Knockdown of PNO1 inhibits esophageal cancer progression
The present study aimed to investigate the role of partner of NOB1 homolog (PNO1) in esophageal cancer (EC). The expression levels of PNO1 in EC were primarily analyzed using data obtained from databases. PNO1 expression was also knocked down in EC cells (Eca‑109 and TE1) to determine the biological...
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| Veröffentlicht in: | Oncology reports 2021-05, Vol.45 (5), p.1, Article 85 |
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| creator | Wang, Guowen Li, Qicai Li, Chuankui Duan, Guixin Sang, Haiwei Dong, Haijun Yang, Yifan Ma, Chang Tao, Tao |
| description | The present study aimed to investigate the role of partner of NOB1 homolog (PNO1) in esophageal cancer (EC). The expression levels of PNO1 in EC were primarily analyzed using data obtained from databases. PNO1 expression was also knocked down in EC cells (Eca‑109 and TE1) to determine the biological effects of PNO1 on tumorigenesis
and
. In addition, possible downstream targets of PNO1 in EC were identified. The expression levels of PNO1 were upregulated in the tumor tissues compared with that noted in normal tissues. Moreover, the knockdown (KD) of PNO1 suppressed cell proliferation, migration and invasion, and promoted cell apoptosis (P < 0.05). Furthermore, the protein expression levels of AKT1, Twist, Myc, mTOR, matrix metalloproteinase 2 (MMP2), nuclear factor (NF)‑κB p65 and β‑catenin 1 (CTNNB1) were downregulated following the KD of PNO1 in Eca‑109 cells (P < 0.05). In addition, the overexpression of CTNNB1 reversed the effects of PNO1 KD in Eca‑109 cells (P < 0.05). In conclusion, the findings of the present study suggest that PNO1 promotes EC progression by regulating AKT1, Twist, Myc, mTOR, MMP2, NF‑κB p65 and CTNNB1 expression. |
| doi_str_mv | 10.3892/or.2021.8036 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8025143</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A659005333</galeid><sourcerecordid>A659005333</sourcerecordid><originalsourceid>FETCH-LOGICAL-c510t-236d8824678591763735951c837b4f74390b1273f673a26a5fbade54ac1722c43</originalsourceid><addsrcrecordid>eNptks1rFTEUxYMotlZ3rmVAEBfOM8nN50YoxS8s1oWCu5DJZN6kzkueyYzif2-G1tonkkXCze-eyz0chB4TvAGl6cuUNxRTslEYxB10TKQmLWVA7tZ3rbcA_OsRelDKJcZUYqHvoyMAJZgQ5BipDzG5b336GZs0NJ8-XpAmxDF0YS6NL2k_2q23U-NsdD43-5y22ZcSUnyI7g12Kv7R9X2Cvrx5_fnsXXt-8fb92el56zjBc0tB9EpRJqTimkgBErjmxCmQHRskA407QiUMQoKlwvKhs73nzDoiKXUMTtCrK9390u1873ycs53MPoedzb9MssEc_sQwmm36YRSmnDCoAs-vBXL6vvgym10ozk-TjT4txayUwAxrUtGn_6CXacmxrlcprJmmgvC_1NZO3oQ4pDrXraLmVHCNMQdYx27-Q9XT-11wKfoh1PpBw7NbDWN1fR5Lmpa5ml0OwRdXoMuplOyHGzMINmskTMpmjYRZI1HxJ7cNvIH_ZAB-A8w7rQc</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2509492615</pqid></control><display><type>article</type><title>Knockdown of PNO1 inhibits esophageal cancer progression</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Wang, Guowen ; Li, Qicai ; Li, Chuankui ; Duan, Guixin ; Sang, Haiwei ; Dong, Haijun ; Yang, Yifan ; Ma, Chang ; Tao, Tao</creator><creatorcontrib>Wang, Guowen ; Li, Qicai ; Li, Chuankui ; Duan, Guixin ; Sang, Haiwei ; Dong, Haijun ; Yang, Yifan ; Ma, Chang ; Tao, Tao</creatorcontrib><description>The present study aimed to investigate the role of partner of NOB1 homolog (PNO1) in esophageal cancer (EC). The expression levels of PNO1 in EC were primarily analyzed using data obtained from databases. PNO1 expression was also knocked down in EC cells (Eca‑109 and TE1) to determine the biological effects of PNO1 on tumorigenesis
and
. In addition, possible downstream targets of PNO1 in EC were identified. The expression levels of PNO1 were upregulated in the tumor tissues compared with that noted in normal tissues. Moreover, the knockdown (KD) of PNO1 suppressed cell proliferation, migration and invasion, and promoted cell apoptosis (P < 0.05). Furthermore, the protein expression levels of AKT1, Twist, Myc, mTOR, matrix metalloproteinase 2 (MMP2), nuclear factor (NF)‑κB p65 and β‑catenin 1 (CTNNB1) were downregulated following the KD of PNO1 in Eca‑109 cells (P < 0.05). In addition, the overexpression of CTNNB1 reversed the effects of PNO1 KD in Eca‑109 cells (P < 0.05). In conclusion, the findings of the present study suggest that PNO1 promotes EC progression by regulating AKT1, Twist, Myc, mTOR, MMP2, NF‑κB p65 and CTNNB1 expression.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2021.8036</identifier><identifier>PMID: 33864661</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Apoptosis ; Biotechnology ; Esophageal cancer ; Experiments ; Laboratory animals ; Medical prognosis ; Proteins ; Scientific equipment and supplies industry ; Software ; Statistical analysis ; Wound healing</subject><ispartof>Oncology reports, 2021-05, Vol.45 (5), p.1, Article 85</ispartof><rights>COPYRIGHT 2021 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2021</rights><rights>Copyright: © Wang et al. 2021</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-236d8824678591763735951c837b4f74390b1273f673a26a5fbade54ac1722c43</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33864661$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Guowen</creatorcontrib><creatorcontrib>Li, Qicai</creatorcontrib><creatorcontrib>Li, Chuankui</creatorcontrib><creatorcontrib>Duan, Guixin</creatorcontrib><creatorcontrib>Sang, Haiwei</creatorcontrib><creatorcontrib>Dong, Haijun</creatorcontrib><creatorcontrib>Yang, Yifan</creatorcontrib><creatorcontrib>Ma, Chang</creatorcontrib><creatorcontrib>Tao, Tao</creatorcontrib><title>Knockdown of PNO1 inhibits esophageal cancer progression</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>The present study aimed to investigate the role of partner of NOB1 homolog (PNO1) in esophageal cancer (EC). The expression levels of PNO1 in EC were primarily analyzed using data obtained from databases. PNO1 expression was also knocked down in EC cells (Eca‑109 and TE1) to determine the biological effects of PNO1 on tumorigenesis
and
. In addition, possible downstream targets of PNO1 in EC were identified. The expression levels of PNO1 were upregulated in the tumor tissues compared with that noted in normal tissues. Moreover, the knockdown (KD) of PNO1 suppressed cell proliferation, migration and invasion, and promoted cell apoptosis (P < 0.05). Furthermore, the protein expression levels of AKT1, Twist, Myc, mTOR, matrix metalloproteinase 2 (MMP2), nuclear factor (NF)‑κB p65 and β‑catenin 1 (CTNNB1) were downregulated following the KD of PNO1 in Eca‑109 cells (P < 0.05). In addition, the overexpression of CTNNB1 reversed the effects of PNO1 KD in Eca‑109 cells (P < 0.05). In conclusion, the findings of the present study suggest that PNO1 promotes EC progression by regulating AKT1, Twist, Myc, mTOR, MMP2, NF‑κB p65 and CTNNB1 expression.</description><subject>Apoptosis</subject><subject>Biotechnology</subject><subject>Esophageal cancer</subject><subject>Experiments</subject><subject>Laboratory animals</subject><subject>Medical prognosis</subject><subject>Proteins</subject><subject>Scientific equipment and supplies industry</subject><subject>Software</subject><subject>Statistical analysis</subject><subject>Wound healing</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptks1rFTEUxYMotlZ3rmVAEBfOM8nN50YoxS8s1oWCu5DJZN6kzkueyYzif2-G1tonkkXCze-eyz0chB4TvAGl6cuUNxRTslEYxB10TKQmLWVA7tZ3rbcA_OsRelDKJcZUYqHvoyMAJZgQ5BipDzG5b336GZs0NJ8-XpAmxDF0YS6NL2k_2q23U-NsdD43-5y22ZcSUnyI7g12Kv7R9X2Cvrx5_fnsXXt-8fb92el56zjBc0tB9EpRJqTimkgBErjmxCmQHRskA407QiUMQoKlwvKhs73nzDoiKXUMTtCrK9390u1873ycs53MPoedzb9MssEc_sQwmm36YRSmnDCoAs-vBXL6vvgym10ozk-TjT4txayUwAxrUtGn_6CXacmxrlcprJmmgvC_1NZO3oQ4pDrXraLmVHCNMQdYx27-Q9XT-11wKfoh1PpBw7NbDWN1fR5Lmpa5ml0OwRdXoMuplOyHGzMINmskTMpmjYRZI1HxJ7cNvIH_ZAB-A8w7rQc</recordid><startdate>20210501</startdate><enddate>20210501</enddate><creator>Wang, Guowen</creator><creator>Li, Qicai</creator><creator>Li, Chuankui</creator><creator>Duan, Guixin</creator><creator>Sang, Haiwei</creator><creator>Dong, Haijun</creator><creator>Yang, Yifan</creator><creator>Ma, Chang</creator><creator>Tao, Tao</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</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><scope>5PM</scope></search><sort><creationdate>20210501</creationdate><title>Knockdown of PNO1 inhibits esophageal cancer progression</title><author>Wang, Guowen ; Li, Qicai ; Li, Chuankui ; Duan, Guixin ; Sang, Haiwei ; Dong, Haijun ; Yang, Yifan ; Ma, Chang ; Tao, Tao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c510t-236d8824678591763735951c837b4f74390b1273f673a26a5fbade54ac1722c43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Apoptosis</topic><topic>Biotechnology</topic><topic>Esophageal cancer</topic><topic>Experiments</topic><topic>Laboratory animals</topic><topic>Medical prognosis</topic><topic>Proteins</topic><topic>Scientific equipment and supplies industry</topic><topic>Software</topic><topic>Statistical analysis</topic><topic>Wound healing</topic><toplevel>online_resources</toplevel><creatorcontrib>Wang, Guowen</creatorcontrib><creatorcontrib>Li, Qicai</creatorcontrib><creatorcontrib>Li, Chuankui</creatorcontrib><creatorcontrib>Duan, Guixin</creatorcontrib><creatorcontrib>Sang, Haiwei</creatorcontrib><creatorcontrib>Dong, Haijun</creatorcontrib><creatorcontrib>Yang, Yifan</creatorcontrib><creatorcontrib>Ma, Chang</creatorcontrib><creatorcontrib>Tao, Tao</creatorcontrib><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>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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Guowen</au><au>Li, Qicai</au><au>Li, Chuankui</au><au>Duan, Guixin</au><au>Sang, Haiwei</au><au>Dong, Haijun</au><au>Yang, Yifan</au><au>Ma, Chang</au><au>Tao, Tao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Knockdown of PNO1 inhibits esophageal cancer progression</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2021-05-01</date><risdate>2021</risdate><volume>45</volume><issue>5</issue><spage>1</spage><pages>1-</pages><artnum>85</artnum><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>The present study aimed to investigate the role of partner of NOB1 homolog (PNO1) in esophageal cancer (EC). The expression levels of PNO1 in EC were primarily analyzed using data obtained from databases. PNO1 expression was also knocked down in EC cells (Eca‑109 and TE1) to determine the biological effects of PNO1 on tumorigenesis
and
. In addition, possible downstream targets of PNO1 in EC were identified. The expression levels of PNO1 were upregulated in the tumor tissues compared with that noted in normal tissues. Moreover, the knockdown (KD) of PNO1 suppressed cell proliferation, migration and invasion, and promoted cell apoptosis (P < 0.05). Furthermore, the protein expression levels of AKT1, Twist, Myc, mTOR, matrix metalloproteinase 2 (MMP2), nuclear factor (NF)‑κB p65 and β‑catenin 1 (CTNNB1) were downregulated following the KD of PNO1 in Eca‑109 cells (P < 0.05). In addition, the overexpression of CTNNB1 reversed the effects of PNO1 KD in Eca‑109 cells (P < 0.05). In conclusion, the findings of the present study suggest that PNO1 promotes EC progression by regulating AKT1, Twist, Myc, mTOR, MMP2, NF‑κB p65 and CTNNB1 expression.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>33864661</pmid><doi>10.3892/or.2021.8036</doi><oa>free_for_read</oa></addata></record> |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Apoptosis Biotechnology Esophageal cancer Experiments Laboratory animals Medical prognosis Proteins Scientific equipment and supplies industry Software Statistical analysis Wound healing |
| title | Knockdown of PNO1 inhibits esophageal cancer progression |
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