A Study on Cytotoxic and Apoptotic Potential of a Triterpenoid Saponin (3-O-α-L-Arabinosyl Oleanolic Acid) Isolated from Schumacheria castaneifolia Vahl in Human Non-Small-Cell Lung Cancer (NCI-H292) Cells
Lung cancer is the major cause of cancer death among men. A number of natural compounds have proven to be useful in the treatmet of lung cancer. This study was aimed to determine cytotoxic and apoptotoic effects of a natural compound 3-O-α-L-arabinosyl oleanolic acid (3-O-L-AO) isolated from Schumac...
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| creator | Karunaratne, Veranja Piyathilaka, Poorna Tennekoon, Kamani H. Bandara, Chamara Janaka Nwokwu, Chukwumaobim Daniel Uzochukwuwulu Ediriweera, Meran K. Samarakoon, Sameera R. Karunaratne, D. Nedra |
| description | Lung cancer is the major cause of cancer death among men. A number of natural compounds have proven to be useful in the treatmet of lung cancer. This study was aimed to determine cytotoxic and apoptotoic effects of a natural compound 3-O-α-L-arabinosyl oleanolic acid (3-O-L-AO) isolated from Schumacheria castaneifolia in non-small-cell lung cancer (NCI-H292) cells. Cytotoxic effects of 3-O-L-AO were determined by Sulforhodamine B (SRB) assay and apoptotic effects were tested by evaluating (a) apoptotsis related morphological changes, (b) caspase 3/7 activity, and (c) expression of Bax, p53, and survivin genes. Oxidative stress markers (reactive oxygen species (ROS), glutathione-S-transferase (GST), and glutathione (GSH)) were also analysed in 3-O-L-AO treated NCI-H292 cells. 3-O-L-AO exerted potent cytotoxic effects in NCI-H292 cells while being less cytotoxic to normal lung (MRC-5) cells. Exposure to 3-O-L-AO caused upregulation of Bax and p53 and downregulation of survivin in NCI-H292 cells. Activation of caspase 3/7 and morphological features related to apoptosis further confirmed 3-O-L-AO induced apoptosis. Furthermore, elevated ROS and GST levels and decreased GSH levels suggested 3-O-L-AO can induce apoptosis, possibly causing oxidative stress in NCI-H292 cells. Overall results suggest that 3-O-L-AO can be considered as an effective anticancer agent for the treatment of lung cancer. |
| doi_str_mv | 10.1155/2017/9854083 |
| format | Article |
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Nedra</creator><contributor>Liu, Gang</contributor><creatorcontrib>Karunaratne, Veranja ; Piyathilaka, Poorna ; Tennekoon, Kamani H. ; Bandara, Chamara Janaka ; Nwokwu, Chukwumaobim Daniel Uzochukwuwulu ; Ediriweera, Meran K. ; Samarakoon, Sameera R. ; Karunaratne, D. Nedra ; Liu, Gang</creatorcontrib><description>Lung cancer is the major cause of cancer death among men. A number of natural compounds have proven to be useful in the treatmet of lung cancer. This study was aimed to determine cytotoxic and apoptotoic effects of a natural compound 3-O-α-L-arabinosyl oleanolic acid (3-O-L-AO) isolated from Schumacheria castaneifolia in non-small-cell lung cancer (NCI-H292) cells. Cytotoxic effects of 3-O-L-AO were determined by Sulforhodamine B (SRB) assay and apoptotic effects were tested by evaluating (a) apoptotsis related morphological changes, (b) caspase 3/7 activity, and (c) expression of Bax, p53, and survivin genes. Oxidative stress markers (reactive oxygen species (ROS), glutathione-S-transferase (GST), and glutathione (GSH)) were also analysed in 3-O-L-AO treated NCI-H292 cells. 3-O-L-AO exerted potent cytotoxic effects in NCI-H292 cells while being less cytotoxic to normal lung (MRC-5) cells. Exposure to 3-O-L-AO caused upregulation of Bax and p53 and downregulation of survivin in NCI-H292 cells. Activation of caspase 3/7 and morphological features related to apoptosis further confirmed 3-O-L-AO induced apoptosis. Furthermore, elevated ROS and GST levels and decreased GSH levels suggested 3-O-L-AO can induce apoptosis, possibly causing oxidative stress in NCI-H292 cells. Overall results suggest that 3-O-L-AO can be considered as an effective anticancer agent for the treatment of lung cancer.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2017/9854083</identifier><identifier>PMID: 29259993</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Acids ; Anticancer properties ; Apoptosis ; Biochemistry ; Biomedical research ; Breast cancer ; Cancer ; Cancer therapies ; Caspase ; Caspase-3 ; Cell culture ; Chemotherapy ; Cytotoxicity ; Gene expression ; Glutathione ; Glutathione transferase ; Lung cancer ; Morphology ; Oleanolic acid ; Oxidative stress ; p53 Protein ; Reactive oxygen species ; Sulforhodamine ; Survivin</subject><ispartof>BioMed research international, 2017-01, Vol.2017 (2017), p.1-8</ispartof><rights>Copyright © 2017 Sameera R. Samarakoon et al.</rights><rights>Copyright © 2017 Sameera R. Samarakoon et al.; This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2017 Sameera R. Samarakoon et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433t-a700f172aaf642a5b94b1b98bbf44249ab2bfcec85eaa5a3f2328b1f3b48d3023</citedby><cites>FETCH-LOGICAL-c433t-a700f172aaf642a5b94b1b98bbf44249ab2bfcec85eaa5a3f2328b1f3b48d3023</cites><orcidid>0000-0003-0608-4340 ; 0000-0002-0092-3361 ; 0000-0002-5278-4770 ; 0000-0001-9393-9516</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5702947/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5702947/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29259993$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Liu, Gang</contributor><creatorcontrib>Karunaratne, Veranja</creatorcontrib><creatorcontrib>Piyathilaka, Poorna</creatorcontrib><creatorcontrib>Tennekoon, Kamani H.</creatorcontrib><creatorcontrib>Bandara, Chamara Janaka</creatorcontrib><creatorcontrib>Nwokwu, Chukwumaobim Daniel Uzochukwuwulu</creatorcontrib><creatorcontrib>Ediriweera, Meran K.</creatorcontrib><creatorcontrib>Samarakoon, Sameera R.</creatorcontrib><creatorcontrib>Karunaratne, D. Nedra</creatorcontrib><title>A Study on Cytotoxic and Apoptotic Potential of a Triterpenoid Saponin (3-O-α-L-Arabinosyl Oleanolic Acid) Isolated from Schumacheria castaneifolia Vahl in Human Non-Small-Cell Lung Cancer (NCI-H292) Cells</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Lung cancer is the major cause of cancer death among men. A number of natural compounds have proven to be useful in the treatmet of lung cancer. This study was aimed to determine cytotoxic and apoptotoic effects of a natural compound 3-O-α-L-arabinosyl oleanolic acid (3-O-L-AO) isolated from Schumacheria castaneifolia in non-small-cell lung cancer (NCI-H292) cells. Cytotoxic effects of 3-O-L-AO were determined by Sulforhodamine B (SRB) assay and apoptotic effects were tested by evaluating (a) apoptotsis related morphological changes, (b) caspase 3/7 activity, and (c) expression of Bax, p53, and survivin genes. Oxidative stress markers (reactive oxygen species (ROS), glutathione-S-transferase (GST), and glutathione (GSH)) were also analysed in 3-O-L-AO treated NCI-H292 cells. 3-O-L-AO exerted potent cytotoxic effects in NCI-H292 cells while being less cytotoxic to normal lung (MRC-5) cells. Exposure to 3-O-L-AO caused upregulation of Bax and p53 and downregulation of survivin in NCI-H292 cells. Activation of caspase 3/7 and morphological features related to apoptosis further confirmed 3-O-L-AO induced apoptosis. Furthermore, elevated ROS and GST levels and decreased GSH levels suggested 3-O-L-AO can induce apoptosis, possibly causing oxidative stress in NCI-H292 cells. Overall results suggest that 3-O-L-AO can be considered as an effective anticancer agent for the treatment of lung cancer.</description><subject>Acids</subject><subject>Anticancer properties</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical research</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell culture</subject><subject>Chemotherapy</subject><subject>Cytotoxicity</subject><subject>Gene expression</subject><subject>Glutathione</subject><subject>Glutathione transferase</subject><subject>Lung cancer</subject><subject>Morphology</subject><subject>Oleanolic acid</subject><subject>Oxidative stress</subject><subject>p53 Protein</subject><subject>Reactive oxygen species</subject><subject>Sulforhodamine</subject><subject>Survivin</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNks2O0zAUhSMEYkZldqyRJTYzgjD-SxNvkKoIaKVqitSBbXTj2FOPHLvYCdDH4kXmmXDVUn5WeGNf3U9H91yfLHtO8BtCiuKaYlJei6rguGKPsnPKCM-nhJPHpzdjZ9lFjPc4nYpMsZg-zc6ooIUQgp1nDzO0HsZuh7xD9W7wg_9uJALXodnWb1Odqo9-UG4wYJHXCNBtMIMKW-W86dAatt4Zhy5ZvsoffuTLfBagNc7HnUUrq8B5myRm0nRXaBG9hUF1SAffo7XcjD3IjQoGkIQ4gFNGJxzQZ9hYlFTnCXDoxrt83YO1ea2sRcvR3aEanFQBXd7Ui3ye7FyhfS8-y55osFFdHO9J9un9u9t6ni9XHxb1bJlLztiQQ4mxJiUF0FNOoWgFb0krqrbVnFMuoKWtlkpWhQIogGnKaNUSzVpedQxTNsneHnS3Y9urTqb9BLDNNpgewq7xYJq_O85smjv_tSlKTAUvk8DlUSD4L6OKQ9ObKJOFtAQ_xoaIUpCSVOn_JtnLf9B7PwaX7CVqKnBBy6pI1OsDJYOPMSh9GobgZp-VZp-V5piVhL_408AJ_pWMBLw6ABvjOvhm_lNOJUZp-E0TJkqO2U-yZ9IQ</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Karunaratne, Veranja</creator><creator>Piyathilaka, Poorna</creator><creator>Tennekoon, Kamani H.</creator><creator>Bandara, Chamara Janaka</creator><creator>Nwokwu, Chukwumaobim Daniel Uzochukwuwulu</creator><creator>Ediriweera, Meran K.</creator><creator>Samarakoon, Sameera R.</creator><creator>Karunaratne, D. 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Nedra</au><au>Liu, Gang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Study on Cytotoxic and Apoptotic Potential of a Triterpenoid Saponin (3-O-α-L-Arabinosyl Oleanolic Acid) Isolated from Schumacheria castaneifolia Vahl in Human Non-Small-Cell Lung Cancer (NCI-H292) Cells</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>2017</volume><issue>2017</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Lung cancer is the major cause of cancer death among men. A number of natural compounds have proven to be useful in the treatmet of lung cancer. This study was aimed to determine cytotoxic and apoptotoic effects of a natural compound 3-O-α-L-arabinosyl oleanolic acid (3-O-L-AO) isolated from Schumacheria castaneifolia in non-small-cell lung cancer (NCI-H292) cells. Cytotoxic effects of 3-O-L-AO were determined by Sulforhodamine B (SRB) assay and apoptotic effects were tested by evaluating (a) apoptotsis related morphological changes, (b) caspase 3/7 activity, and (c) expression of Bax, p53, and survivin genes. Oxidative stress markers (reactive oxygen species (ROS), glutathione-S-transferase (GST), and glutathione (GSH)) were also analysed in 3-O-L-AO treated NCI-H292 cells. 3-O-L-AO exerted potent cytotoxic effects in NCI-H292 cells while being less cytotoxic to normal lung (MRC-5) cells. Exposure to 3-O-L-AO caused upregulation of Bax and p53 and downregulation of survivin in NCI-H292 cells. Activation of caspase 3/7 and morphological features related to apoptosis further confirmed 3-O-L-AO induced apoptosis. Furthermore, elevated ROS and GST levels and decreased GSH levels suggested 3-O-L-AO can induce apoptosis, possibly causing oxidative stress in NCI-H292 cells. Overall results suggest that 3-O-L-AO can be considered as an effective anticancer agent for the treatment of lung cancer.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>29259993</pmid><doi>10.1155/2017/9854083</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-0608-4340</orcidid><orcidid>https://orcid.org/0000-0002-0092-3361</orcidid><orcidid>https://orcid.org/0000-0002-5278-4770</orcidid><orcidid>https://orcid.org/0000-0001-9393-9516</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acids Anticancer properties Apoptosis Biochemistry Biomedical research Breast cancer Cancer Cancer therapies Caspase Caspase-3 Cell culture Chemotherapy Cytotoxicity Gene expression Glutathione Glutathione transferase Lung cancer Morphology Oleanolic acid Oxidative stress p53 Protein Reactive oxygen species Sulforhodamine Survivin |
| title | A Study on Cytotoxic and Apoptotic Potential of a Triterpenoid Saponin (3-O-α-L-Arabinosyl Oleanolic Acid) Isolated from Schumacheria castaneifolia Vahl in Human Non-Small-Cell Lung Cancer (NCI-H292) Cells |
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