Sanggenol L Induces Apoptosis and Cell Cycle Arrest via Activation of p53 and Suppression of PI3K/Akt/mTOR Signaling in Human Prostate Cancer Cells
Prostate cancer is the most common cancer in Western countries. Recently, Asian countries are being affected by Western habits, which have had an important role in the rapid increase in cancer incidence. Sanggenol L (San L) is a natural flavonoid present in the root barks of , which induces anti-can...
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| Veröffentlicht in: | Nutrients 2020-02, Vol.12 (2), p.488 |
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| description | Prostate cancer is the most common cancer in Western countries. Recently, Asian countries are being affected by Western habits, which have had an important role in the rapid increase in cancer incidence. Sanggenol L (San L) is a natural flavonoid present in the root barks of
, which induces anti-cancer activities in ovarian cancer cells. However, the molecular and cellular mechanisms of the effects of sanggenol L on human prostate cancer cells have not been elucidated. In this study, we investigated whether sanggenol L exerts anti-cancer activity in human prostate cancer cells via apoptosis and cell cycle arrest. Sanggenol L induced caspase-dependent apoptosis (up-regulation of PARP and Bax or down-regulation of procaspase-3, -8, -9, Bid, and Bcl-2), induction of caspase-independent apoptosis (up-regulation of AIF and Endo G on cytosol), suppression of cell cycle (down-regulation of CDK1/2, CDK4, CDK6, cyclin D1, cyclin E, cyclin A, and cyclin B1 or up-regulation of p53 and p21), and inhibition of PI3K/Akt/mTOR signaling (down-regulation of PI3K, p-Akt, and p-mTOR) in prostate cancer cells. These results suggest the induction of apoptosis via suppression of PI3K/Akt/mTOR signaling and cell cycle arrest via activation of p53 in response to sanggenol L in prostate cancer cells. |
| doi_str_mv | 10.3390/nu12020488 |
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, which induces anti-cancer activities in ovarian cancer cells. However, the molecular and cellular mechanisms of the effects of sanggenol L on human prostate cancer cells have not been elucidated. In this study, we investigated whether sanggenol L exerts anti-cancer activity in human prostate cancer cells via apoptosis and cell cycle arrest. Sanggenol L induced caspase-dependent apoptosis (up-regulation of PARP and Bax or down-regulation of procaspase-3, -8, -9, Bid, and Bcl-2), induction of caspase-independent apoptosis (up-regulation of AIF and Endo G on cytosol), suppression of cell cycle (down-regulation of CDK1/2, CDK4, CDK6, cyclin D1, cyclin E, cyclin A, and cyclin B1 or up-regulation of p53 and p21), and inhibition of PI3K/Akt/mTOR signaling (down-regulation of PI3K, p-Akt, and p-mTOR) in prostate cancer cells. These results suggest the induction of apoptosis via suppression of PI3K/Akt/mTOR signaling and cell cycle arrest via activation of p53 in response to sanggenol L in prostate cancer cells.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu12020488</identifier><identifier>PMID: 32075054</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>1-Phosphatidylinositol 3-kinase ; aif ; AKT protein ; Apoptosis ; Apoptosis - genetics ; Apoptosis-inducing factor ; Bcl-2 protein ; Cancer therapies ; Caspase ; Caspase-3 ; Cell activation ; Cell culture ; Cell cycle ; Cell Cycle Checkpoints - genetics ; Cell Line, Tumor ; Cyclin A ; Cyclin B1 ; Cyclin D1 ; Cyclin E ; Cyclin-dependent kinase 4 ; Cytosol ; Cytotoxicity ; Deoxyribonucleic acid ; DNA ; Flavanones - isolation & purification ; Flavanones - pharmacology ; Flavanones - therapeutic use ; Flavonoids ; Humans ; Male ; Metastasis ; Morus - chemistry ; Ovarian cancer ; p53 ; p53 Protein ; Penicillin ; Phosphatidylinositol 3-Kinases - metabolism ; Physiology ; Phytotherapy ; pi3k/akt/mtor ; Plant Roots - chemistry ; Poly(ADP-ribose) polymerase ; Prostate cancer ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - pathology ; Proto-Oncogene Proteins c-akt - metabolism ; sanggenol l ; Signal Transduction - drug effects ; Signal Transduction - genetics ; TOR protein ; TOR Serine-Threonine Kinases ; Tumor Suppressor Protein p53 - metabolism ; Tumors</subject><ispartof>Nutrients, 2020-02, Vol.12 (2), p.488</ispartof><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 by the authors. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-440103637402eb8ec1ffde2ac38cfde08ef37c5e662b80d67c97dc8bb0e4f5bf3</citedby><cites>FETCH-LOGICAL-c472t-440103637402eb8ec1ffde2ac38cfde08ef37c5e662b80d67c97dc8bb0e4f5bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071324/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071324/$$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/32075054$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Won, Yeong-Seon</creatorcontrib><creatorcontrib>Seo, Kwon-Il</creatorcontrib><title>Sanggenol L Induces Apoptosis and Cell Cycle Arrest via Activation of p53 and Suppression of PI3K/Akt/mTOR Signaling in Human Prostate Cancer Cells</title><title>Nutrients</title><addtitle>Nutrients</addtitle><description>Prostate cancer is the most common cancer in Western countries. Recently, Asian countries are being affected by Western habits, which have had an important role in the rapid increase in cancer incidence. Sanggenol L (San L) is a natural flavonoid present in the root barks of
, which induces anti-cancer activities in ovarian cancer cells. However, the molecular and cellular mechanisms of the effects of sanggenol L on human prostate cancer cells have not been elucidated. In this study, we investigated whether sanggenol L exerts anti-cancer activity in human prostate cancer cells via apoptosis and cell cycle arrest. Sanggenol L induced caspase-dependent apoptosis (up-regulation of PARP and Bax or down-regulation of procaspase-3, -8, -9, Bid, and Bcl-2), induction of caspase-independent apoptosis (up-regulation of AIF and Endo G on cytosol), suppression of cell cycle (down-regulation of CDK1/2, CDK4, CDK6, cyclin D1, cyclin E, cyclin A, and cyclin B1 or up-regulation of p53 and p21), and inhibition of PI3K/Akt/mTOR signaling (down-regulation of PI3K, p-Akt, and p-mTOR) in prostate cancer cells. These results suggest the induction of apoptosis via suppression of PI3K/Akt/mTOR signaling and cell cycle arrest via activation of p53 in response to sanggenol L in prostate cancer cells.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>aif</subject><subject>AKT protein</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis-inducing factor</subject><subject>Bcl-2 protein</subject><subject>Cancer therapies</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell activation</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cyclin A</subject><subject>Cyclin B1</subject><subject>Cyclin D1</subject><subject>Cyclin E</subject><subject>Cyclin-dependent kinase 4</subject><subject>Cytosol</subject><subject>Cytotoxicity</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Flavanones - isolation & purification</subject><subject>Flavanones - pharmacology</subject><subject>Flavanones - therapeutic use</subject><subject>Flavonoids</subject><subject>Humans</subject><subject>Male</subject><subject>Metastasis</subject><subject>Morus - chemistry</subject><subject>Ovarian cancer</subject><subject>p53</subject><subject>p53 Protein</subject><subject>Penicillin</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Physiology</subject><subject>Phytotherapy</subject><subject>pi3k/akt/mtor</subject><subject>Plant Roots - chemistry</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>sanggenol l</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>TOR protein</subject><subject>TOR Serine-Threonine Kinases</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumors</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>DOA</sourceid><recordid>eNpdks9u1DAQxiMEolXphQdAlrggpGVtjxMnF6QognbFSq3YcrYcxwleEjvYyUp9Dl643j-UFl88mvnpm_HnSZK3BH8CKPDSzoRiilmev0jOKeZ0kWUMXj6Jz5LLELZ4fzjmGbxOziAWU5yy8-TPRtqu09b1aI1WtpmVDqgc3Ti5YAKStkGV7ntU3ateo9J7HSa0MxKVajI7ORlnkWvRmMKB3czjGJFwSt-u4Nuy_DUth7ub72hjOit7YztkLLqeB2nRrXdhkpNGlbRK-0Ov8CZ51co-6MvTfZH8-PrlrrperG-uVlW5XijG6bRgDBMMGXCGqa5zrUjbNppKBbmKAc51C1ylOstoneMm46rgjcrrGmvWpnULF8nqqNs4uRWjN4P098JJIw4J5zsh_WTiw4UklBZ1zhiVBaOaSeBQNylvGeQ1YWnU-nzUGud60I3SdvKyfyb6vGLNT9G5nYhfQoCyKPDhJODd7zm6LAYTVLRDWu3mICikBSMpAxzR9_-hWzf7aO2eKlJMAUgeqY9HSkWPg9ft4zAEi_3qiH-rE-F3T8d_RP8uCjwAyNi-EQ</recordid><startdate>20200214</startdate><enddate>20200214</enddate><creator>Won, Yeong-Seon</creator><creator>Seo, Kwon-Il</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20200214</creationdate><title>Sanggenol L Induces Apoptosis and Cell Cycle Arrest via Activation of p53 and Suppression of PI3K/Akt/mTOR Signaling in Human Prostate Cancer Cells</title><author>Won, Yeong-Seon ; Seo, Kwon-Il</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-440103637402eb8ec1ffde2ac38cfde08ef37c5e662b80d67c97dc8bb0e4f5bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>aif</topic><topic>AKT protein</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis-inducing factor</topic><topic>Bcl-2 protein</topic><topic>Cancer therapies</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Cell activation</topic><topic>Cell culture</topic><topic>Cell cycle</topic><topic>Cell Cycle Checkpoints - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cyclin A</topic><topic>Cyclin B1</topic><topic>Cyclin D1</topic><topic>Cyclin E</topic><topic>Cyclin-dependent kinase 4</topic><topic>Cytosol</topic><topic>Cytotoxicity</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Flavanones - isolation & purification</topic><topic>Flavanones - pharmacology</topic><topic>Flavanones - therapeutic use</topic><topic>Flavonoids</topic><topic>Humans</topic><topic>Male</topic><topic>Metastasis</topic><topic>Morus - chemistry</topic><topic>Ovarian cancer</topic><topic>p53</topic><topic>p53 Protein</topic><topic>Penicillin</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Physiology</topic><topic>Phytotherapy</topic><topic>pi3k/akt/mtor</topic><topic>Plant Roots - chemistry</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>sanggenol l</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>TOR protein</topic><topic>TOR Serine-Threonine Kinases</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Won, Yeong-Seon</creatorcontrib><creatorcontrib>Seo, Kwon-Il</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Nutrients</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Won, Yeong-Seon</au><au>Seo, Kwon-Il</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sanggenol L Induces Apoptosis and Cell Cycle Arrest via Activation of p53 and Suppression of PI3K/Akt/mTOR Signaling in Human Prostate Cancer Cells</atitle><jtitle>Nutrients</jtitle><addtitle>Nutrients</addtitle><date>2020-02-14</date><risdate>2020</risdate><volume>12</volume><issue>2</issue><spage>488</spage><pages>488-</pages><issn>2072-6643</issn><eissn>2072-6643</eissn><abstract>Prostate cancer is the most common cancer in Western countries. Recently, Asian countries are being affected by Western habits, which have had an important role in the rapid increase in cancer incidence. Sanggenol L (San L) is a natural flavonoid present in the root barks of
, which induces anti-cancer activities in ovarian cancer cells. However, the molecular and cellular mechanisms of the effects of sanggenol L on human prostate cancer cells have not been elucidated. In this study, we investigated whether sanggenol L exerts anti-cancer activity in human prostate cancer cells via apoptosis and cell cycle arrest. Sanggenol L induced caspase-dependent apoptosis (up-regulation of PARP and Bax or down-regulation of procaspase-3, -8, -9, Bid, and Bcl-2), induction of caspase-independent apoptosis (up-regulation of AIF and Endo G on cytosol), suppression of cell cycle (down-regulation of CDK1/2, CDK4, CDK6, cyclin D1, cyclin E, cyclin A, and cyclin B1 or up-regulation of p53 and p21), and inhibition of PI3K/Akt/mTOR signaling (down-regulation of PI3K, p-Akt, and p-mTOR) in prostate cancer cells. These results suggest the induction of apoptosis via suppression of PI3K/Akt/mTOR signaling and cell cycle arrest via activation of p53 in response to sanggenol L in prostate cancer cells.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>32075054</pmid><doi>10.3390/nu12020488</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase aif AKT protein Apoptosis Apoptosis - genetics Apoptosis-inducing factor Bcl-2 protein Cancer therapies Caspase Caspase-3 Cell activation Cell culture Cell cycle Cell Cycle Checkpoints - genetics Cell Line, Tumor Cyclin A Cyclin B1 Cyclin D1 Cyclin E Cyclin-dependent kinase 4 Cytosol Cytotoxicity Deoxyribonucleic acid DNA Flavanones - isolation & purification Flavanones - pharmacology Flavanones - therapeutic use Flavonoids Humans Male Metastasis Morus - chemistry Ovarian cancer p53 p53 Protein Penicillin Phosphatidylinositol 3-Kinases - metabolism Physiology Phytotherapy pi3k/akt/mtor Plant Roots - chemistry Poly(ADP-ribose) polymerase Prostate cancer Prostatic Neoplasms - drug therapy Prostatic Neoplasms - genetics Prostatic Neoplasms - pathology Proto-Oncogene Proteins c-akt - metabolism sanggenol l Signal Transduction - drug effects Signal Transduction - genetics TOR protein TOR Serine-Threonine Kinases Tumor Suppressor Protein p53 - metabolism Tumors |
| title | Sanggenol L Induces Apoptosis and Cell Cycle Arrest via Activation of p53 and Suppression of PI3K/Akt/mTOR Signaling in Human Prostate Cancer Cells |
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