Rapamycin may inhibit murine S180 sarcoma growth by regulating the pathways associated with autophagy and cancer stem cells
Objective: The objective of this study was to investigate the molecular mechanisms involved in rapamycin-induced inhibition of tumor growth. Materials and Methods: Murine S180 sarcoma cells were subcutaneously injected into mice, and the tumor-bearing mice were randomly divided into three groups (ve...
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| Veröffentlicht in: | Journal of cancer research and therapeutics 2019-04, Vol.15 (2), p.398-403 |
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| description | Objective: The objective of this study was to investigate the molecular mechanisms involved in rapamycin-induced inhibition of tumor growth.
Materials and Methods: Murine S180 sarcoma cells were subcutaneously injected into mice, and the tumor-bearing mice were randomly divided into three groups (vehicle control, 2 mg/kg rapamycin, and 4 mg/kg rapamycin). The effect of rapamycin on tumor growth was determined by measuring tumor volume. Mammalian target of rapamycin (mTOR), Beclin1, ULK1, LC3, Notch1, CD133, and CD90 expressions was confirmed using confocal microscopy and Western blotting.
Results: The tumor growth inhibition rates induced by high-dose and low-dose rapamycin were 48.8% and 30.1%, respectively. Beclin1 and ULK1 expressions and the LC3-II/LC3-I ratio in tumor tissues were altered by rapamycin, whereas mTOR, Notch1, CD133, and CD90 expressions were significantly inhibited by rapamycin in immunofluorescence assays. Western blotting also showed similar results.
Conclusion: Tumor growth delay induced by rapamycin may be associated with the suppression of the cancer stem cell phenotype (Notch1, CD133, and CD90) and promotion of autophagy (mTOR, Beclin1, ULK1, and LC3-II/LC3-I ratio) in the murine S180 sarcoma model. |
| doi_str_mv | 10.4103/jcrt.JCRT_639_18 |
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Materials and Methods: Murine S180 sarcoma cells were subcutaneously injected into mice, and the tumor-bearing mice were randomly divided into three groups (vehicle control, 2 mg/kg rapamycin, and 4 mg/kg rapamycin). The effect of rapamycin on tumor growth was determined by measuring tumor volume. Mammalian target of rapamycin (mTOR), Beclin1, ULK1, LC3, Notch1, CD133, and CD90 expressions was confirmed using confocal microscopy and Western blotting.
Results: The tumor growth inhibition rates induced by high-dose and low-dose rapamycin were 48.8% and 30.1%, respectively. Beclin1 and ULK1 expressions and the LC3-II/LC3-I ratio in tumor tissues were altered by rapamycin, whereas mTOR, Notch1, CD133, and CD90 expressions were significantly inhibited by rapamycin in immunofluorescence assays. Western blotting also showed similar results.
Conclusion: Tumor growth delay induced by rapamycin may be associated with the suppression of the cancer stem cell phenotype (Notch1, CD133, and CD90) and promotion of autophagy (mTOR, Beclin1, ULK1, and LC3-II/LC3-I ratio) in the murine S180 sarcoma model.</description><identifier>ISSN: 0973-1482</identifier><identifier>EISSN: 1998-4138</identifier><identifier>DOI: 10.4103/jcrt.JCRT_639_18</identifier><identifier>PMID: 30964118</identifier><language>eng</language><publisher>India: Wolters Kluwer India Pvt. Ltd</publisher><subject>Animals ; Apoptosis ; Autophagy ; Autophagy - drug effects ; Biomarkers ; Cancer therapies ; Cell culture ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Chemotherapy ; Dosage and administration ; Dose-Response Relationship, Drug ; Drug dosages ; Genotype & phenotype ; Health aspects ; Immunoglobulins ; Immunophenotyping ; Laboratory animals ; Male ; Medical research ; Mice ; Neoplastic Stem Cells - drug effects ; Neoplastic Stem Cells - metabolism ; Penicillin ; Proteins ; Rapamycin ; Rats as laboratory animals ; Sarcoma ; Sarcoma - metabolism ; Signal Transduction - drug effects ; Sirolimus - pharmacology ; Stem cells ; Transforming growth factors ; Tumors</subject><ispartof>Journal of cancer research and therapeutics, 2019-04, Vol.15 (2), p.398-403</ispartof><rights>COPYRIGHT 2019 Medknow Publications and Media Pvt. Ltd.</rights><rights>2019. This work is published under https://creativecommons.org/licenses/by-nc-sa/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463i-8a527faba6015d706c4db26eaa4f19a5c3c629c0a7c1b0a8f68eeec90f87b1e73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27435,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30964118$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Hubo</creatorcontrib><creatorcontrib>Zhang, Lulu</creatorcontrib><creatorcontrib>Zhang, Chengke</creatorcontrib><creatorcontrib>Hao, Yingtao</creatorcontrib><creatorcontrib>Zhao, Xiaogang</creatorcontrib><title>Rapamycin may inhibit murine S180 sarcoma growth by regulating the pathways associated with autophagy and cancer stem cells</title><title>Journal of cancer research and therapeutics</title><addtitle>J Cancer Res Ther</addtitle><description>Objective: The objective of this study was to investigate the molecular mechanisms involved in rapamycin-induced inhibition of tumor growth.
Materials and Methods: Murine S180 sarcoma cells were subcutaneously injected into mice, and the tumor-bearing mice were randomly divided into three groups (vehicle control, 2 mg/kg rapamycin, and 4 mg/kg rapamycin). The effect of rapamycin on tumor growth was determined by measuring tumor volume. Mammalian target of rapamycin (mTOR), Beclin1, ULK1, LC3, Notch1, CD133, and CD90 expressions was confirmed using confocal microscopy and Western blotting.
Results: The tumor growth inhibition rates induced by high-dose and low-dose rapamycin were 48.8% and 30.1%, respectively. Beclin1 and ULK1 expressions and the LC3-II/LC3-I ratio in tumor tissues were altered by rapamycin, whereas mTOR, Notch1, CD133, and CD90 expressions were significantly inhibited by rapamycin in immunofluorescence assays. Western blotting also showed similar results.
Conclusion: Tumor growth delay induced by rapamycin may be associated with the suppression of the cancer stem cell phenotype (Notch1, CD133, and CD90) and promotion of autophagy (mTOR, Beclin1, ULK1, and LC3-II/LC3-I ratio) in the murine S180 sarcoma model.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Biomarkers</subject><subject>Cancer therapies</subject><subject>Cell culture</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemotherapy</subject><subject>Dosage and administration</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug dosages</subject><subject>Genotype & phenotype</subject><subject>Health aspects</subject><subject>Immunoglobulins</subject><subject>Immunophenotyping</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Medical research</subject><subject>Mice</subject><subject>Neoplastic Stem Cells - drug effects</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Penicillin</subject><subject>Proteins</subject><subject>Rapamycin</subject><subject>Rats as laboratory animals</subject><subject>Sarcoma</subject><subject>Sarcoma - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Sirolimus - pharmacology</subject><subject>Stem cells</subject><subject>Transforming growth factors</subject><subject>Tumors</subject><issn>0973-1482</issn><issn>1998-4138</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp10s2L1DAYBvAiiju7evckAc8dk6YfyXEdVldZENb1HN6mbzuZbZOapJTiP2-X2fUDRnIIhN_zhvAkSd4wus0Z5e8P2sftl93tnSq5VEw8SzZMSpHmjIvnyYbKiqcsF9lZch7CgdKiyjLxMjnjVJY5Y2KT_LyFEYZFG0sGWIixe1ObSIbJG4vkGxOUBPDaDUA67-a4J_VCPHZTD9HYjsQ9khHifoYlEAjBaQMRGzKblcIU3biHbiFgG6LBavQkRByIxr4Pr5IXLfQBXz_uF8n3j1d3u-v05uunz7vLm1TnJTepgCKrWqihpKxoKlrqvKmzEgHylkkoNNdlJjWFSrOagmhLgYha0lZUNcOKXyTvjnNH735MGKI6uMnb9UqVZTRjtMwp_6M66FEZ27roQQ8maHVZCColLQu2qvSE6tCih95ZbM16_I_fnvDranAw-mSAHgPauxA8tmr0ZgC_KEbVQ-nqoXT1V-lr5O3j-6Z6wOZ34KnlFXw4gtn1EX2476cZvVrtvXXzfwcrLoV6-h_8F4wawOk</recordid><startdate>20190401</startdate><enddate>20190401</enddate><creator>Shi, Hubo</creator><creator>Zhang, Lulu</creator><creator>Zhang, Chengke</creator><creator>Hao, Yingtao</creator><creator>Zhao, Xiaogang</creator><general>Wolters Kluwer India Pvt. 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drug effects</topic><topic>Biomarkers</topic><topic>Cancer therapies</topic><topic>Cell culture</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Chemotherapy</topic><topic>Dosage and administration</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug dosages</topic><topic>Genotype & phenotype</topic><topic>Health aspects</topic><topic>Immunoglobulins</topic><topic>Immunophenotyping</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Medical research</topic><topic>Mice</topic><topic>Neoplastic Stem Cells - drug effects</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Penicillin</topic><topic>Proteins</topic><topic>Rapamycin</topic><topic>Rats as laboratory animals</topic><topic>Sarcoma</topic><topic>Sarcoma - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Sirolimus - pharmacology</topic><topic>Stem cells</topic><topic>Transforming growth factors</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Hubo</creatorcontrib><creatorcontrib>Zhang, Lulu</creatorcontrib><creatorcontrib>Zhang, Chengke</creatorcontrib><creatorcontrib>Hao, Yingtao</creatorcontrib><creatorcontrib>Zhao, Xiaogang</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>ProQuest 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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</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</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest research library</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><jtitle>Journal of cancer research and therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, Hubo</au><au>Zhang, Lulu</au><au>Zhang, Chengke</au><au>Hao, Yingtao</au><au>Zhao, Xiaogang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rapamycin may inhibit murine S180 sarcoma growth by regulating the pathways associated with autophagy and cancer stem cells</atitle><jtitle>Journal of cancer research and therapeutics</jtitle><addtitle>J Cancer Res Ther</addtitle><date>2019-04-01</date><risdate>2019</risdate><volume>15</volume><issue>2</issue><spage>398</spage><epage>403</epage><pages>398-403</pages><issn>0973-1482</issn><eissn>1998-4138</eissn><abstract>Objective: The objective of this study was to investigate the molecular mechanisms involved in rapamycin-induced inhibition of tumor growth.
Materials and Methods: Murine S180 sarcoma cells were subcutaneously injected into mice, and the tumor-bearing mice were randomly divided into three groups (vehicle control, 2 mg/kg rapamycin, and 4 mg/kg rapamycin). The effect of rapamycin on tumor growth was determined by measuring tumor volume. Mammalian target of rapamycin (mTOR), Beclin1, ULK1, LC3, Notch1, CD133, and CD90 expressions was confirmed using confocal microscopy and Western blotting.
Results: The tumor growth inhibition rates induced by high-dose and low-dose rapamycin were 48.8% and 30.1%, respectively. Beclin1 and ULK1 expressions and the LC3-II/LC3-I ratio in tumor tissues were altered by rapamycin, whereas mTOR, Notch1, CD133, and CD90 expressions were significantly inhibited by rapamycin in immunofluorescence assays. Western blotting also showed similar results.
Conclusion: Tumor growth delay induced by rapamycin may be associated with the suppression of the cancer stem cell phenotype (Notch1, CD133, and CD90) and promotion of autophagy (mTOR, Beclin1, ULK1, and LC3-II/LC3-I ratio) in the murine S180 sarcoma model.</abstract><cop>India</cop><pub>Wolters Kluwer India Pvt. Ltd</pub><pmid>30964118</pmid><doi>10.4103/jcrt.JCRT_639_18</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Autophagy Autophagy - drug effects Biomarkers Cancer therapies Cell culture Cell growth Cell Line, Tumor Cell Proliferation - drug effects Chemotherapy Dosage and administration Dose-Response Relationship, Drug Drug dosages Genotype & phenotype Health aspects Immunoglobulins Immunophenotyping Laboratory animals Male Medical research Mice Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - metabolism Penicillin Proteins Rapamycin Rats as laboratory animals Sarcoma Sarcoma - metabolism Signal Transduction - drug effects Sirolimus - pharmacology Stem cells Transforming growth factors Tumors |
| title | Rapamycin may inhibit murine S180 sarcoma growth by regulating the pathways associated with autophagy and cancer stem cells |
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