Time-Dependent Effects of POT1 Knockdown on Proliferation, Tumorigenicity, and HDACi Response of SK-OV3 Ovarian Cancer Cells

The roles of protection of telomeres 1 (POT1) in human ovarian cancer have not been fully elucidated. Here, we investigated the impact of POT1 knockdown (POT1-KD) on in vitro cell proliferation, tumorigenesis, and histone deacetylase inhibitor (HDACi) response in human ovarian cancer-derived SK-OV3...

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Published in:BioMed research international 2018-01, Vol.2018 (2018), p.1-12
Main Authors: Liu, Xuefeng, Alhawas, Lama, Dakic, Aleksandra, Mondal, Abdul, Zhou, Hua, He, Zhixu
Format: Article
Language:English
Subjects:
Apoptosis
c-Myc protein
Cancer
Cell growth
Cell proliferation
Gene expression
Health aspects
Histone deacetylase
Human behavior
Lymphoma
Medical research
mRNA
Myc protein
Ovarian cancer
Population
Pot1 gene
Prevention
Researchers
RNA
Studies
Telomerase
Telomerase reverse transcriptase
Telomeres
Tumorigenesis
Tumorigenicity
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creator Liu, Xuefeng
Alhawas, Lama
Dakic, Aleksandra
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He, Zhixu
description The roles of protection of telomeres 1 (POT1) in human ovarian cancer have not been fully elucidated. Here, we investigated the impact of POT1 knockdown (POT1-KD) on in vitro cell proliferation, tumorigenesis, and histone deacetylase inhibitor (HDACi) response in human ovarian cancer-derived SK-OV3 cells. The POT1 gene was knocked down by infection with POT1 lenti-shRNA. POT1, c-Myc, and hTERT mRNA levels and relative telomere length were determined by qRT-PCR; POT1 protein levels were determined by western blot. The relative telomerase activity levels were detected using qTRAP; cell proliferation was assessed using cumulative population doubling (cPD) experiments. Cell tumorigenicity was evaluated by anchorage-independent cell growth assays, and cell response to HDACi was determined by luminescence cell viability assays. Results indicate that lenti-shRNA-mediated POT1-KD significantly reduced POT1 mRNA and protein expression. POT1-KD immediately downregulated c-Myc expression, which led to the inhibition of cell proliferation, tumorigenesis, and HDACi response. However, after brief suppression, c-Myc expression increased in the medium term, which resulted in enhanced cell proliferation, tumorigenesis, and HDACi response in the POT1-KD cells. Furthermore, we discovered that c-Myc regulated cell proliferation and tumorigenesis via hTERT/telomerase/telomere pathway.
doi_str_mv 10.1155/2018/7184253
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Here, we investigated the impact of POT1 knockdown (POT1-KD) on in vitro cell proliferation, tumorigenesis, and histone deacetylase inhibitor (HDACi) response in human ovarian cancer-derived SK-OV3 cells. The POT1 gene was knocked down by infection with POT1 lenti-shRNA. POT1, c-Myc, and hTERT mRNA levels and relative telomere length were determined by qRT-PCR; POT1 protein levels were determined by western blot. The relative telomerase activity levels were detected using qTRAP; cell proliferation was assessed using cumulative population doubling (cPD) experiments. Cell tumorigenicity was evaluated by anchorage-independent cell growth assays, and cell response to HDACi was determined by luminescence cell viability assays. Results indicate that lenti-shRNA-mediated POT1-KD significantly reduced POT1 mRNA and protein expression. POT1-KD immediately downregulated c-Myc expression, which led to the inhibition of cell proliferation, tumorigenesis, and HDACi response. However, after brief suppression, c-Myc expression increased in the medium term, which resulted in enhanced cell proliferation, tumorigenesis, and HDACi response in the POT1-KD cells. Furthermore, we discovered that c-Myc regulated cell proliferation and tumorigenesis via hTERT/telomerase/telomere pathway.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2018/7184253</identifier><identifier>PMID: 29546066</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Apoptosis ; c-Myc protein ; Cancer ; Cell growth ; Cell proliferation ; Gene expression ; Health aspects ; Histone deacetylase ; Human behavior ; Lymphoma ; Medical research ; mRNA ; Myc protein ; Ovarian cancer ; Population ; Pot1 gene ; Prevention ; Researchers ; RNA ; Studies ; Telomerase ; Telomerase reverse transcriptase ; Telomeres ; Tumorigenesis ; Tumorigenicity</subject><ispartof>BioMed research international, 2018-01, Vol.2018 (2018), p.1-12</ispartof><rights>Copyright © 2018 Hua Zhou et al.</rights><rights>COPYRIGHT 2018 John Wiley &amp; Sons, Inc.</rights><rights>Copyright © 2018 Hua Zhou et al.; This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2018 Hua Zhou et al. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-b53cde65c36ba6e9d9dd80c3a5748706cd8ec4a6dd4c0e5c2d2eb01dbe222dd3</citedby><cites>FETCH-LOGICAL-c499t-b53cde65c36ba6e9d9dd80c3a5748706cd8ec4a6dd4c0e5c2d2eb01dbe222dd3</cites><orcidid>0000-0003-2292-7504 ; 0000-0002-9922-9627</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2002923639/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2002923639?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,25752,27923,27924,37011,37012,44589,74897</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29546066$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Wimberger, Pauline</contributor><contributor>Pauline Wimberger</contributor><creatorcontrib>Liu, Xuefeng</creatorcontrib><creatorcontrib>Alhawas, Lama</creatorcontrib><creatorcontrib>Dakic, Aleksandra</creatorcontrib><creatorcontrib>Mondal, Abdul</creatorcontrib><creatorcontrib>Zhou, Hua</creatorcontrib><creatorcontrib>He, Zhixu</creatorcontrib><title>Time-Dependent Effects of POT1 Knockdown on Proliferation, Tumorigenicity, and HDACi Response of SK-OV3 Ovarian Cancer Cells</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>The roles of protection of telomeres 1 (POT1) in human ovarian cancer have not been fully elucidated. Here, we investigated the impact of POT1 knockdown (POT1-KD) on in vitro cell proliferation, tumorigenesis, and histone deacetylase inhibitor (HDACi) response in human ovarian cancer-derived SK-OV3 cells. The POT1 gene was knocked down by infection with POT1 lenti-shRNA. POT1, c-Myc, and hTERT mRNA levels and relative telomere length were determined by qRT-PCR; POT1 protein levels were determined by western blot. The relative telomerase activity levels were detected using qTRAP; cell proliferation was assessed using cumulative population doubling (cPD) experiments. Cell tumorigenicity was evaluated by anchorage-independent cell growth assays, and cell response to HDACi was determined by luminescence cell viability assays. Results indicate that lenti-shRNA-mediated POT1-KD significantly reduced POT1 mRNA and protein expression. POT1-KD immediately downregulated c-Myc expression, which led to the inhibition of cell proliferation, tumorigenesis, and HDACi response. 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Here, we investigated the impact of POT1 knockdown (POT1-KD) on in vitro cell proliferation, tumorigenesis, and histone deacetylase inhibitor (HDACi) response in human ovarian cancer-derived SK-OV3 cells. The POT1 gene was knocked down by infection with POT1 lenti-shRNA. POT1, c-Myc, and hTERT mRNA levels and relative telomere length were determined by qRT-PCR; POT1 protein levels were determined by western blot. The relative telomerase activity levels were detected using qTRAP; cell proliferation was assessed using cumulative population doubling (cPD) experiments. Cell tumorigenicity was evaluated by anchorage-independent cell growth assays, and cell response to HDACi was determined by luminescence cell viability assays. Results indicate that lenti-shRNA-mediated POT1-KD significantly reduced POT1 mRNA and protein expression. POT1-KD immediately downregulated c-Myc expression, which led to the inhibition of cell proliferation, tumorigenesis, and HDACi response. However, after brief suppression, c-Myc expression increased in the medium term, which resulted in enhanced cell proliferation, tumorigenesis, and HDACi response in the POT1-KD cells. Furthermore, we discovered that c-Myc regulated cell proliferation and tumorigenesis via hTERT/telomerase/telomere pathway.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>29546066</pmid><doi>10.1155/2018/7184253</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-2292-7504</orcidid><orcidid>https://orcid.org/0000-0002-9922-9627</orcidid><oa>free_for_read</oa></addata></record>
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subjects Apoptosis
c-Myc protein
Cancer
Cell growth
Cell proliferation
Gene expression
Health aspects
Histone deacetylase
Human behavior
Lymphoma
Medical research
mRNA
Myc protein
Ovarian cancer
Population
Pot1 gene
Prevention
Researchers
RNA
Studies
Telomerase
Telomerase reverse transcriptase
Telomeres
Tumorigenesis
Tumorigenicity
title Time-Dependent Effects of POT1 Knockdown on Proliferation, Tumorigenicity, and HDACi Response of SK-OV3 Ovarian Cancer Cells
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