[6]‐Gingerol enhances the cisplatin sensitivity of gastric cancer cells through inhibition of proliferation and invasion via PI3K/AKT signaling pathway
Cisplatin‐based chemotherapy is a widely used chemotherapeutic regimen for gastric cancer; however, drug resistance limits its efficacy. [6]‐Gingerol has been found to exhibit anticancer effects. Here, we aim to explore the potential of [6]‐gingerol in combination with cisplatin as a new regimen for...
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| Veröffentlicht in: | Phytotherapy research 2019-05, Vol.33 (5), p.1353-1362 |
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| creator | Luo, Youjun Zha, Lin Luo, Lumeng Chen, Xue Zhang, Qi Gao, Caixia Zhuang, Xibing Yuan, Sujuan Qiao, Tiankui |
| description | Cisplatin‐based chemotherapy is a widely used chemotherapeutic regimen for gastric cancer; however, drug resistance limits its efficacy. [6]‐Gingerol has been found to exhibit anticancer effects. Here, we aim to explore the potential of [6]‐gingerol in combination with cisplatin as a new regimen for gastric cancer. CCK‐8 assay and colony formation assay were used to determine the effect of [6]‐gingerol in combination with cisplatin on cell viability of gastric cancer cells. Flow cytometry was performed to assess cell cycle distribution. Wound‐healing assay and transwell invasion assay were conducted to examine the migration and invasion abilities. Cell cycle and invasion‐related proteins and mRNAs, as well as PI3K/AKT signaling proteins, were assessed by western blotting and quantitative real‐time polymerase chain reaction. Combination of [6]‐gingerol with cisplatin inhibited cell viability and enhanced cell cycle arrest at G1 phase compared with cisplatin alone. The combination treatment inhibited cell migration and invasion ability and decreased cyclin D1, cyclin A2, matrix metalloproteinase‐9, p‐PI3K, AKT, and p‐AKT protein expressions and increased P21 and P27 mRNA levels. Our study demonstrates that [6]‐gingerol enhances the cisplatin sensitivity of gastric cancer cells and that the mechanisms involve G1 phase arrest, migration and invasion suppression via PI3K/AKT signaling pathway. |
| doi_str_mv | 10.1002/ptr.6325 |
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[6]‐Gingerol has been found to exhibit anticancer effects. Here, we aim to explore the potential of [6]‐gingerol in combination with cisplatin as a new regimen for gastric cancer. CCK‐8 assay and colony formation assay were used to determine the effect of [6]‐gingerol in combination with cisplatin on cell viability of gastric cancer cells. Flow cytometry was performed to assess cell cycle distribution. Wound‐healing assay and transwell invasion assay were conducted to examine the migration and invasion abilities. Cell cycle and invasion‐related proteins and mRNAs, as well as PI3K/AKT signaling proteins, were assessed by western blotting and quantitative real‐time polymerase chain reaction. Combination of [6]‐gingerol with cisplatin inhibited cell viability and enhanced cell cycle arrest at G1 phase compared with cisplatin alone. The combination treatment inhibited cell migration and invasion ability and decreased cyclin D1, cyclin A2, matrix metalloproteinase‐9, p‐PI3K, AKT, and p‐AKT protein expressions and increased P21 and P27 mRNA levels. Our study demonstrates that [6]‐gingerol enhances the cisplatin sensitivity of gastric cancer cells and that the mechanisms involve G1 phase arrest, migration and invasion suppression via PI3K/AKT signaling pathway.</description><identifier>ISSN: 0951-418X</identifier><identifier>EISSN: 1099-1573</identifier><identifier>DOI: 10.1002/ptr.6325</identifier><identifier>PMID: 30811726</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Anticancer properties ; Assaying ; Cell adhesion & migration ; Cell cycle ; Cell migration ; Cell proliferation ; Cell viability ; Chemotherapy ; Cholecystokinin ; Cisplatin ; Cyclin D1 ; Drug resistance ; Flow cytometry ; G1 phase ; Gastric cancer ; gastric cancer cells ; Gingerol ; GTP-binding protein ; invasion ; Matrix metalloproteinase ; Matrix metalloproteinases ; Metalloproteinase ; mRNA ; PI3K/AKT signaling pathway ; Polymerase chain reaction ; proliferation ; Proteins ; Sensitivity ; Sensitivity enhancement ; Signal transduction ; Signaling ; Western blotting ; Wound healing</subject><ispartof>Phytotherapy research, 2019-05, Vol.33 (5), p.1353-1362</ispartof><rights>2019 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0002-4460-2826</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fptr.6325$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fptr.6325$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30811726$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Luo, Youjun</creatorcontrib><creatorcontrib>Zha, Lin</creatorcontrib><creatorcontrib>Luo, Lumeng</creatorcontrib><creatorcontrib>Chen, Xue</creatorcontrib><creatorcontrib>Zhang, Qi</creatorcontrib><creatorcontrib>Gao, Caixia</creatorcontrib><creatorcontrib>Zhuang, Xibing</creatorcontrib><creatorcontrib>Yuan, Sujuan</creatorcontrib><creatorcontrib>Qiao, Tiankui</creatorcontrib><title>[6]‐Gingerol enhances the cisplatin sensitivity of gastric cancer cells through inhibition of proliferation and invasion via PI3K/AKT signaling pathway</title><title>Phytotherapy research</title><addtitle>Phytother Res</addtitle><description>Cisplatin‐based chemotherapy is a widely used chemotherapeutic regimen for gastric cancer; however, drug resistance limits its efficacy. [6]‐Gingerol has been found to exhibit anticancer effects. Here, we aim to explore the potential of [6]‐gingerol in combination with cisplatin as a new regimen for gastric cancer. CCK‐8 assay and colony formation assay were used to determine the effect of [6]‐gingerol in combination with cisplatin on cell viability of gastric cancer cells. Flow cytometry was performed to assess cell cycle distribution. Wound‐healing assay and transwell invasion assay were conducted to examine the migration and invasion abilities. Cell cycle and invasion‐related proteins and mRNAs, as well as PI3K/AKT signaling proteins, were assessed by western blotting and quantitative real‐time polymerase chain reaction. Combination of [6]‐gingerol with cisplatin inhibited cell viability and enhanced cell cycle arrest at G1 phase compared with cisplatin alone. The combination treatment inhibited cell migration and invasion ability and decreased cyclin D1, cyclin A2, matrix metalloproteinase‐9, p‐PI3K, AKT, and p‐AKT protein expressions and increased P21 and P27 mRNA levels. Our study demonstrates that [6]‐gingerol enhances the cisplatin sensitivity of gastric cancer cells and that the mechanisms involve G1 phase arrest, migration and invasion suppression via PI3K/AKT signaling pathway.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Anticancer properties</subject><subject>Assaying</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Cell viability</subject><subject>Chemotherapy</subject><subject>Cholecystokinin</subject><subject>Cisplatin</subject><subject>Cyclin D1</subject><subject>Drug resistance</subject><subject>Flow cytometry</subject><subject>G1 phase</subject><subject>Gastric cancer</subject><subject>gastric cancer cells</subject><subject>Gingerol</subject><subject>GTP-binding protein</subject><subject>invasion</subject><subject>Matrix metalloproteinase</subject><subject>Matrix metalloproteinases</subject><subject>Metalloproteinase</subject><subject>mRNA</subject><subject>PI3K/AKT signaling pathway</subject><subject>Polymerase chain reaction</subject><subject>proliferation</subject><subject>Proteins</subject><subject>Sensitivity</subject><subject>Sensitivity enhancement</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Western blotting</subject><subject>Wound healing</subject><issn>0951-418X</issn><issn>1099-1573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNpdkc1KxDAQx4Mo7voBPoEEvHip5qNJ2qOIrqKgyAqCSMlm022km9ak3WVvPoJXX88nMfHr4GmYmd8M_5k_AHsYHWGEyHHbuSNOCVsDQ4zyPMFM0HUwRDnDSYqzhwHY8v4ZIZQTlG6CAUUZxoLwIXh_5E8fr28jY2faNTXUtpJWaQ-7SkNlfFvLzljotfWmMwvTrWBTwpn0nTMKqsg6qHRdxwnX9LMKGluZSYAbG9E2bDWldvKrIO009BfSx2RhJLy9pFfHJ1dj6M3MyjrIgK3sqqVc7YCNUtZe7_7EbXB_fjY-vUiub0aXpyfXSUuEYIkimnORcsaYILnIEAmXMZ1qIlhGNSsVl4zlimCqMoIELklKGEf5VFDMhaDb4PB7b1D60mvfFXPj40XS6qb3BcGZQITnPAvowT_0ueldkB0oQjFNGcWR2v-h-slcT4vWmbl0q-L36QFIvoGlqfXqr49REc0sgplFNLO4Hd_FSD8BDv2RxQ</recordid><startdate>201905</startdate><enddate>201905</enddate><creator>Luo, Youjun</creator><creator>Zha, Lin</creator><creator>Luo, Lumeng</creator><creator>Chen, Xue</creator><creator>Zhang, Qi</creator><creator>Gao, Caixia</creator><creator>Zhuang, Xibing</creator><creator>Yuan, Sujuan</creator><creator>Qiao, Tiankui</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>7QO</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4460-2826</orcidid></search><sort><creationdate>201905</creationdate><title>[6]‐Gingerol enhances the cisplatin sensitivity of gastric cancer cells through inhibition of proliferation and invasion via PI3K/AKT signaling pathway</title><author>Luo, Youjun ; Zha, Lin ; Luo, Lumeng ; Chen, Xue ; Zhang, Qi ; Gao, Caixia ; Zhuang, Xibing ; Yuan, Sujuan ; Qiao, Tiankui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p2775-c2e6674655572978021175e4e27583e5fc6a559c213c82071f2425609d7316773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Anticancer properties</topic><topic>Assaying</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Cell viability</topic><topic>Chemotherapy</topic><topic>Cholecystokinin</topic><topic>Cisplatin</topic><topic>Cyclin D1</topic><topic>Drug resistance</topic><topic>Flow cytometry</topic><topic>G1 phase</topic><topic>Gastric cancer</topic><topic>gastric cancer cells</topic><topic>Gingerol</topic><topic>GTP-binding protein</topic><topic>invasion</topic><topic>Matrix metalloproteinase</topic><topic>Matrix metalloproteinases</topic><topic>Metalloproteinase</topic><topic>mRNA</topic><topic>PI3K/AKT signaling pathway</topic><topic>Polymerase chain reaction</topic><topic>proliferation</topic><topic>Proteins</topic><topic>Sensitivity</topic><topic>Sensitivity enhancement</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Western blotting</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luo, Youjun</creatorcontrib><creatorcontrib>Zha, Lin</creatorcontrib><creatorcontrib>Luo, Lumeng</creatorcontrib><creatorcontrib>Chen, Xue</creatorcontrib><creatorcontrib>Zhang, Qi</creatorcontrib><creatorcontrib>Gao, Caixia</creatorcontrib><creatorcontrib>Zhuang, Xibing</creatorcontrib><creatorcontrib>Yuan, Sujuan</creatorcontrib><creatorcontrib>Qiao, Tiankui</creatorcontrib><collection>PubMed</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Phytotherapy research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luo, Youjun</au><au>Zha, Lin</au><au>Luo, Lumeng</au><au>Chen, Xue</au><au>Zhang, Qi</au><au>Gao, Caixia</au><au>Zhuang, Xibing</au><au>Yuan, Sujuan</au><au>Qiao, Tiankui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>[6]‐Gingerol enhances the cisplatin sensitivity of gastric cancer cells through inhibition of proliferation and invasion via PI3K/AKT signaling pathway</atitle><jtitle>Phytotherapy research</jtitle><addtitle>Phytother Res</addtitle><date>2019-05</date><risdate>2019</risdate><volume>33</volume><issue>5</issue><spage>1353</spage><epage>1362</epage><pages>1353-1362</pages><issn>0951-418X</issn><eissn>1099-1573</eissn><abstract>Cisplatin‐based chemotherapy is a widely used chemotherapeutic regimen for gastric cancer; however, drug resistance limits its efficacy. [6]‐Gingerol has been found to exhibit anticancer effects. Here, we aim to explore the potential of [6]‐gingerol in combination with cisplatin as a new regimen for gastric cancer. CCK‐8 assay and colony formation assay were used to determine the effect of [6]‐gingerol in combination with cisplatin on cell viability of gastric cancer cells. Flow cytometry was performed to assess cell cycle distribution. Wound‐healing assay and transwell invasion assay were conducted to examine the migration and invasion abilities. Cell cycle and invasion‐related proteins and mRNAs, as well as PI3K/AKT signaling proteins, were assessed by western blotting and quantitative real‐time polymerase chain reaction. Combination of [6]‐gingerol with cisplatin inhibited cell viability and enhanced cell cycle arrest at G1 phase compared with cisplatin alone. The combination treatment inhibited cell migration and invasion ability and decreased cyclin D1, cyclin A2, matrix metalloproteinase‐9, p‐PI3K, AKT, and p‐AKT protein expressions and increased P21 and P27 mRNA levels. Our study demonstrates that [6]‐gingerol enhances the cisplatin sensitivity of gastric cancer cells and that the mechanisms involve G1 phase arrest, migration and invasion suppression via PI3K/AKT signaling pathway.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30811726</pmid><doi>10.1002/ptr.6325</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-4460-2826</orcidid></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Anticancer properties Assaying Cell adhesion & migration Cell cycle Cell migration Cell proliferation Cell viability Chemotherapy Cholecystokinin Cisplatin Cyclin D1 Drug resistance Flow cytometry G1 phase Gastric cancer gastric cancer cells Gingerol GTP-binding protein invasion Matrix metalloproteinase Matrix metalloproteinases Metalloproteinase mRNA PI3K/AKT signaling pathway Polymerase chain reaction proliferation Proteins Sensitivity Sensitivity enhancement Signal transduction Signaling Western blotting Wound healing |
| title | [6]‐Gingerol enhances the cisplatin sensitivity of gastric cancer cells through inhibition of proliferation and invasion via PI3K/AKT signaling pathway |
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