Knockdown of immature colon carcinoma transcript 1 induces suppression of proliferation, S-phase arrest and apoptosis in leukemia cells
Immature colon carcinoma transcript 1 (ICT1), a human mitochondrial translation release factor, is a ribosome-dependent codon-independent peptidyl-tRNA hydrolase. ICT1-deficiency has been recognized as a cell growth inhibitor of hepatoblastoma and glioblastoma multiforme. To explore the role of ICT1...
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| Veröffentlicht in: | Oncology reports 2018-03, Vol.39 (3), p.1269-1275 |
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| creator | Li, Guang-Yao Liu, Ji-Zhu Zhang, Li Liu, Guo-Zhen Li, Shuang-Jing Xiao, Tai-Wu Wang, Jing-Xia Wang, Le-Xin Hou, Ming |
| description | Immature colon carcinoma transcript 1 (ICT1), a human mitochondrial translation release factor, is a ribosome-dependent codon-independent peptidyl-tRNA hydrolase. ICT1-deficiency has been recognized as a cell growth inhibitor of hepatoblastoma and glioblastoma multiforme. To explore the role of ICT1 in human leukemia, 2 short hairpin RNAs (shRNAs) targeting ICT1 sequences were designed in leukemia U937 cells. The successful infection of ICT1 in the U937 cells was observed under a fluorescence microscope and further quantified by western blotting and quantitative real-time PCR (qRT-PCR) analysis. Tetrazolium dye (MTT) assay revealed a significant decrease in proliferation of ICT1-knockdown U937 cells on the fourth and fifth day as compared with the control. Depletion of ICT1 resulted in an increase in S phase and sub-G1 (representing cell apoptosis) fractions. Annexin V-APC/7-AAD staining assay confirmed that knockdown of ICT1 played a crucial role in boosting early and late apoptotic programs in U937 cells. Downregulation of ICT1 also altered cyclin A2 transcription expression, caspase-3 activity and p21 protein expression. Additionally, decreased levels of heat shock protein 27 (HSP27) phosphorylation at Ser78 was correlated with knockdown of ICT1 in U937 cells. Thus, we concluded that the regulatory role of ICT1 in leukemia may be used as a potential therapeutic target for the treatment of leukemia. |
| doi_str_mv | 10.3892/or.2018.6185 |
| format | Article |
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ICT1-deficiency has been recognized as a cell growth inhibitor of hepatoblastoma and glioblastoma multiforme. To explore the role of ICT1 in human leukemia, 2 short hairpin RNAs (shRNAs) targeting ICT1 sequences were designed in leukemia U937 cells. The successful infection of ICT1 in the U937 cells was observed under a fluorescence microscope and further quantified by western blotting and quantitative real-time PCR (qRT-PCR) analysis. Tetrazolium dye (MTT) assay revealed a significant decrease in proliferation of ICT1-knockdown U937 cells on the fourth and fifth day as compared with the control. Depletion of ICT1 resulted in an increase in S phase and sub-G1 (representing cell apoptosis) fractions. Annexin V-APC/7-AAD staining assay confirmed that knockdown of ICT1 played a crucial role in boosting early and late apoptotic programs in U937 cells. Downregulation of ICT1 also altered cyclin A2 transcription expression, caspase-3 activity and p21 protein expression. Additionally, decreased levels of heat shock protein 27 (HSP27) phosphorylation at Ser78 was correlated with knockdown of ICT1 in U937 cells. Thus, we concluded that the regulatory role of ICT1 in leukemia may be used as a potential therapeutic target for the treatment of leukemia.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2018.6185</identifier><identifier>PMID: 29328466</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Apoptosis ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Cancer therapies ; Care and treatment ; Cell cycle ; Cell Cycle Checkpoints ; Cell Proliferation ; Chemotherapy ; Colorectal cancer ; Cytochrome ; Development and progression ; Gene expression ; Gene therapy ; Genetic aspects ; Health aspects ; Humans ; Infections ; Kinases ; Leukemia ; Leukemia - genetics ; Leukemia - metabolism ; Leukemia - pathology ; Medical prognosis ; Membranes ; Phosphorylation ; Proteins ; Proteins - antagonists & inhibitors ; Proteins - genetics ; S Phase ; Transcription factors ; Tumor Cells, Cultured ; Vectors (Biology)</subject><ispartof>Oncology reports, 2018-03, Vol.39 (3), p.1269-1275</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29328466$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Guang-Yao</creatorcontrib><creatorcontrib>Liu, Ji-Zhu</creatorcontrib><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Liu, Guo-Zhen</creatorcontrib><creatorcontrib>Li, Shuang-Jing</creatorcontrib><creatorcontrib>Xiao, Tai-Wu</creatorcontrib><creatorcontrib>Wang, Jing-Xia</creatorcontrib><creatorcontrib>Wang, Le-Xin</creatorcontrib><creatorcontrib>Hou, Ming</creatorcontrib><title>Knockdown of immature colon carcinoma transcript 1 induces suppression of proliferation, S-phase arrest and apoptosis in leukemia cells</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Immature colon carcinoma transcript 1 (ICT1), a human mitochondrial translation release factor, is a ribosome-dependent codon-independent peptidyl-tRNA hydrolase. ICT1-deficiency has been recognized as a cell growth inhibitor of hepatoblastoma and glioblastoma multiforme. To explore the role of ICT1 in human leukemia, 2 short hairpin RNAs (shRNAs) targeting ICT1 sequences were designed in leukemia U937 cells. The successful infection of ICT1 in the U937 cells was observed under a fluorescence microscope and further quantified by western blotting and quantitative real-time PCR (qRT-PCR) analysis. Tetrazolium dye (MTT) assay revealed a significant decrease in proliferation of ICT1-knockdown U937 cells on the fourth and fifth day as compared with the control. Depletion of ICT1 resulted in an increase in S phase and sub-G1 (representing cell apoptosis) fractions. Annexin V-APC/7-AAD staining assay confirmed that knockdown of ICT1 played a crucial role in boosting early and late apoptotic programs in U937 cells. Downregulation of ICT1 also altered cyclin A2 transcription expression, caspase-3 activity and p21 protein expression. Additionally, decreased levels of heat shock protein 27 (HSP27) phosphorylation at Ser78 was correlated with knockdown of ICT1 in U937 cells. Thus, we concluded that the regulatory role of ICT1 in leukemia may be used as a potential therapeutic target for the treatment of leukemia.</description><subject>Apoptosis</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints</subject><subject>Cell Proliferation</subject><subject>Chemotherapy</subject><subject>Colorectal cancer</subject><subject>Cytochrome</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Gene therapy</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Infections</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Leukemia - genetics</subject><subject>Leukemia - metabolism</subject><subject>Leukemia - pathology</subject><subject>Medical prognosis</subject><subject>Membranes</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Proteins - antagonists & inhibitors</subject><subject>Proteins - genetics</subject><subject>S Phase</subject><subject>Transcription factors</subject><subject>Tumor Cells, Cultured</subject><subject>Vectors (Biology)</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkc1qFjEYhQdR7I_uXEtAKF04n_mbZLIsxaq04EIFd8M7mXf6pc0kYzKDeAdehtfSK2s-rWhFskh4ec7JyUlVPWN0I1rDX8W04ZS1G8Xa5kG1z7RhNZeCPSxnylktRPN5rzrI-YpSrqkyj6s9bgRvpVL71ffzEO31EL8GEkfipgmWNSGx0cdALCTrQpyALAlCtsnNy80PRlwYVouZ5HWeE-bs4k_1nKJ3IyZYyuAl-VDPW8hIIBVmIRAGAnOcl5hdLhbE43qNkwNi0fv8pHo0gs_49G4_rD6dvf54-ra-eP_m3enJRX0phF7qUSkpB9X0XALSXg-jNq020AsFSmE_lJdjbxpJGVqK1FqJg7aAhqPUWojD6viXb0n7ZS3BusnlXQIIGNfcMdMaRRvNTEFf_INexTWFkq5QRmqhlKJ_qEvw2LkwxlKW3Zl2Jw0vZoyy3bWb_1BlDaUCGwOOrszvCY7-EmwR_LLN0a-7bvN98PldyrWfcOjm5CZI37rffyxuAR1uqTM</recordid><startdate>20180301</startdate><enddate>20180301</enddate><creator>Li, Guang-Yao</creator><creator>Liu, Ji-Zhu</creator><creator>Zhang, Li</creator><creator>Liu, Guo-Zhen</creator><creator>Li, Shuang-Jing</creator><creator>Xiao, Tai-Wu</creator><creator>Wang, Jing-Xia</creator><creator>Wang, Le-Xin</creator><creator>Hou, Ming</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20180301</creationdate><title>Knockdown of immature colon carcinoma transcript 1 induces suppression of proliferation, S-phase arrest and apoptosis in leukemia cells</title><author>Li, Guang-Yao ; Liu, Ji-Zhu ; Zhang, Li ; Liu, Guo-Zhen ; Li, Shuang-Jing ; Xiao, Tai-Wu ; Wang, Jing-Xia ; Wang, Le-Xin ; Hou, Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g337t-f6644d65b24ae0b7df79879ab36a66ebd431eb95401ec0e0cc4ed7cae92e47733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Apoptosis</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell Cycle Checkpoints</topic><topic>Cell Proliferation</topic><topic>Chemotherapy</topic><topic>Colorectal cancer</topic><topic>Cytochrome</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>Gene therapy</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Infections</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Leukemia - genetics</topic><topic>Leukemia - metabolism</topic><topic>Leukemia - pathology</topic><topic>Medical prognosis</topic><topic>Membranes</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Proteins - antagonists & inhibitors</topic><topic>Proteins - genetics</topic><topic>S Phase</topic><topic>Transcription factors</topic><topic>Tumor Cells, Cultured</topic><topic>Vectors (Biology)</topic><toplevel>online_resources</toplevel><creatorcontrib>Li, Guang-Yao</creatorcontrib><creatorcontrib>Liu, Ji-Zhu</creatorcontrib><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Liu, Guo-Zhen</creatorcontrib><creatorcontrib>Li, Shuang-Jing</creatorcontrib><creatorcontrib>Xiao, Tai-Wu</creatorcontrib><creatorcontrib>Wang, Jing-Xia</creatorcontrib><creatorcontrib>Wang, Le-Xin</creatorcontrib><creatorcontrib>Hou, Ming</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</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>Medical 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><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Guang-Yao</au><au>Liu, Ji-Zhu</au><au>Zhang, Li</au><au>Liu, Guo-Zhen</au><au>Li, Shuang-Jing</au><au>Xiao, Tai-Wu</au><au>Wang, Jing-Xia</au><au>Wang, Le-Xin</au><au>Hou, Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Knockdown of immature colon carcinoma transcript 1 induces suppression of proliferation, S-phase arrest and apoptosis in leukemia cells</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2018-03-01</date><risdate>2018</risdate><volume>39</volume><issue>3</issue><spage>1269</spage><epage>1275</epage><pages>1269-1275</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Immature colon carcinoma transcript 1 (ICT1), a human mitochondrial translation release factor, is a ribosome-dependent codon-independent peptidyl-tRNA hydrolase. ICT1-deficiency has been recognized as a cell growth inhibitor of hepatoblastoma and glioblastoma multiforme. To explore the role of ICT1 in human leukemia, 2 short hairpin RNAs (shRNAs) targeting ICT1 sequences were designed in leukemia U937 cells. The successful infection of ICT1 in the U937 cells was observed under a fluorescence microscope and further quantified by western blotting and quantitative real-time PCR (qRT-PCR) analysis. Tetrazolium dye (MTT) assay revealed a significant decrease in proliferation of ICT1-knockdown U937 cells on the fourth and fifth day as compared with the control. Depletion of ICT1 resulted in an increase in S phase and sub-G1 (representing cell apoptosis) fractions. Annexin V-APC/7-AAD staining assay confirmed that knockdown of ICT1 played a crucial role in boosting early and late apoptotic programs in U937 cells. Downregulation of ICT1 also altered cyclin A2 transcription expression, caspase-3 activity and p21 protein expression. Additionally, decreased levels of heat shock protein 27 (HSP27) phosphorylation at Ser78 was correlated with knockdown of ICT1 in U937 cells. Thus, we concluded that the regulatory role of ICT1 in leukemia may be used as a potential therapeutic target for the treatment of leukemia.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29328466</pmid><doi>10.3892/or.2018.6185</doi><tpages>7</tpages></addata></record> |
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| subjects | Apoptosis Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Cancer therapies Care and treatment Cell cycle Cell Cycle Checkpoints Cell Proliferation Chemotherapy Colorectal cancer Cytochrome Development and progression Gene expression Gene therapy Genetic aspects Health aspects Humans Infections Kinases Leukemia Leukemia - genetics Leukemia - metabolism Leukemia - pathology Medical prognosis Membranes Phosphorylation Proteins Proteins - antagonists & inhibitors Proteins - genetics S Phase Transcription factors Tumor Cells, Cultured Vectors (Biology) |
| title | Knockdown of immature colon carcinoma transcript 1 induces suppression of proliferation, S-phase arrest and apoptosis in leukemia cells |
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