Anti-tumor Activity of Bufalin by Inhibiting c-MET Mediated MEK/ERK and PI3K/AKT Signaling Pathways in Gallbladder Cancer
Gallbladder cancer is one of the most common malignant tumors in the biliary tract. In recent years, the chemotherapy treatment for gallbladder carcinoma has exhibited obvious characteristics of drug resistance and insensitivity, and one of the main factors is the existence of cancer stem cells. Her...
Gespeichert in:
| Veröffentlicht in: | Journal of Cancer 2020-01, Vol.11 (11), p.3114-3123 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 3123 |
|---|---|
| container_issue | 11 |
| container_start_page | 3114 |
| container_title | Journal of Cancer |
| container_volume | 11 |
| creator | Qian, Liqiang Su, Haoyuan Wang, Gang Li, Bin Shen, Genhai Gao, Quangen |
| description | Gallbladder cancer is one of the most common malignant tumors in the biliary tract. In recent years, the chemotherapy treatment for gallbladder carcinoma has exhibited obvious characteristics of drug resistance and insensitivity, and one of the main factors is the existence of cancer stem cells. Here in this study, the effect of Bufalin on gallbladder cancer (GBC-SD) cells and the related mechanism were studied. The results indicated that Bufalin could inhibit the growth of gallbladder carcinoma both
and
. According to the biological behavior analysis, Bufalin induced apoptosis, inhibited the propagation, migration and invasion of GBC-SD cells, and blocked cell cycle at the G2/M stage. Besides, Bufalin inhibited the tumor sphere formation capability of gallbladder carcinoma in matrigel, reduced the expression of multiple stemness-associated proteins, including Oct4, Sox2 and the stem cell-surface marker proteins CD133 and CD44. Western blot assay showed that Bufalin inhibited MEK/ERK and PI3-K/AKT signaling pathways by inhibiting the expression of p-c-Met, which in turn affected the expression of apoptosis-related protein Mcl-1, and the invasion-associated proteins E-cadherin, MMP9 and Snail. Bufalin was found to have an inhibitory effect on the GBC-SD cell growth and reduce the self-renewal and characteristic of gallbladder cancer stem cells. It enhanced the chemotherapeutic sensitivity and reduced the metastasis of gallbladder carcinoma. In conclusion, Bufalin can be used as a new promising anticancer drug for gallbladder cancer patients who are resistant to traditional chemotherapy. |
| doi_str_mv | 10.7150/jca.38393 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7097950</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2385275557</sourcerecordid><originalsourceid>FETCH-LOGICAL-c469t-2b1de1f38bbb5575c0df0d33b50484c30f2de3bd5e929ba05c410a375987c1b03</originalsourceid><addsrcrecordid>eNpdkU9vEzEQxS0EolXpgS-ALHGBwza2Zx3vXpBCFEqURlQQzpb_beJo42293qL99nXaUhV8GUvzmzdP8xB6T8mFoJxM9kZdQAU1vEKntAJR1NNp-frF_wSd9_2e5Ac1EyW8RSfAGFBBp6donIXkizQcuohnJvk7n0bcNfjr0KjWB6xHvAw7r33yYYtNsV5s8NpZr5KzeL1YTRY_V1gFi6-XsJrMVhv8y2_DcXSLr1Xa_VFjj7POpWpb3SprXcRzFYyL79CbvKJ350_1DP3-ttjMvxdXPy6X89lVYcppnQqmqXW0gUprzbnghtiGWADNSVmVBkjDrANtuatZrRXhpqREgeB1JQzVBM7Ql0fdm0EfnDUupKhaeRP9QcVRdsrLfzvB7-S2u5OC1KLmR4FPTwKxux1cn-TB98a1rQquG3rJoOJM8Gwuox__Q_fdEPM5MpUNQUkEO1KfHykTu76Prnk2Q4k8ZipzpvIh08x-eOn-mfybINwDW7-bLw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2598340727</pqid></control><display><type>article</type><title>Anti-tumor Activity of Bufalin by Inhibiting c-MET Mediated MEK/ERK and PI3K/AKT Signaling Pathways in Gallbladder Cancer</title><source>PubMed Central Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Qian, Liqiang ; Su, Haoyuan ; Wang, Gang ; Li, Bin ; Shen, Genhai ; Gao, Quangen</creator><creatorcontrib>Qian, Liqiang ; Su, Haoyuan ; Wang, Gang ; Li, Bin ; Shen, Genhai ; Gao, Quangen</creatorcontrib><description>Gallbladder cancer is one of the most common malignant tumors in the biliary tract. In recent years, the chemotherapy treatment for gallbladder carcinoma has exhibited obvious characteristics of drug resistance and insensitivity, and one of the main factors is the existence of cancer stem cells. Here in this study, the effect of Bufalin on gallbladder cancer (GBC-SD) cells and the related mechanism were studied. The results indicated that Bufalin could inhibit the growth of gallbladder carcinoma both
and
. According to the biological behavior analysis, Bufalin induced apoptosis, inhibited the propagation, migration and invasion of GBC-SD cells, and blocked cell cycle at the G2/M stage. Besides, Bufalin inhibited the tumor sphere formation capability of gallbladder carcinoma in matrigel, reduced the expression of multiple stemness-associated proteins, including Oct4, Sox2 and the stem cell-surface marker proteins CD133 and CD44. Western blot assay showed that Bufalin inhibited MEK/ERK and PI3-K/AKT signaling pathways by inhibiting the expression of p-c-Met, which in turn affected the expression of apoptosis-related protein Mcl-1, and the invasion-associated proteins E-cadherin, MMP9 and Snail. Bufalin was found to have an inhibitory effect on the GBC-SD cell growth and reduce the self-renewal and characteristic of gallbladder cancer stem cells. It enhanced the chemotherapeutic sensitivity and reduced the metastasis of gallbladder carcinoma. In conclusion, Bufalin can be used as a new promising anticancer drug for gallbladder cancer patients who are resistant to traditional chemotherapy.</description><identifier>ISSN: 1837-9664</identifier><identifier>EISSN: 1837-9664</identifier><identifier>DOI: 10.7150/jca.38393</identifier><identifier>PMID: 32231716</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Antibodies ; Apoptosis ; Biotechnology ; Bone cancer ; Cancer therapies ; Cell cycle ; Cell growth ; Chemotherapy ; Drugs ; Gallbladder ; Gallbladder cancer ; Medical prognosis ; Metastasis ; Pancreatic cancer ; Research Paper ; Stem cells</subject><ispartof>Journal of Cancer, 2020-01, Vol.11 (11), p.3114-3123</ispartof><rights>The author(s).</rights><rights>2020. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-2b1de1f38bbb5575c0df0d33b50484c30f2de3bd5e929ba05c410a375987c1b03</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7097950/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7097950/$$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/32231716$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qian, Liqiang</creatorcontrib><creatorcontrib>Su, Haoyuan</creatorcontrib><creatorcontrib>Wang, Gang</creatorcontrib><creatorcontrib>Li, Bin</creatorcontrib><creatorcontrib>Shen, Genhai</creatorcontrib><creatorcontrib>Gao, Quangen</creatorcontrib><title>Anti-tumor Activity of Bufalin by Inhibiting c-MET Mediated MEK/ERK and PI3K/AKT Signaling Pathways in Gallbladder Cancer</title><title>Journal of Cancer</title><addtitle>J Cancer</addtitle><description>Gallbladder cancer is one of the most common malignant tumors in the biliary tract. In recent years, the chemotherapy treatment for gallbladder carcinoma has exhibited obvious characteristics of drug resistance and insensitivity, and one of the main factors is the existence of cancer stem cells. Here in this study, the effect of Bufalin on gallbladder cancer (GBC-SD) cells and the related mechanism were studied. The results indicated that Bufalin could inhibit the growth of gallbladder carcinoma both
and
. According to the biological behavior analysis, Bufalin induced apoptosis, inhibited the propagation, migration and invasion of GBC-SD cells, and blocked cell cycle at the G2/M stage. Besides, Bufalin inhibited the tumor sphere formation capability of gallbladder carcinoma in matrigel, reduced the expression of multiple stemness-associated proteins, including Oct4, Sox2 and the stem cell-surface marker proteins CD133 and CD44. Western blot assay showed that Bufalin inhibited MEK/ERK and PI3-K/AKT signaling pathways by inhibiting the expression of p-c-Met, which in turn affected the expression of apoptosis-related protein Mcl-1, and the invasion-associated proteins E-cadherin, MMP9 and Snail. Bufalin was found to have an inhibitory effect on the GBC-SD cell growth and reduce the self-renewal and characteristic of gallbladder cancer stem cells. It enhanced the chemotherapeutic sensitivity and reduced the metastasis of gallbladder carcinoma. In conclusion, Bufalin can be used as a new promising anticancer drug for gallbladder cancer patients who are resistant to traditional chemotherapy.</description><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Biotechnology</subject><subject>Bone cancer</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Chemotherapy</subject><subject>Drugs</subject><subject>Gallbladder</subject><subject>Gallbladder cancer</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Pancreatic cancer</subject><subject>Research Paper</subject><subject>Stem cells</subject><issn>1837-9664</issn><issn>1837-9664</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNpdkU9vEzEQxS0EolXpgS-ALHGBwza2Zx3vXpBCFEqURlQQzpb_beJo42293qL99nXaUhV8GUvzmzdP8xB6T8mFoJxM9kZdQAU1vEKntAJR1NNp-frF_wSd9_2e5Ac1EyW8RSfAGFBBp6donIXkizQcuohnJvk7n0bcNfjr0KjWB6xHvAw7r33yYYtNsV5s8NpZr5KzeL1YTRY_V1gFi6-XsJrMVhv8y2_DcXSLr1Xa_VFjj7POpWpb3SprXcRzFYyL79CbvKJ350_1DP3-ttjMvxdXPy6X89lVYcppnQqmqXW0gUprzbnghtiGWADNSVmVBkjDrANtuatZrRXhpqREgeB1JQzVBM7Ql0fdm0EfnDUupKhaeRP9QcVRdsrLfzvB7-S2u5OC1KLmR4FPTwKxux1cn-TB98a1rQquG3rJoOJM8Gwuox__Q_fdEPM5MpUNQUkEO1KfHykTu76Prnk2Q4k8ZipzpvIh08x-eOn-mfybINwDW7-bLw</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Qian, Liqiang</creator><creator>Su, Haoyuan</creator><creator>Wang, Gang</creator><creator>Li, Bin</creator><creator>Shen, Genhai</creator><creator>Gao, Quangen</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</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>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200101</creationdate><title>Anti-tumor Activity of Bufalin by Inhibiting c-MET Mediated MEK/ERK and PI3K/AKT Signaling Pathways in Gallbladder Cancer</title><author>Qian, Liqiang ; Su, Haoyuan ; Wang, Gang ; Li, Bin ; Shen, Genhai ; Gao, Quangen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-2b1de1f38bbb5575c0df0d33b50484c30f2de3bd5e929ba05c410a375987c1b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Biotechnology</topic><topic>Bone cancer</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Chemotherapy</topic><topic>Drugs</topic><topic>Gallbladder</topic><topic>Gallbladder cancer</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Pancreatic cancer</topic><topic>Research Paper</topic><topic>Stem cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qian, Liqiang</creatorcontrib><creatorcontrib>Su, Haoyuan</creatorcontrib><creatorcontrib>Wang, Gang</creatorcontrib><creatorcontrib>Li, Bin</creatorcontrib><creatorcontrib>Shen, Genhai</creatorcontrib><creatorcontrib>Gao, Quangen</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>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><jtitle>Journal of Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qian, Liqiang</au><au>Su, Haoyuan</au><au>Wang, Gang</au><au>Li, Bin</au><au>Shen, Genhai</au><au>Gao, Quangen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anti-tumor Activity of Bufalin by Inhibiting c-MET Mediated MEK/ERK and PI3K/AKT Signaling Pathways in Gallbladder Cancer</atitle><jtitle>Journal of Cancer</jtitle><addtitle>J Cancer</addtitle><date>2020-01-01</date><risdate>2020</risdate><volume>11</volume><issue>11</issue><spage>3114</spage><epage>3123</epage><pages>3114-3123</pages><issn>1837-9664</issn><eissn>1837-9664</eissn><abstract>Gallbladder cancer is one of the most common malignant tumors in the biliary tract. In recent years, the chemotherapy treatment for gallbladder carcinoma has exhibited obvious characteristics of drug resistance and insensitivity, and one of the main factors is the existence of cancer stem cells. Here in this study, the effect of Bufalin on gallbladder cancer (GBC-SD) cells and the related mechanism were studied. The results indicated that Bufalin could inhibit the growth of gallbladder carcinoma both
and
. According to the biological behavior analysis, Bufalin induced apoptosis, inhibited the propagation, migration and invasion of GBC-SD cells, and blocked cell cycle at the G2/M stage. Besides, Bufalin inhibited the tumor sphere formation capability of gallbladder carcinoma in matrigel, reduced the expression of multiple stemness-associated proteins, including Oct4, Sox2 and the stem cell-surface marker proteins CD133 and CD44. Western blot assay showed that Bufalin inhibited MEK/ERK and PI3-K/AKT signaling pathways by inhibiting the expression of p-c-Met, which in turn affected the expression of apoptosis-related protein Mcl-1, and the invasion-associated proteins E-cadherin, MMP9 and Snail. Bufalin was found to have an inhibitory effect on the GBC-SD cell growth and reduce the self-renewal and characteristic of gallbladder cancer stem cells. It enhanced the chemotherapeutic sensitivity and reduced the metastasis of gallbladder carcinoma. In conclusion, Bufalin can be used as a new promising anticancer drug for gallbladder cancer patients who are resistant to traditional chemotherapy.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>32231716</pmid><doi>10.7150/jca.38393</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1837-9664 |
| ispartof | Journal of Cancer, 2020-01, Vol.11 (11), p.3114-3123 |
| issn | 1837-9664 1837-9664 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7097950 |
| source | PubMed Central Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Antibodies Apoptosis Biotechnology Bone cancer Cancer therapies Cell cycle Cell growth Chemotherapy Drugs Gallbladder Gallbladder cancer Medical prognosis Metastasis Pancreatic cancer Research Paper Stem cells |
| title | Anti-tumor Activity of Bufalin by Inhibiting c-MET Mediated MEK/ERK and PI3K/AKT Signaling Pathways in Gallbladder Cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-27T07%3A42%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Anti-tumor%20Activity%20of%20Bufalin%20by%20Inhibiting%20c-MET%20Mediated%20MEK/ERK%20and%20PI3K/AKT%20Signaling%20Pathways%20in%20Gallbladder%20Cancer&rft.jtitle=Journal%20of%20Cancer&rft.au=Qian,%20Liqiang&rft.date=2020-01-01&rft.volume=11&rft.issue=11&rft.spage=3114&rft.epage=3123&rft.pages=3114-3123&rft.issn=1837-9664&rft.eissn=1837-9664&rft_id=info:doi/10.7150/jca.38393&rft_dat=%3Cproquest_pubme%3E2385275557%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2598340727&rft_id=info:pmid/32231716&rfr_iscdi=true |