Ganodermanontriol inhibits expression of special AT rich sequence binding protein 1 gene in human hepatocellular carcinoma
Context: The metastasis of liver cancer is a major cause of clinical treatment failure, restrain, and control the cancer metastasis is the major strategy of the treatment and prevention of the disease. Special AT-rich sequence-binding protein 1 (SATB1) gene was overexpressed in many malignant tumors...
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creator | Xu, Chengkai Guo, Hanbin Kong, Danli Pang, Dong Ding, Yuanlin |
description | Context: The metastasis of liver cancer is a major cause of clinical treatment failure, restrain, and control the cancer metastasis is the major strategy of the treatment and prevention of the disease. Special AT-rich sequence-binding protein 1 (SATB1) gene was overexpressed in many malignant tumors and considered as a potential target of anticancer drug. This study investigated the mechanism how ganodermanontriol effect the expression of SATB1 and thus inhibits the growth and metastasis in hepatocellular carcinoma (HCC).
Aims: This study explored mainly on the mechanism how ganodermanontriol affects the expression of SATB1 and inhibits proliferation of tumor on human hepatoma cell line HepG2.
Settings and Design: The cancer cells were treated with ganodermanontriol. The status of the cells was detected by different methods. The mechanism was checked by various methods.
Materials and Methods: In HepG2 cancer cells treated with various concentrations of ganodermanontriol, the cell proliferation of was detected by MTT assay, cell apoptosis was analyzed by flow cytometry; the mRNA of SATB1, Bcl-2, Bax were detected by reverse transcription-polymerase chain reaction (RT-PCR) and the protein level of SATB1, Bcl-2, Bax, and caspase 3 were analyzed by Western blot.
Statistical Analysis Used: Data are presented as the mean ± standard deviation. The data were analyzed using SPSS 18.0 software (SPSS, Inc., Chicago, IL, USA) and GraphPad Prism software (GraphPad Software, Inc., La Jolla, CA, USA). A one-way analysis of variance test was used to compare the differences among groups.
Results: This study showed that ganodermanontriol could significantly reduce the expression level of SATB1.
Conclusion: Therefore, downregulate the cascade effect caused by the expression level of Bcl-2 in HCC HepG2 cells. |
doi_str_mv | 10.4103/0973-1482.203597 |
format | Article |
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Aims: This study explored mainly on the mechanism how ganodermanontriol affects the expression of SATB1 and inhibits proliferation of tumor on human hepatoma cell line HepG2.
Settings and Design: The cancer cells were treated with ganodermanontriol. The status of the cells was detected by different methods. The mechanism was checked by various methods.
Materials and Methods: In HepG2 cancer cells treated with various concentrations of ganodermanontriol, the cell proliferation of was detected by MTT assay, cell apoptosis was analyzed by flow cytometry; the mRNA of SATB1, Bcl-2, Bax were detected by reverse transcription-polymerase chain reaction (RT-PCR) and the protein level of SATB1, Bcl-2, Bax, and caspase 3 were analyzed by Western blot.
Statistical Analysis Used: Data are presented as the mean ± standard deviation. The data were analyzed using SPSS 18.0 software (SPSS, Inc., Chicago, IL, USA) and GraphPad Prism software (GraphPad Software, Inc., La Jolla, CA, USA). A one-way analysis of variance test was used to compare the differences among groups.
Results: This study showed that ganodermanontriol could significantly reduce the expression level of SATB1.
Conclusion: Therefore, downregulate the cascade effect caused by the expression level of Bcl-2 in HCC HepG2 cells.</description><identifier>ISSN: 0973-1482</identifier><identifier>EISSN: 1998-4138</identifier><identifier>DOI: 10.4103/0973-1482.203597</identifier><identifier>PMID: 30539830</identifier><language>eng</language><publisher>India: Wolters Kluwer India Pvt. Ltd</publisher><subject>Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Apoptosis ; Apoptosis - drug effects ; Biotechnology ; Cancer ; Cancer genetics ; Cancer metastasis ; Cancer treatment ; Carcinoma ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - pathology ; Cell growth ; Diagnosis ; Down-Regulation ; Drug Screening Assays, Antitumor ; Gene amplification ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Genes ; Genetic aspects ; Hep G2 Cells ; Hepatocellular carcinoma ; Humans ; Lanosterol - analogs & derivatives ; Lanosterol - pharmacology ; Lanosterol - therapeutic use ; Liver cancer ; Liver Neoplasms - drug therapy ; Liver Neoplasms - pathology ; Matrix Attachment Region Binding Proteins - metabolism ; Metastasis ; Polymerase chain reaction ; Protein binding ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Software ; Studies ; Tumors</subject><ispartof>Journal of cancer research and therapeutics, 2018-12, Vol.14 (12), p.964-968</ispartof><rights>COPYRIGHT 2018 Medknow Publications and Media Pvt. Ltd.</rights><rights>2018. 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-c533m-8cd8ca324a4332014af130e55baf44fc912076fa2ec167baaecba05094b3ca933</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27462,27928,27929</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30539830$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Chengkai</creatorcontrib><creatorcontrib>Guo, Hanbin</creatorcontrib><creatorcontrib>Kong, Danli</creatorcontrib><creatorcontrib>Pang, Dong</creatorcontrib><creatorcontrib>Ding, Yuanlin</creatorcontrib><title>Ganodermanontriol inhibits expression of special AT rich sequence binding protein 1 gene in human hepatocellular carcinoma</title><title>Journal of cancer research and therapeutics</title><addtitle>J Cancer Res Ther</addtitle><description>Context: The metastasis of liver cancer is a major cause of clinical treatment failure, restrain, and control the cancer metastasis is the major strategy of the treatment and prevention of the disease. Special AT-rich sequence-binding protein 1 (SATB1) gene was overexpressed in many malignant tumors and considered as a potential target of anticancer drug. This study investigated the mechanism how ganodermanontriol effect the expression of SATB1 and thus inhibits the growth and metastasis in hepatocellular carcinoma (HCC).
Aims: This study explored mainly on the mechanism how ganodermanontriol affects the expression of SATB1 and inhibits proliferation of tumor on human hepatoma cell line HepG2.
Settings and Design: The cancer cells were treated with ganodermanontriol. The status of the cells was detected by different methods. The mechanism was checked by various methods.
Materials and Methods: In HepG2 cancer cells treated with various concentrations of ganodermanontriol, the cell proliferation of was detected by MTT assay, cell apoptosis was analyzed by flow cytometry; the mRNA of SATB1, Bcl-2, Bax were detected by reverse transcription-polymerase chain reaction (RT-PCR) and the protein level of SATB1, Bcl-2, Bax, and caspase 3 were analyzed by Western blot.
Statistical Analysis Used: Data are presented as the mean ± standard deviation. The data were analyzed using SPSS 18.0 software (SPSS, Inc., Chicago, IL, USA) and GraphPad Prism software (GraphPad Software, Inc., La Jolla, CA, USA). A one-way analysis of variance test was used to compare the differences among groups.
Results: This study showed that ganodermanontriol could significantly reduce the expression level of SATB1.
Conclusion: Therefore, downregulate the cascade effect caused by the expression level of Bcl-2 in HCC HepG2 cells.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biotechnology</subject><subject>Cancer</subject><subject>Cancer genetics</subject><subject>Cancer metastasis</subject><subject>Cancer treatment</subject><subject>Carcinoma</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell growth</subject><subject>Diagnosis</subject><subject>Down-Regulation</subject><subject>Drug Screening Assays, Antitumor</subject><subject>Gene amplification</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Hep G2 Cells</subject><subject>Hepatocellular carcinoma</subject><subject>Humans</subject><subject>Lanosterol - analogs & derivatives</subject><subject>Lanosterol - pharmacology</subject><subject>Lanosterol - therapeutic use</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - pathology</subject><subject>Matrix Attachment Region Binding Proteins - metabolism</subject><subject>Metastasis</subject><subject>Polymerase chain reaction</subject><subject>Protein binding</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Software</subject><subject>Studies</subject><subject>Tumors</subject><issn>0973-1482</issn><issn>1998-4138</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptks1v1DAQxS0EokvhzglZ4pzFn5v4uFS0RarEpZwtx5nsunXsYCfawl-Po20LlVY-jGT_3vOMnxH6SMlaUMK_EFXzioqGrRnhUtWv0Ioq1VSC8uY1Wj0fn6F3Od8RImvGmrfojBPJVcPJCv25MiF2kIZSwpRc9NiFvWvdlDE8jAlydjHg2OM8gnXG4-0tTs7ucYZfMwQLuHWhc2GHxxQncAFTvIMAxQbv52KL9zCaKVrwfvYmYWuSdSEO5j160xuf4cNjPUc_L7_dXlxXNz-uvl9sbyorOR-qxnaNNZwJIzhnhArTU05Aytb0QvRWUUbqTW8YWLqpW2PAtoZIokTLrVGcn6PPR9_SYGk5T_ouzimUKzWj5UWUkFT9o3bGg3ahj1MydnDZ6q3cSMVpzRav6gS1zJuMjwF6V7Zf8OsTfFkdDM6eFJCjwKaYc4Jej8kNJv3WlOglc72EqpdQ9THzIvn0ON_cDtA9C55CLsDXI3CIfoKU7_18gKQLex_i4YVx9Z-xVhuhn74H_wt8lLvc</recordid><startdate>20181201</startdate><enddate>20181201</enddate><creator>Xu, Chengkai</creator><creator>Guo, Hanbin</creator><creator>Kong, Danli</creator><creator>Pang, Dong</creator><creator>Ding, Yuanlin</creator><general>Wolters Kluwer India Pvt. Ltd</general><general>Medknow Publications and Media Pvt. Ltd</general><general>Medknow Publications & Media Pvt. 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pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biotechnology</topic><topic>Cancer</topic><topic>Cancer genetics</topic><topic>Cancer metastasis</topic><topic>Cancer treatment</topic><topic>Carcinoma</topic><topic>Carcinoma, Hepatocellular - drug therapy</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell growth</topic><topic>Diagnosis</topic><topic>Down-Regulation</topic><topic>Drug Screening Assays, Antitumor</topic><topic>Gene amplification</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Hep G2 Cells</topic><topic>Hepatocellular carcinoma</topic><topic>Humans</topic><topic>Lanosterol - analogs & derivatives</topic><topic>Lanosterol - pharmacology</topic><topic>Lanosterol - therapeutic use</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - drug therapy</topic><topic>Liver Neoplasms - pathology</topic><topic>Matrix Attachment Region Binding Proteins - metabolism</topic><topic>Metastasis</topic><topic>Polymerase chain reaction</topic><topic>Protein binding</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Software</topic><topic>Studies</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Chengkai</creatorcontrib><creatorcontrib>Guo, Hanbin</creatorcontrib><creatorcontrib>Kong, Danli</creatorcontrib><creatorcontrib>Pang, Dong</creatorcontrib><creatorcontrib>Ding, Yuanlin</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>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 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 Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Access via ProQuest (Open Access)</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>Xu, Chengkai</au><au>Guo, Hanbin</au><au>Kong, Danli</au><au>Pang, Dong</au><au>Ding, Yuanlin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ganodermanontriol inhibits expression of special AT rich sequence binding protein 1 gene in human hepatocellular carcinoma</atitle><jtitle>Journal of cancer research and therapeutics</jtitle><addtitle>J Cancer Res Ther</addtitle><date>2018-12-01</date><risdate>2018</risdate><volume>14</volume><issue>12</issue><spage>964</spage><epage>968</epage><pages>964-968</pages><issn>0973-1482</issn><eissn>1998-4138</eissn><abstract>Context: The metastasis of liver cancer is a major cause of clinical treatment failure, restrain, and control the cancer metastasis is the major strategy of the treatment and prevention of the disease. Special AT-rich sequence-binding protein 1 (SATB1) gene was overexpressed in many malignant tumors and considered as a potential target of anticancer drug. This study investigated the mechanism how ganodermanontriol effect the expression of SATB1 and thus inhibits the growth and metastasis in hepatocellular carcinoma (HCC).
Aims: This study explored mainly on the mechanism how ganodermanontriol affects the expression of SATB1 and inhibits proliferation of tumor on human hepatoma cell line HepG2.
Settings and Design: The cancer cells were treated with ganodermanontriol. The status of the cells was detected by different methods. The mechanism was checked by various methods.
Materials and Methods: In HepG2 cancer cells treated with various concentrations of ganodermanontriol, the cell proliferation of was detected by MTT assay, cell apoptosis was analyzed by flow cytometry; the mRNA of SATB1, Bcl-2, Bax were detected by reverse transcription-polymerase chain reaction (RT-PCR) and the protein level of SATB1, Bcl-2, Bax, and caspase 3 were analyzed by Western blot.
Statistical Analysis Used: Data are presented as the mean ± standard deviation. The data were analyzed using SPSS 18.0 software (SPSS, Inc., Chicago, IL, USA) and GraphPad Prism software (GraphPad Software, Inc., La Jolla, CA, USA). A one-way analysis of variance test was used to compare the differences among groups.
Results: This study showed that ganodermanontriol could significantly reduce the expression level of SATB1.
Conclusion: Therefore, downregulate the cascade effect caused by the expression level of Bcl-2 in HCC HepG2 cells.</abstract><cop>India</cop><pub>Wolters Kluwer India Pvt. Ltd</pub><pmid>30539830</pmid><doi>10.4103/0973-1482.203597</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Apoptosis Apoptosis - drug effects Biotechnology Cancer Cancer genetics Cancer metastasis Cancer treatment Carcinoma Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - pathology Cell growth Diagnosis Down-Regulation Drug Screening Assays, Antitumor Gene amplification Gene expression Gene Expression Regulation, Neoplastic - drug effects Genes Genetic aspects Hep G2 Cells Hepatocellular carcinoma Humans Lanosterol - analogs & derivatives Lanosterol - pharmacology Lanosterol - therapeutic use Liver cancer Liver Neoplasms - drug therapy Liver Neoplasms - pathology Matrix Attachment Region Binding Proteins - metabolism Metastasis Polymerase chain reaction Protein binding Proteins Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism Software Studies Tumors |
title | Ganodermanontriol inhibits expression of special AT rich sequence binding protein 1 gene in human hepatocellular carcinoma |
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