3 and poly-ADP-ribose polymerase, and autophagic marker, microtubule-associated protein 1 light chain 3 A/B, wAS determined to clarify the cell death pathways responsible for AE-SN induced tumor cell death. Results indicated that AE-SN-treatment has significant cytotoxicity on the tested endometrial cancer cells with accumulation of LC3 A/B II and demonstrated a synergistic effect of AE-SN and docetaxel in HEC1A and HEC1B cells, but not KLE cells. In conclusion, AE-SN treatment was effective in suppressing endometrial cancer cells via the autophagic pathway and was also capable of enhancing the cytotoxicity of docetaxel in human endometrial cancer cells. Our results provide meaningful evidence for integrative cancer therapy in the future.

No MeSH data available.


Related in: MedlinePlus

Cytotoxicity of AE-SN and docetaxel cotreatment in human endometrial cancer cells. (a) HEC1A cells. (b) HEC1B cells. (c) KLE cells. Tested cells were treated with serial doses of docetaxel from 0 to 100 nM together with 0, 0.2, or 0.5 mg/mL AE-SN for 48 hr. Cell cytotoxicity was determined by MTT assay and presented as mean ± SD. Experiments were performed in triplicate.
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fig5: Cytotoxicity of AE-SN and docetaxel cotreatment in human endometrial cancer cells. (a) HEC1A cells. (b) HEC1B cells. (c) KLE cells. Tested cells were treated with serial doses of docetaxel from 0 to 100 nM together with 0, 0.2, or 0.5 mg/mL AE-SN for 48 hr. Cell cytotoxicity was determined by MTT assay and presented as mean ± SD. Experiments were performed in triplicate.

Mentions: Since previous results verified that AE-SN treatment resulted in significant cell cytotoxicity in HEC1A, HEC1B, and KLE cells and was associated with autophagic cell death, the next step was to clarify the combination effect of AE-SN and a chemotherapeutic regimen with docetaxel in human endometrial adenocarcinoma cells. According to the IC50 determined by the cell viability study, doses of 0.2 and 0.5 mg/mL AE-SN which covered the IC50 dosage were chosen for cells treated with 0 to 100 nM docetaxel. The results shown in Figure 5 demonstrated that a combination effect was observed in HEC1A and HEC1B cells, whereas KLE cells were not only less sensitive to AE-SN, but also resistant to docetaxel treatment. The CI was calculated for AE-SN and docetaxel-treated cells and showed that a synergistic effect occurred in both 0.2 and 0.5 mg/mL AE-SN-treated HEC1A and HEC1B cells treated with 1 to 100 nM docetaxel (Table 1). These results suggested that cotreatment with AE-SN further enhanced the cell cytotoxicity of docetaxel in HEC1A and HEC1B cells.


Aqueous Extract of Solanum nigrum Leaf Activates Autophagic Cell Death and Enhances Docetaxel-Induced Cytotoxicity in Human Endometrial Carcinoma Cells.

Tai CJ, Wang CK, Chang YJ, Lin CS, Tai CJ - Evid Based Complement Alternat Med (2012)

Cytotoxicity of AE-SN and docetaxel cotreatment in human endometrial cancer cells. (a) HEC1A cells. (b) HEC1B cells. (c) KLE cells. Tested cells were treated with serial doses of docetaxel from 0 to 100 nM together with 0, 0.2, or 0.5 mg/mL AE-SN for 48 hr. Cell cytotoxicity was determined by MTT assay and presented as mean ± SD. Experiments were performed in triplicate.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3526186&req=5

fig5: Cytotoxicity of AE-SN and docetaxel cotreatment in human endometrial cancer cells. (a) HEC1A cells. (b) HEC1B cells. (c) KLE cells. Tested cells were treated with serial doses of docetaxel from 0 to 100 nM together with 0, 0.2, or 0.5 mg/mL AE-SN for 48 hr. Cell cytotoxicity was determined by MTT assay and presented as mean ± SD. Experiments were performed in triplicate.
Mentions: Since previous results verified that AE-SN treatment resulted in significant cell cytotoxicity in HEC1A, HEC1B, and KLE cells and was associated with autophagic cell death, the next step was to clarify the combination effect of AE-SN and a chemotherapeutic regimen with docetaxel in human endometrial adenocarcinoma cells. According to the IC50 determined by the cell viability study, doses of 0.2 and 0.5 mg/mL AE-SN which covered the IC50 dosage were chosen for cells treated with 0 to 100 nM docetaxel. The results shown in Figure 5 demonstrated that a combination effect was observed in HEC1A and HEC1B cells, whereas KLE cells were not only less sensitive to AE-SN, but also resistant to docetaxel treatment. The CI was calculated for AE-SN and docetaxel-treated cells and showed that a synergistic effect occurred in both 0.2 and 0.5 mg/mL AE-SN-treated HEC1A and HEC1B cells treated with 1 to 100 nM docetaxel (Table 1). These results suggested that cotreatment with AE-SN further enhanced the cell cytotoxicity of docetaxel in HEC1A and HEC1B cells.

Bottom Line: An effective complementary ingredient can be helpful in improving the clinical outcome.Aqueous extract of Solanum nigrum leaf (AE-SN) is a principal ingredient for treating cancer patients in traditional Chinese medicinal practice but lacks sufficient evidence to verify its tumor suppression efficacy.The activation of apoptotic markers, caspase-3 and poly-ADP-ribose polymerase, and autophagic marker, microtubule-associated protein 1 light chain 3 A/B, wAS determined to clarify the cell death pathways responsible for AE-SN induced tumor cell death.

View Article: PubMed Central - PubMed

Affiliation: Division of Hematology and Oncology, Department of Internal Medicine, Taipei Medical University Hospital, Taipei 110, Taiwan ; Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.

ABSTRACT
Chemotherapy is the main approach in dealing with advanced and recurrent endometrial cancer. An effective complementary ingredient can be helpful in improving the clinical outcome. Aqueous extract of Solanum nigrum leaf (AE-SN) is a principal ingredient for treating cancer patients in traditional Chinese medicinal practice but lacks sufficient evidence to verify its tumor suppression efficacy. This study evaluated the antitumor effects of AE-SN and also assessed the synergistic effects of AE-SN with docetaxel On the human endometrial cancer cell lines, HEC1A, HEC1B, and KLE. The activation of apoptotic markers, caspase-3 and poly-ADP-ribose polymerase, and autophagic marker, microtubule-associated protein 1 light chain 3 A/B, wAS determined to clarify the cell death pathways responsible for AE-SN induced tumor cell death. Results indicated that AE-SN-treatment has significant cytotoxicity on the tested endometrial cancer cells with accumulation of LC3 A/B II and demonstrated a synergistic effect of AE-SN and docetaxel in HEC1A and HEC1B cells, but not KLE cells. In conclusion, AE-SN treatment was effective in suppressing endometrial cancer cells via the autophagic pathway and was also capable of enhancing the cytotoxicity of docetaxel in human endometrial cancer cells. Our results provide meaningful evidence for integrative cancer therapy in the future.

No MeSH data available.


Related in: MedlinePlus