Publication: Inhibitory effects on chondrosarcoma cell metastasis by Senna alata extract
2
0
Issued Date
2021
Resource Type
Language
eng
File Type
application/pdf
ISSN
7533322
Other identifier(s)
2-s2.0-85100802120
Rights Holder(s)
มหาวิทยาลัยศรีนครินทรวิโรฒ
Bibliographic Citation
Biomedicine and Pharmacotherapy. Vol 137, No. (2021)
Suggested Citation
Kittiwattanokhun A., Samosorn S., Innajak S., Watanapokasin R. Inhibitory effects on chondrosarcoma cell metastasis by Senna alata extract. Biomedicine and Pharmacotherapy. Vol 137, No. (2021). doi:10.1016/j.biopha.2021.111337 Retrieved from: https://hdl.handle.net/20.500.14740/7817
Abstract
Background: Senna alata L. Roxb or candle bush is a traditional medicinal plant with a wide range of biological activities including anti-inflammatory, antimicrobial and antifungal. Leaf extract of S. alata showed the anti-tumor activity in various cancer cell lines. In this study, we focused on the inhibitory mechanism of S. alata extract (SAE) on cancer metastasis including cell migration, cell invasion and signaling pathways in chondrosarcoma SW1353 cells. Purpose: This study aimed to evaluate the anti-metastatic mechanisms of Senna alata extract on chondrosarcoma SW1353 cells. Methods: Screening for phytochemicals in biologically active fraction of SAE was analysed by 1H NMR spectroscopy. Cell viability and cytoxicity were determined by using MTT assay. Cell migration was observed by scratch wound healing and transwell migration assay. Cell invasion and cell adhesion assay were examined by Matrigel coated transwell chambers or plates. The expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), MAPKs and PI3K/Akt signaling pathways and NF-κB were detected by Western blot analysis. Results: The SAE treatment at the sub-cytoxic and non-cytotoxic concentrations significantly inhibited cell migration, cell invasion and cell adhesion of SW1353 cells in a dose-dependent manner. The results from Western blot analysis showed decreased MMP-2 and MMP-9 expression, while increased TIMP-1 and TIMP-2 expression in SAE treated cells. Moreover, SAE suppressed phosphorylation of ERK1/2, p38 and Akt but decreased NF-κB transcription factor expression in SW1353 cells. Conclusion: These results revealed that SAE could reduce MMP-2 and MMP-9 expression by downregulation of NF-κB which is downstream of MAPKs and PI3K/Akt signaling pathway in SW1353 cells resulting in reduced cancer cell migration and invasion. Therefore, SAE may have the potential use as an alternative treatment of chondrosarcoma metastasis. © 2021
Subject(s)
Antineoplastic agent
Chloroform
Gelatinase A
Gelatinase B
Immunoglobulin enhancer binding protein
Mitogen activated protein kinase 1
Mitogen activated protein kinase 3
Plant extract
Senna alata extract
Tissue inhibitor of metalloproteinase 1
Tissue inhibitor of metalloproteinase 2
Unclassified drug
Gelatinase A
Gelatinase B
Immunoglobulin enhancer binding protein
Mitogen activated protein kinase
MMP2 protein, human
MMP9 protein, human
Oncoprotein
Phosphatidylinositol 3 kinase
Senna extract
TIMP1 protein, human
TIMP2 protein, human
Tissue inhibitor of metalloproteinase 1
Tissue inhibitor of metalloproteinase 2
Article
Cell adhesion assay
Cell invasion
Cell migration
Cell proliferation
Cell viability
Chondrosarcoma
Controlled study
Down regulation
Drug mechanism
Drug screening
Human
Human cell
In vitro study
Metastasis
Metastasis inhibition
MTT assay
Pi3K/Akt signaling
Plant leaf
Priority journal
Protein expression
Proton nuclear magnetic resonance
SW1353 cell line
Thin layer chromatography
Transwell assay
Tumor microenvironment
Western blotting
Wound closure
Wound healing assay
Cell adhesion
Cell motion
Cell survival
Chemistry
Chondrosarcoma
Drug effect
Metabolism
Metastasis
Signal transduction
Tumor cell line
Cell Adhesion
Cell Line, Tumor
Cell Movement
Cell Proliferation
Cell Survival
Chondrosarcoma
Humans
Matrix Metalloproteinase 2
Matrix Metalloproteinase 9
Mitogen-Activated Protein Kinases
Neoplasm Metastasis
NF-kappa B
Oncogene Protein v-akt
Phosphatidylinositol 3-Kinase
Senna Extract
Signal Transduction
Tissue Inhibitor of Metalloproteinase-1
Tissue Inhibitor of Metalloproteinase-2
Chloroform
Gelatinase A
Gelatinase B
Immunoglobulin enhancer binding protein
Mitogen activated protein kinase 1
Mitogen activated protein kinase 3
Plant extract
Senna alata extract
Tissue inhibitor of metalloproteinase 1
Tissue inhibitor of metalloproteinase 2
Unclassified drug
Gelatinase A
Gelatinase B
Immunoglobulin enhancer binding protein
Mitogen activated protein kinase
MMP2 protein, human
MMP9 protein, human
Oncoprotein
Phosphatidylinositol 3 kinase
Senna extract
TIMP1 protein, human
TIMP2 protein, human
Tissue inhibitor of metalloproteinase 1
Tissue inhibitor of metalloproteinase 2
Article
Cell adhesion assay
Cell invasion
Cell migration
Cell proliferation
Cell viability
Chondrosarcoma
Controlled study
Down regulation
Drug mechanism
Drug screening
Human
Human cell
In vitro study
Metastasis
Metastasis inhibition
MTT assay
Pi3K/Akt signaling
Plant leaf
Priority journal
Protein expression
Proton nuclear magnetic resonance
SW1353 cell line
Thin layer chromatography
Transwell assay
Tumor microenvironment
Western blotting
Wound closure
Wound healing assay
Cell adhesion
Cell motion
Cell survival
Chemistry
Chondrosarcoma
Drug effect
Metabolism
Metastasis
Signal transduction
Tumor cell line
Cell Adhesion
Cell Line, Tumor
Cell Movement
Cell Proliferation
Cell Survival
Chondrosarcoma
Humans
Matrix Metalloproteinase 2
Matrix Metalloproteinase 9
Mitogen-Activated Protein Kinases
Neoplasm Metastasis
NF-kappa B
Oncogene Protein v-akt
Phosphatidylinositol 3-Kinase
Senna Extract
Signal Transduction
Tissue Inhibitor of Metalloproteinase-1
Tissue Inhibitor of Metalloproteinase-2
