RING finger protein 128 (RNF128) regulates malignant biological behaviors of colorectal cancer cells via PI3K/AKT signaling pathway
This study was designed and conducted to clarify the impact of RNF128 expression on malignant biological behaviors of colorectal cancer (CRC) cells and the underlying mechanism. The expression of RNF128 in CRC tissues was analyzed using mRNA sequencing data of TCGA database and was validated by West...
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| Veröffentlicht in: | Cell biology international 2022-10, Vol.46 (10), p.1604-1611 |
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| creator | Zhuang, Yan Liu, Peng‐fei Zhan, Yang Kong, Da‐lu Tian, Fei Zhao, Peng |
| description | This study was designed and conducted to clarify the impact of RNF128 expression on malignant biological behaviors of colorectal cancer (CRC) cells and the underlying mechanism. The expression of RNF128 in CRC tissues was analyzed using mRNA sequencing data of TCGA database and was validated by Western blot assay. The experimental studies on biological functions of RNF128 in vitro were conducted to assess its impact on the proliferation, apoptosis, and metastasis of CRC cells. Furthermore, tumor xenograft models in nude mice were established to investigate the relationship between RNF128 expression and tumor growth in vivo. The expression levels of both RNF128 mRNA and protein were significantly increased in CRC tissues (p |
| doi_str_mv | 10.1002/cbin.11835 |
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The expression of RNF128 in CRC tissues was analyzed using mRNA sequencing data of TCGA database and was validated by Western blot assay. The experimental studies on biological functions of RNF128 in vitro were conducted to assess its impact on the proliferation, apoptosis, and metastasis of CRC cells. Furthermore, tumor xenograft models in nude mice were established to investigate the relationship between RNF128 expression and tumor growth in vivo. The expression levels of both RNF128 mRNA and protein were significantly increased in CRC tissues (p < .001). The knockdown of RNF128 markedly suppressed the malignant phenotype of HCT116 and SW480 cells in vitro, including cell growth, antiapoptosis, migration, and invasion (p < .001). On the other hand, knockdown of RNF128 exerted a remarkable effect on the growth inhibition of tumor xenografts in vivo (p < .001). Further investigation revealed that RNF128 knockdown lead to a significant decrease in the expression of p‐AKT and p‐PI3K protein. More importantly, the proliferative, antiapoptotic, metastatic abilities of RNF128‐knockdown cells were markedly increased by 740 Y‐P treatment (p < .001). These findings further suggested that PI3K/AKT signaling pathway played a key role in RNF128‐mediated aggressive phenotype of CRC cells. RNF128 functions as a tumor promoter in the pathogenesis of CRC via regulating PI3K/AKT pathway, and it could be a valuable target for CRC treatment.</description><identifier>ISSN: 1065-6995</identifier><identifier>EISSN: 1095-8355</identifier><identifier>DOI: 10.1002/cbin.11835</identifier><language>eng</language><publisher>London: Wiley Subscription Services, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Animal models ; Apoptosis ; Cell culture ; Cell migration ; Cell proliferation ; Colorectal cancer ; Colorectal carcinoma ; Kinases ; Metastases ; mRNA ; oncogenesis ; Phenotypes ; PI3K/AKT signaling ; progression ; Proteins ; RING finger proteins ; Signal transduction ; the RING finger protein 128 (RNF128) ; Xenografts</subject><ispartof>Cell biology international, 2022-10, Vol.46 (10), p.1604-1611</ispartof><rights>2022 International Federation for Cell Biology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3345-c8af7ac01bfc12d1b10b415b817a078bbcc299536945d7f50bb5d800f2f6f5ac3</citedby><cites>FETCH-LOGICAL-c3345-c8af7ac01bfc12d1b10b415b817a078bbcc299536945d7f50bb5d800f2f6f5ac3</cites><orcidid>0000-0002-5766-7039</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fcbin.11835$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcbin.11835$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids></links><search><creatorcontrib>Zhuang, Yan</creatorcontrib><creatorcontrib>Liu, Peng‐fei</creatorcontrib><creatorcontrib>Zhan, Yang</creatorcontrib><creatorcontrib>Kong, Da‐lu</creatorcontrib><creatorcontrib>Tian, Fei</creatorcontrib><creatorcontrib>Zhao, Peng</creatorcontrib><title>RING finger protein 128 (RNF128) regulates malignant biological behaviors of colorectal cancer cells via PI3K/AKT signaling pathway</title><title>Cell biology international</title><description>This study was designed and conducted to clarify the impact of RNF128 expression on malignant biological behaviors of colorectal cancer (CRC) cells and the underlying mechanism. The expression of RNF128 in CRC tissues was analyzed using mRNA sequencing data of TCGA database and was validated by Western blot assay. The experimental studies on biological functions of RNF128 in vitro were conducted to assess its impact on the proliferation, apoptosis, and metastasis of CRC cells. Furthermore, tumor xenograft models in nude mice were established to investigate the relationship between RNF128 expression and tumor growth in vivo. The expression levels of both RNF128 mRNA and protein were significantly increased in CRC tissues (p < .001). The knockdown of RNF128 markedly suppressed the malignant phenotype of HCT116 and SW480 cells in vitro, including cell growth, antiapoptosis, migration, and invasion (p < .001). On the other hand, knockdown of RNF128 exerted a remarkable effect on the growth inhibition of tumor xenografts in vivo (p < .001). Further investigation revealed that RNF128 knockdown lead to a significant decrease in the expression of p‐AKT and p‐PI3K protein. More importantly, the proliferative, antiapoptotic, metastatic abilities of RNF128‐knockdown cells were markedly increased by 740 Y‐P treatment (p < .001). These findings further suggested that PI3K/AKT signaling pathway played a key role in RNF128‐mediated aggressive phenotype of CRC cells. RNF128 functions as a tumor promoter in the pathogenesis of CRC via regulating PI3K/AKT pathway, and it could be a valuable target for CRC treatment.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Animal models</subject><subject>Apoptosis</subject><subject>Cell culture</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Kinases</subject><subject>Metastases</subject><subject>mRNA</subject><subject>oncogenesis</subject><subject>Phenotypes</subject><subject>PI3K/AKT signaling</subject><subject>progression</subject><subject>Proteins</subject><subject>RING finger proteins</subject><subject>Signal transduction</subject><subject>the RING finger protein 128 (RNF128)</subject><subject>Xenografts</subject><issn>1065-6995</issn><issn>1095-8355</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNp9kU9PwzAMxSsEEjC48AkicQGkDrtt-ucIExsVaCA0zlWSJVtQ1o6k27QzX5yUcuLAyZb18_OzXhBcIAwRILoVXNdDxDymB8EJQkFD39LDrk9pmBYFPQ5OnfsAQEzy9CT4eiunE6J0vZCWrG3TSl0TjHJy9TYd-3pNrFxsDGulIytm9KJmdUu4bkyz0IIZwuWSbXVjHWkUEX5spWj9XLBaeEkhjXFkqxl5LeOn27unGXGdiPEXyZq1yx3bnwVHihknz3_rIHgfP8xGj-Hzy6Qc3T2HIo4TGoqcqYwJQK4ERnPkCDxBynPMGGQ550JE_sE4LRI6zxQFzuk8B1CRShVlIh4EV72u__NzI11brbTrDLJaNhtXRWmWZ3ERU_Do5R_0o9lYb9tTGUYARQqRp256StjGOStVtbZ6xey-Qqi6PKouj-onDw9jD--0kft_yGp0X077nW-0-Iwq</recordid><startdate>202210</startdate><enddate>202210</enddate><creator>Zhuang, Yan</creator><creator>Liu, Peng‐fei</creator><creator>Zhan, Yang</creator><creator>Kong, Da‐lu</creator><creator>Tian, Fei</creator><creator>Zhao, Peng</creator><general>Wiley Subscription Services, Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5766-7039</orcidid></search><sort><creationdate>202210</creationdate><title>RING finger protein 128 (RNF128) regulates malignant biological behaviors of colorectal cancer cells via PI3K/AKT signaling pathway</title><author>Zhuang, Yan ; Liu, Peng‐fei ; Zhan, Yang ; Kong, Da‐lu ; Tian, Fei ; Zhao, Peng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3345-c8af7ac01bfc12d1b10b415b817a078bbcc299536945d7f50bb5d800f2f6f5ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Animal models</topic><topic>Apoptosis</topic><topic>Cell culture</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Kinases</topic><topic>Metastases</topic><topic>mRNA</topic><topic>oncogenesis</topic><topic>Phenotypes</topic><topic>PI3K/AKT signaling</topic><topic>progression</topic><topic>Proteins</topic><topic>RING finger proteins</topic><topic>Signal transduction</topic><topic>the RING finger protein 128 (RNF128)</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhuang, Yan</creatorcontrib><creatorcontrib>Liu, Peng‐fei</creatorcontrib><creatorcontrib>Zhan, Yang</creatorcontrib><creatorcontrib>Kong, Da‐lu</creatorcontrib><creatorcontrib>Tian, Fei</creatorcontrib><creatorcontrib>Zhao, Peng</creatorcontrib><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhuang, Yan</au><au>Liu, Peng‐fei</au><au>Zhan, Yang</au><au>Kong, Da‐lu</au><au>Tian, Fei</au><au>Zhao, Peng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RING finger protein 128 (RNF128) regulates malignant biological behaviors of colorectal cancer cells via PI3K/AKT signaling pathway</atitle><jtitle>Cell biology international</jtitle><date>2022-10</date><risdate>2022</risdate><volume>46</volume><issue>10</issue><spage>1604</spage><epage>1611</epage><pages>1604-1611</pages><issn>1065-6995</issn><eissn>1095-8355</eissn><abstract>This study was designed and conducted to clarify the impact of RNF128 expression on malignant biological behaviors of colorectal cancer (CRC) cells and the underlying mechanism. The expression of RNF128 in CRC tissues was analyzed using mRNA sequencing data of TCGA database and was validated by Western blot assay. The experimental studies on biological functions of RNF128 in vitro were conducted to assess its impact on the proliferation, apoptosis, and metastasis of CRC cells. Furthermore, tumor xenograft models in nude mice were established to investigate the relationship between RNF128 expression and tumor growth in vivo. The expression levels of both RNF128 mRNA and protein were significantly increased in CRC tissues (p < .001). The knockdown of RNF128 markedly suppressed the malignant phenotype of HCT116 and SW480 cells in vitro, including cell growth, antiapoptosis, migration, and invasion (p < .001). On the other hand, knockdown of RNF128 exerted a remarkable effect on the growth inhibition of tumor xenografts in vivo (p < .001). Further investigation revealed that RNF128 knockdown lead to a significant decrease in the expression of p‐AKT and p‐PI3K protein. More importantly, the proliferative, antiapoptotic, metastatic abilities of RNF128‐knockdown cells were markedly increased by 740 Y‐P treatment (p < .001). These findings further suggested that PI3K/AKT signaling pathway played a key role in RNF128‐mediated aggressive phenotype of CRC cells. RNF128 functions as a tumor promoter in the pathogenesis of CRC via regulating PI3K/AKT pathway, and it could be a valuable target for CRC treatment.</abstract><cop>London</cop><pub>Wiley Subscription Services, Inc</pub><doi>10.1002/cbin.11835</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-5766-7039</orcidid></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Animal models Apoptosis Cell culture Cell migration Cell proliferation Colorectal cancer Colorectal carcinoma Kinases Metastases mRNA oncogenesis Phenotypes PI3K/AKT signaling progression Proteins RING finger proteins Signal transduction the RING finger protein 128 (RNF128) Xenografts |
| title | RING finger protein 128 (RNF128) regulates malignant biological behaviors of colorectal cancer cells via PI3K/AKT signaling pathway |
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