Chemosensitivity to doxorubicin in primary cells derived from tumor of FVB/N-Trp53tm1Hw1 with TALEN-mediated Trp53 mutant gene

BACKGROUNDTo evaluate the chemosensitivity to doxorubicin (DOX) in two primary cells derived from a tumor of FVB/N-Trp53tm1Hw1 knockout (KO) mice with TALEN-mediated Trp53 mutant gene, we evaluated the cell survivability, cell cycle distribution, apoptotic cell numbers and apoptotic protein expressi...

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Published in:Laboratory animal research 2023, 39(4), , pp.287-297
Main Authors: Yun, Woobin, Kim, Ji Eun, Jin, You Jeong, Roh, Yu Jeong, Song, Hee Jin, Seol, Ayun, Kim, Tae Ryeol, Min, Kyeong Seon, Park, Eun Seo, Park, Gi Ho, Kang, Hyun Gu, Choi, Yeon Shik, Hwang, Dae Youn
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Language:English
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Ascetic tumor
Chemosensitivity
Doxorubicin
G2 arrest
Solid tumor
Trp53
수의학
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container_title Laboratory animal research
container_volume 39
creator Yun, Woobin
Kim, Ji Eun
Jin, You Jeong
Roh, Yu Jeong
Song, Hee Jin
Seol, Ayun
Kim, Tae Ryeol
Min, Kyeong Seon
Park, Eun Seo
Park, Gi Ho
Kang, Hyun Gu
Choi, Yeon Shik
Hwang, Dae Youn
description BACKGROUNDTo evaluate the chemosensitivity to doxorubicin (DOX) in two primary cells derived from a tumor of FVB/N-Trp53tm1Hw1 knockout (KO) mice with TALEN-mediated Trp53 mutant gene, we evaluated the cell survivability, cell cycle distribution, apoptotic cell numbers and apoptotic protein expression in solid tumor cells and ascetic tumor cells treated with DOX.RESULTSThe primary tumor cells showed a significant (P 
doi_str_mv 10.1186/s42826-023-00175-2
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The IC50 level to DOX was lower in both primary cells (IC50 = 0.12 μM and 0.20 μM) as compared to the CT26 cells (IC50 = 0.32 μM), although the solid tumor was more sensitive. Also, the number of cells arrested at the G0/G1 stage was significantly decreased (24.7-23.1% in primary tumor cells treated with DOX, P &lt; 0.05) while arrest at the G2 stage was enhanced to 296.8-254.3% in DOX-treated primary tumor cells compared with DOX-treated CT26 cells. Furthermore, apoptotic cells of early and late stage were greatly increased in the two primary cell-lines treated with DOX when compared to same conditions for CT26 cells. However, the Bax/Bcl-2 expression level was maintained constant in the primary tumor and CT26 cells.CONCLUSIONSTo the best of our knowledge, these results are the first to successfully detect an alteration in chemosensitivity to DOX in solid tumor cells and ascetic tumor cells derived from tumor of FVB/N-Trp53tm1Hw1 mice TALEN-mediated Trp53 mutant gene.</description><identifier>ISSN: 2233-7660</identifier><identifier>ISSN: 1738-6055</identifier><identifier>EISSN: 2233-7660</identifier><identifier>DOI: 10.1186/s42826-023-00175-2</identifier><identifier>PMID: 37864254</identifier><language>eng</language><publisher>London: BioMed Central</publisher><subject>Ascetic tumor ; Chemosensitivity ; Doxorubicin ; G2 arrest ; Solid tumor ; Trp53 ; 수의학</subject><ispartof>Laboratory Animal Research, 2023, 39(4), , pp.287-297</ispartof><rights>Korean Association for Laboratory Animal Science 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c411t-4a0c1831ec61e03fb3794926e5c3fc49dcbf1453423731a83c853c6849326f433</citedby><cites>FETCH-LOGICAL-c411t-4a0c1831ec61e03fb3794926e5c3fc49dcbf1453423731a83c853c6849326f433</cites><orcidid>0000-0002-5144-1725</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10588074/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10588074/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,37013,53791,53793</link.rule.ids><backlink>$$Uhttps://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART003039313$$DAccess content in National Research Foundation of Korea (NRF)$$Hfree_for_read</backlink></links><search><creatorcontrib>Yun, Woobin</creatorcontrib><creatorcontrib>Kim, Ji Eun</creatorcontrib><creatorcontrib>Jin, You Jeong</creatorcontrib><creatorcontrib>Roh, Yu Jeong</creatorcontrib><creatorcontrib>Song, Hee Jin</creatorcontrib><creatorcontrib>Seol, Ayun</creatorcontrib><creatorcontrib>Kim, Tae Ryeol</creatorcontrib><creatorcontrib>Min, Kyeong Seon</creatorcontrib><creatorcontrib>Park, Eun Seo</creatorcontrib><creatorcontrib>Park, Gi Ho</creatorcontrib><creatorcontrib>Kang, Hyun Gu</creatorcontrib><creatorcontrib>Choi, Yeon Shik</creatorcontrib><creatorcontrib>Hwang, Dae Youn</creatorcontrib><title>Chemosensitivity to doxorubicin in primary cells derived from tumor of FVB/N-Trp53tm1Hw1 with TALEN-mediated Trp53 mutant gene</title><title>Laboratory animal research</title><description>BACKGROUNDTo evaluate the chemosensitivity to doxorubicin (DOX) in two primary cells derived from a tumor of FVB/N-Trp53tm1Hw1 knockout (KO) mice with TALEN-mediated Trp53 mutant gene, we evaluated the cell survivability, cell cycle distribution, apoptotic cell numbers and apoptotic protein expression in solid tumor cells and ascetic tumor cells treated with DOX.RESULTSThe primary tumor cells showed a significant (P &lt; 0.05) defect for UV-induced upregulation of the Trp53 protein, and consisted of different ratios of leukocytes, fibroblasts, epithelial cells and mesenchymal cells. The IC50 level to DOX was lower in both primary cells (IC50 = 0.12 μM and 0.20 μM) as compared to the CT26 cells (IC50 = 0.32 μM), although the solid tumor was more sensitive. Also, the number of cells arrested at the G0/G1 stage was significantly decreased (24.7-23.1% in primary tumor cells treated with DOX, P &lt; 0.05) while arrest at the G2 stage was enhanced to 296.8-254.3% in DOX-treated primary tumor cells compared with DOX-treated CT26 cells. Furthermore, apoptotic cells of early and late stage were greatly increased in the two primary cell-lines treated with DOX when compared to same conditions for CT26 cells. However, the Bax/Bcl-2 expression level was maintained constant in the primary tumor and CT26 cells.CONCLUSIONSTo the best of our knowledge, these results are the first to successfully detect an alteration in chemosensitivity to DOX in solid tumor cells and ascetic tumor cells derived from tumor of FVB/N-Trp53tm1Hw1 mice TALEN-mediated Trp53 mutant gene.</description><subject>Ascetic tumor</subject><subject>Chemosensitivity</subject><subject>Doxorubicin</subject><subject>G2 arrest</subject><subject>Solid tumor</subject><subject>Trp53</subject><subject>수의학</subject><issn>2233-7660</issn><issn>1738-6055</issn><issn>2233-7660</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVkl1rHCEUhofS0oQ0f6BXXpbCNOpRZ-aqbJd8LCwplG1vxXF012Rm3KqzaW7y2-t-UBoRjnje83jUtyg-EvyFkFpcRUZrKkpMocSYVLykb4pzSgHKSgj89r_1WXEZ4wPOg-MKGH5fnEFVC0Y5Oy9e5hsz-GjG6JLbufSMkked_-PD1DrtRpTnNrhBhWekTd9H1JngdqZDNvgBpWnwAXmLbn59u7ovV2HLIQ3k7omgJ5c2aDVbXt-Xg-mcSrnmkEfDlNSY0NqM5kPxzqo-mstTvCh-3lyv5nfl8vvtYj5blpoRkkqmsCY1EKMFMRhsC1XDGioM12A1azrdWsI4MAoVEFWDrjloUbMGqLAM4KL4fOSOwcpH7aRX7hDXXj4GOfuxWkiCgdOmolm8OIo7rx7k6faHisOGD2upQnK6N7IFBrg2imkjmO14w4Slhllb8YorYTLr65G1ndr8DNqMKaj-FfR1ZnSb3NQud8PrGlcsEz6dCMH_nkxMcnBx_xVqNH6KkmYZwZTBvnF6lOrgYwzG_juHYLl3jTy6RmbXyINrJIW_n1uyZA</recordid><startdate>20231020</startdate><enddate>20231020</enddate><creator>Yun, Woobin</creator><creator>Kim, Ji Eun</creator><creator>Jin, You Jeong</creator><creator>Roh, Yu Jeong</creator><creator>Song, Hee Jin</creator><creator>Seol, Ayun</creator><creator>Kim, Tae Ryeol</creator><creator>Min, Kyeong Seon</creator><creator>Park, Eun Seo</creator><creator>Park, Gi Ho</creator><creator>Kang, Hyun Gu</creator><creator>Choi, Yeon Shik</creator><creator>Hwang, Dae Youn</creator><general>BioMed Central</general><general>BMC</general><general>한국실험동물학회</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><scope>ACYCR</scope><orcidid>https://orcid.org/0000-0002-5144-1725</orcidid></search><sort><creationdate>20231020</creationdate><title>Chemosensitivity to doxorubicin in primary cells derived from tumor of FVB/N-Trp53tm1Hw1 with TALEN-mediated Trp53 mutant gene</title><author>Yun, Woobin ; Kim, Ji Eun ; Jin, You Jeong ; Roh, Yu Jeong ; Song, Hee Jin ; Seol, Ayun ; Kim, Tae Ryeol ; Min, Kyeong Seon ; Park, Eun Seo ; Park, Gi Ho ; Kang, Hyun Gu ; Choi, Yeon Shik ; Hwang, Dae Youn</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c411t-4a0c1831ec61e03fb3794926e5c3fc49dcbf1453423731a83c853c6849326f433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Ascetic tumor</topic><topic>Chemosensitivity</topic><topic>Doxorubicin</topic><topic>G2 arrest</topic><topic>Solid tumor</topic><topic>Trp53</topic><topic>수의학</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yun, Woobin</creatorcontrib><creatorcontrib>Kim, Ji Eun</creatorcontrib><creatorcontrib>Jin, You Jeong</creatorcontrib><creatorcontrib>Roh, Yu Jeong</creatorcontrib><creatorcontrib>Song, Hee Jin</creatorcontrib><creatorcontrib>Seol, Ayun</creatorcontrib><creatorcontrib>Kim, Tae Ryeol</creatorcontrib><creatorcontrib>Min, Kyeong Seon</creatorcontrib><creatorcontrib>Park, Eun Seo</creatorcontrib><creatorcontrib>Park, Gi Ho</creatorcontrib><creatorcontrib>Kang, Hyun Gu</creatorcontrib><creatorcontrib>Choi, Yeon Shik</creatorcontrib><creatorcontrib>Hwang, Dae Youn</creatorcontrib><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><collection>Korean Citation Index</collection><jtitle>Laboratory animal research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yun, Woobin</au><au>Kim, Ji Eun</au><au>Jin, You Jeong</au><au>Roh, Yu Jeong</au><au>Song, Hee Jin</au><au>Seol, Ayun</au><au>Kim, Tae Ryeol</au><au>Min, Kyeong Seon</au><au>Park, Eun Seo</au><au>Park, Gi Ho</au><au>Kang, Hyun Gu</au><au>Choi, Yeon Shik</au><au>Hwang, Dae Youn</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chemosensitivity to doxorubicin in primary cells derived from tumor of FVB/N-Trp53tm1Hw1 with TALEN-mediated Trp53 mutant gene</atitle><jtitle>Laboratory animal research</jtitle><date>2023-10-20</date><risdate>2023</risdate><volume>39</volume><issue>1</issue><spage>23</spage><epage>23</epage><pages>23-23</pages><artnum>23</artnum><issn>2233-7660</issn><issn>1738-6055</issn><eissn>2233-7660</eissn><abstract>BACKGROUNDTo evaluate the chemosensitivity to doxorubicin (DOX) in two primary cells derived from a tumor of FVB/N-Trp53tm1Hw1 knockout (KO) mice with TALEN-mediated Trp53 mutant gene, we evaluated the cell survivability, cell cycle distribution, apoptotic cell numbers and apoptotic protein expression in solid tumor cells and ascetic tumor cells treated with DOX.RESULTSThe primary tumor cells showed a significant (P &lt; 0.05) defect for UV-induced upregulation of the Trp53 protein, and consisted of different ratios of leukocytes, fibroblasts, epithelial cells and mesenchymal cells. The IC50 level to DOX was lower in both primary cells (IC50 = 0.12 μM and 0.20 μM) as compared to the CT26 cells (IC50 = 0.32 μM), although the solid tumor was more sensitive. Also, the number of cells arrested at the G0/G1 stage was significantly decreased (24.7-23.1% in primary tumor cells treated with DOX, P &lt; 0.05) while arrest at the G2 stage was enhanced to 296.8-254.3% in DOX-treated primary tumor cells compared with DOX-treated CT26 cells. Furthermore, apoptotic cells of early and late stage were greatly increased in the two primary cell-lines treated with DOX when compared to same conditions for CT26 cells. However, the Bax/Bcl-2 expression level was maintained constant in the primary tumor and CT26 cells.CONCLUSIONSTo the best of our knowledge, these results are the first to successfully detect an alteration in chemosensitivity to DOX in solid tumor cells and ascetic tumor cells derived from tumor of FVB/N-Trp53tm1Hw1 mice TALEN-mediated Trp53 mutant gene.</abstract><cop>London</cop><pub>BioMed Central</pub><pmid>37864254</pmid><doi>10.1186/s42826-023-00175-2</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-5144-1725</orcidid><oa>free_for_read</oa></addata></record>
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subjects Ascetic tumor
Chemosensitivity
Doxorubicin
G2 arrest
Solid tumor
Trp53
수의학
title Chemosensitivity to doxorubicin in primary cells derived from tumor of FVB/N-Trp53tm1Hw1 with TALEN-mediated Trp53 mutant gene
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