Leaf Extract from European Olive (Olea europaea L.) Post-Transcriptionally Suppresses the Epithelial-Mesenchymal Transition and Sensitizes Gastric Cancer Cells to Chemotherapy
The overall survival of patients with the advanced and recurrent gastric cancer (GC) remains unfavorable. In particular, this is due to cancer spreading and resistance to chemotherapy associated with the epithelial-mesenchymal transition (EMT) of tumor cells. EMT can be identified by the transcripto...
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| Veröffentlicht in: | Biochemistry (Moscow) 2024, Vol.89 (1), p.97-115 |
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| creator | Tekin, Cagla Ercelik, Melis Dunaev, Pavel Galembikova, Aigul Tezcan, Gulcin Aksoy, Secil Ak Budak, Ferah Isık, Ozgen Ugras, Nesrin Boichuk, Sergei Tunca, Berrin |
| description | The overall survival of patients with the advanced and recurrent gastric cancer (GC) remains unfavorable. In particular, this is due to cancer spreading and resistance to chemotherapy associated with the epithelial-mesenchymal transition (EMT) of tumor cells. EMT can be identified by the transcriptome profiling of GC for EMT markers. Indeed, analysis of the TCGA and GTEx databases (
n
= 408) and a cohort of GC patients (
n
= 43) revealed that expression of the
CDH2
gene was significantly decreased in the tumors vs. non-tumor tissues and correlated with the overall survival of GC patients. Expression of the EMT-promoting transcription factors SNAIL and ZEB1 was significantly increased in GC. These data suggest that targeting the EMT might be an attractive therapeutic approach for patients with GC. Previously, we demonstrated a potent anti-cancer activity of the olive leaf extract (OLE). However, its effect on the EMT regulation in GC remained unknown. Here, we showed that OLE efficiently potentiated the inhibitory effect of the chemotherapeutic agents 5-fluorouracil (5-FU) and cisplatin (Cis) on the EMT and their pro-apoptotic activity, as was demonstrated by changes in the expression of the EMT markers (E- and N-cadherins, vimentin, claudin-1) in GC cells treated with the aforementioned chemotherapeutic agents in the presence of OLE. Thus, culturing GC cells with 5-FU + OLE or Cis + OLE attenuated the invasive properties of cancer cells. Importantly, upregulation of expression of the apoptotic markers (PARP cleaved form) and increase in the number of cells undergoing apoptosis (annexin V-positive) were observed for GC cells treated with a combination of OLE and 5-FU or Cis. Collectively, our data illustrate that OLE efficiently interferes with the EMT in GC cells and potentiates the pro-apoptotic activity of certain chemotherapeutic agents used for GC therapy. |
| doi_str_mv | 10.1134/S0006297924010061 |
| format | Article |
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n
= 408) and a cohort of GC patients (
n
= 43) revealed that expression of the
CDH2
gene was significantly decreased in the tumors vs. non-tumor tissues and correlated with the overall survival of GC patients. Expression of the EMT-promoting transcription factors SNAIL and ZEB1 was significantly increased in GC. These data suggest that targeting the EMT might be an attractive therapeutic approach for patients with GC. Previously, we demonstrated a potent anti-cancer activity of the olive leaf extract (OLE). However, its effect on the EMT regulation in GC remained unknown. Here, we showed that OLE efficiently potentiated the inhibitory effect of the chemotherapeutic agents 5-fluorouracil (5-FU) and cisplatin (Cis) on the EMT and their pro-apoptotic activity, as was demonstrated by changes in the expression of the EMT markers (E- and N-cadherins, vimentin, claudin-1) in GC cells treated with the aforementioned chemotherapeutic agents in the presence of OLE. Thus, culturing GC cells with 5-FU + OLE or Cis + OLE attenuated the invasive properties of cancer cells. Importantly, upregulation of expression of the apoptotic markers (PARP cleaved form) and increase in the number of cells undergoing apoptosis (annexin V-positive) were observed for GC cells treated with a combination of OLE and 5-FU or Cis. Collectively, our data illustrate that OLE efficiently interferes with the EMT in GC cells and potentiates the pro-apoptotic activity of certain chemotherapeutic agents used for GC therapy.</description><identifier>ISSN: 0006-2979</identifier><identifier>EISSN: 1608-3040</identifier><identifier>DOI: 10.1134/S0006297924010061</identifier><identifier>PMID: 38467548</identifier><language>eng</language><publisher>Moscow: Pleiades Publishing</publisher><subject>5-Fluorouracil ; Annexin V ; Anticancer properties ; Antineoplastic drugs ; Antitumor activity ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Bioorganic Chemistry ; Cadherins ; Cadherins - metabolism ; Cancer therapies ; Cell Line, Tumor ; Cell Movement ; Chemotherapy ; Cisplatin ; Cisplatin - pharmacology ; Epithelial-Mesenchymal Transition ; Fluorouracil - pharmacology ; Gastric cancer ; Gene expression ; Gene Expression Regulation, Neoplastic ; Herbal medicine ; Humans ; Invasiveness ; Leaves ; Life Sciences ; Microbiology ; Olea - metabolism ; Plant extracts ; Plant Extracts - pharmacology ; Post-transcription ; Snail protein ; Stomach Neoplasms - drug therapy ; Stomach Neoplasms - genetics ; Stomach Neoplasms - metabolism ; Survival ; Survival analysis ; Transcription factors ; Transcriptomes ; Tumor cells ; Tumors ; Vimentin</subject><ispartof>Biochemistry (Moscow), 2024, Vol.89 (1), p.97-115</ispartof><rights>Pleiades Publishing, Ltd. 2024</rights><rights>Pleiades Publishing, Ltd. 2024.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c324t-e2ca48e5acd4a06a2c1faf456130cbba8095bd1e9a595bbdd934c7c06b15c8603</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1134/S0006297924010061$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1134/S0006297924010061$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38467548$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tekin, Cagla</creatorcontrib><creatorcontrib>Ercelik, Melis</creatorcontrib><creatorcontrib>Dunaev, Pavel</creatorcontrib><creatorcontrib>Galembikova, Aigul</creatorcontrib><creatorcontrib>Tezcan, Gulcin</creatorcontrib><creatorcontrib>Aksoy, Secil Ak</creatorcontrib><creatorcontrib>Budak, Ferah</creatorcontrib><creatorcontrib>Isık, Ozgen</creatorcontrib><creatorcontrib>Ugras, Nesrin</creatorcontrib><creatorcontrib>Boichuk, Sergei</creatorcontrib><creatorcontrib>Tunca, Berrin</creatorcontrib><title>Leaf Extract from European Olive (Olea europaea L.) Post-Transcriptionally Suppresses the Epithelial-Mesenchymal Transition and Sensitizes Gastric Cancer Cells to Chemotherapy</title><title>Biochemistry (Moscow)</title><addtitle>Biochemistry Moscow</addtitle><addtitle>Biochemistry (Mosc)</addtitle><description>The overall survival of patients with the advanced and recurrent gastric cancer (GC) remains unfavorable. In particular, this is due to cancer spreading and resistance to chemotherapy associated with the epithelial-mesenchymal transition (EMT) of tumor cells. EMT can be identified by the transcriptome profiling of GC for EMT markers. Indeed, analysis of the TCGA and GTEx databases (
n
= 408) and a cohort of GC patients (
n
= 43) revealed that expression of the
CDH2
gene was significantly decreased in the tumors vs. non-tumor tissues and correlated with the overall survival of GC patients. Expression of the EMT-promoting transcription factors SNAIL and ZEB1 was significantly increased in GC. These data suggest that targeting the EMT might be an attractive therapeutic approach for patients with GC. Previously, we demonstrated a potent anti-cancer activity of the olive leaf extract (OLE). However, its effect on the EMT regulation in GC remained unknown. Here, we showed that OLE efficiently potentiated the inhibitory effect of the chemotherapeutic agents 5-fluorouracil (5-FU) and cisplatin (Cis) on the EMT and their pro-apoptotic activity, as was demonstrated by changes in the expression of the EMT markers (E- and N-cadherins, vimentin, claudin-1) in GC cells treated with the aforementioned chemotherapeutic agents in the presence of OLE. Thus, culturing GC cells with 5-FU + OLE or Cis + OLE attenuated the invasive properties of cancer cells. Importantly, upregulation of expression of the apoptotic markers (PARP cleaved form) and increase in the number of cells undergoing apoptosis (annexin V-positive) were observed for GC cells treated with a combination of OLE and 5-FU or Cis. Collectively, our data illustrate that OLE efficiently interferes with the EMT in GC cells and potentiates the pro-apoptotic activity of certain chemotherapeutic agents used for GC therapy.</description><subject>5-Fluorouracil</subject><subject>Annexin V</subject><subject>Anticancer properties</subject><subject>Antineoplastic drugs</subject><subject>Antitumor activity</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bioorganic Chemistry</subject><subject>Cadherins</subject><subject>Cadherins - metabolism</subject><subject>Cancer therapies</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>Cisplatin - pharmacology</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Fluorouracil - pharmacology</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Herbal medicine</subject><subject>Humans</subject><subject>Invasiveness</subject><subject>Leaves</subject><subject>Life Sciences</subject><subject>Microbiology</subject><subject>Olea - metabolism</subject><subject>Plant extracts</subject><subject>Plant Extracts - pharmacology</subject><subject>Post-transcription</subject><subject>Snail protein</subject><subject>Stomach Neoplasms - drug therapy</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Survival</subject><subject>Survival analysis</subject><subject>Transcription factors</subject><subject>Transcriptomes</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>Vimentin</subject><issn>0006-2979</issn><issn>1608-3040</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</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>GNUQQ</sourceid><recordid>eNp1kU2O1DAQhS0EYpqBA7BBltgMiwz-iztZoqgZkBo1Ug_rqOJUaI-cONgJojkNR-AMnAxnegAJxKqq_L73bLkIecrZJedSvdwzxrQo16VQjKeW3yMrrlmRSabYfbJa5GzRz8ijGG_SKFgpH5IzWSi9zlWxIt-3CB3dfJkCmIl2wfd0Mwc_Igx05-xnpBc7h0BxOQSEH9-2ly_oex-n7DrAEE2w42T9AM4d6X4ex4AxYqTTAelmtKk4Cy57hxEHczj24Oitzy4mCkNL93g7fU2mK4hTsIZWMBgMtELnUpKn1QF7n6ICjMfH5EEHLuKTu3pOPrzeXFdvsu3u6m31apsZKdSUoTCgCszBtAqYBmF4B53KNZfMNA0UrMyblmMJeWqati2lMmvDdMNzU2gmz8nFKXcM_tOMcap7G016EQzo51iLMmXlpRJFQp__hd74OaQvWSihpWBK60TxE2WCjzFgV4_B9hCONWf1ss76n3Umz7O75Lnpsf3t-LW_BIgTEJM0fMTw5-r_p_4EV_OteQ</recordid><startdate>2024</startdate><enddate>2024</enddate><creator>Tekin, Cagla</creator><creator>Ercelik, Melis</creator><creator>Dunaev, Pavel</creator><creator>Galembikova, Aigul</creator><creator>Tezcan, Gulcin</creator><creator>Aksoy, Secil Ak</creator><creator>Budak, Ferah</creator><creator>Isık, Ozgen</creator><creator>Ugras, Nesrin</creator><creator>Boichuk, Sergei</creator><creator>Tunca, Berrin</creator><general>Pleiades Publishing</general><general>Springer Nature B.V</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>7QL</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>2024</creationdate><title>Leaf Extract from European Olive (Olea europaea L.) Post-Transcriptionally Suppresses the Epithelial-Mesenchymal Transition and Sensitizes Gastric Cancer Cells to Chemotherapy</title><author>Tekin, Cagla ; Ercelik, Melis ; Dunaev, Pavel ; Galembikova, Aigul ; Tezcan, Gulcin ; Aksoy, Secil Ak ; Budak, Ferah ; Isık, Ozgen ; Ugras, Nesrin ; Boichuk, Sergei ; Tunca, Berrin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c324t-e2ca48e5acd4a06a2c1faf456130cbba8095bd1e9a595bbdd934c7c06b15c8603</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>5-Fluorouracil</topic><topic>Annexin V</topic><topic>Anticancer properties</topic><topic>Antineoplastic drugs</topic><topic>Antitumor activity</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bioorganic Chemistry</topic><topic>Cadherins</topic><topic>Cadherins - metabolism</topic><topic>Cancer therapies</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Chemotherapy</topic><topic>Cisplatin</topic><topic>Cisplatin - pharmacology</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Fluorouracil - pharmacology</topic><topic>Gastric cancer</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Herbal medicine</topic><topic>Humans</topic><topic>Invasiveness</topic><topic>Leaves</topic><topic>Life Sciences</topic><topic>Microbiology</topic><topic>Olea - metabolism</topic><topic>Plant extracts</topic><topic>Plant Extracts - pharmacology</topic><topic>Post-transcription</topic><topic>Snail protein</topic><topic>Stomach Neoplasms - drug therapy</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Survival</topic><topic>Survival analysis</topic><topic>Transcription factors</topic><topic>Transcriptomes</topic><topic>Tumor cells</topic><topic>Tumors</topic><topic>Vimentin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tekin, Cagla</creatorcontrib><creatorcontrib>Ercelik, Melis</creatorcontrib><creatorcontrib>Dunaev, Pavel</creatorcontrib><creatorcontrib>Galembikova, Aigul</creatorcontrib><creatorcontrib>Tezcan, Gulcin</creatorcontrib><creatorcontrib>Aksoy, Secil Ak</creatorcontrib><creatorcontrib>Budak, Ferah</creatorcontrib><creatorcontrib>Isık, Ozgen</creatorcontrib><creatorcontrib>Ugras, Nesrin</creatorcontrib><creatorcontrib>Boichuk, Sergei</creatorcontrib><creatorcontrib>Tunca, Berrin</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</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 Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science 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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemistry (Moscow)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tekin, Cagla</au><au>Ercelik, Melis</au><au>Dunaev, Pavel</au><au>Galembikova, Aigul</au><au>Tezcan, Gulcin</au><au>Aksoy, Secil Ak</au><au>Budak, Ferah</au><au>Isık, Ozgen</au><au>Ugras, Nesrin</au><au>Boichuk, Sergei</au><au>Tunca, Berrin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leaf Extract from European Olive (Olea europaea L.) Post-Transcriptionally Suppresses the Epithelial-Mesenchymal Transition and Sensitizes Gastric Cancer Cells to Chemotherapy</atitle><jtitle>Biochemistry (Moscow)</jtitle><stitle>Biochemistry Moscow</stitle><addtitle>Biochemistry (Mosc)</addtitle><date>2024</date><risdate>2024</risdate><volume>89</volume><issue>1</issue><spage>97</spage><epage>115</epage><pages>97-115</pages><issn>0006-2979</issn><eissn>1608-3040</eissn><abstract>The overall survival of patients with the advanced and recurrent gastric cancer (GC) remains unfavorable. In particular, this is due to cancer spreading and resistance to chemotherapy associated with the epithelial-mesenchymal transition (EMT) of tumor cells. EMT can be identified by the transcriptome profiling of GC for EMT markers. Indeed, analysis of the TCGA and GTEx databases (
n
= 408) and a cohort of GC patients (
n
= 43) revealed that expression of the
CDH2
gene was significantly decreased in the tumors vs. non-tumor tissues and correlated with the overall survival of GC patients. Expression of the EMT-promoting transcription factors SNAIL and ZEB1 was significantly increased in GC. These data suggest that targeting the EMT might be an attractive therapeutic approach for patients with GC. Previously, we demonstrated a potent anti-cancer activity of the olive leaf extract (OLE). However, its effect on the EMT regulation in GC remained unknown. Here, we showed that OLE efficiently potentiated the inhibitory effect of the chemotherapeutic agents 5-fluorouracil (5-FU) and cisplatin (Cis) on the EMT and their pro-apoptotic activity, as was demonstrated by changes in the expression of the EMT markers (E- and N-cadherins, vimentin, claudin-1) in GC cells treated with the aforementioned chemotherapeutic agents in the presence of OLE. Thus, culturing GC cells with 5-FU + OLE or Cis + OLE attenuated the invasive properties of cancer cells. Importantly, upregulation of expression of the apoptotic markers (PARP cleaved form) and increase in the number of cells undergoing apoptosis (annexin V-positive) were observed for GC cells treated with a combination of OLE and 5-FU or Cis. Collectively, our data illustrate that OLE efficiently interferes with the EMT in GC cells and potentiates the pro-apoptotic activity of certain chemotherapeutic agents used for GC therapy.</abstract><cop>Moscow</cop><pub>Pleiades Publishing</pub><pmid>38467548</pmid><doi>10.1134/S0006297924010061</doi><tpages>19</tpages></addata></record> |
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| subjects | 5-Fluorouracil Annexin V Anticancer properties Antineoplastic drugs Antitumor activity Apoptosis Biochemistry Biomedical and Life Sciences Biomedicine Bioorganic Chemistry Cadherins Cadherins - metabolism Cancer therapies Cell Line, Tumor Cell Movement Chemotherapy Cisplatin Cisplatin - pharmacology Epithelial-Mesenchymal Transition Fluorouracil - pharmacology Gastric cancer Gene expression Gene Expression Regulation, Neoplastic Herbal medicine Humans Invasiveness Leaves Life Sciences Microbiology Olea - metabolism Plant extracts Plant Extracts - pharmacology Post-transcription Snail protein Stomach Neoplasms - drug therapy Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Survival Survival analysis Transcription factors Transcriptomes Tumor cells Tumors Vimentin |
| title | Leaf Extract from European Olive (Olea europaea L.) Post-Transcriptionally Suppresses the Epithelial-Mesenchymal Transition and Sensitizes Gastric Cancer Cells to Chemotherapy |
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