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Inhibition of Ribosomal RNA Processing 15 Homolog (RRP15) Suppressed Tumor Growth, Invasion and Epithelial to Mesenchymal Transition (EMT) of Colon Cancer
Although ribosomal RNA processing 15 Homolog (RRP15) has been implicated in the occurrence of various cancers and is considered a potential target for cancer treatment, its significance in colon cancer (CC) is unclear. Thus, this present study aims to determine RRP15 expression and biological functi...
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Published in: | International journal of molecular sciences 2023-02, Vol.24 (4), p.3528 |
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description | Although ribosomal RNA processing 15 Homolog (RRP15) has been implicated in the occurrence of various cancers and is considered a potential target for cancer treatment, its significance in colon cancer (CC) is unclear. Thus, this present study aims to determine RRP15 expression and biological function in CC. The results demonstrated a strong expression of RRP15 in CC compared to normal colon specimens, which was correlated with poorer overall survival (OS) and disease-free survival (DFS) of the patients. Among the nine investigated CC cell lines, RRP15 demonstrated the highest and lowest expression in HCT15 and HCT116 cells, respectively. In vitro assays demonstrated that the knockdown of RRP15 inhibited the growth, colony-forming ability and invasive ability of the CC cells whereas its overexpression enhanced the above oncogenic function. Moreover, subcutaneous tumors in nude mice showed that RRP15 knockdown inhibited the CC growth while its overexpression enhanced their growth. Additionally, the knockdown of RRP15 inhibited the epithelial-mesenchymal transition (EMT), whereas overexpression of RRP15 promoted the EMT process in CC. Collectively, inhibition of RRP15 suppressed tumor growth, invasion and EMT of CC, and might be considered a promising therapeutic target for treating CC. |
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Thus, this present study aims to determine RRP15 expression and biological function in CC. The results demonstrated a strong expression of RRP15 in CC compared to normal colon specimens, which was correlated with poorer overall survival (OS) and disease-free survival (DFS) of the patients. Among the nine investigated CC cell lines, RRP15 demonstrated the highest and lowest expression in HCT15 and HCT116 cells, respectively. In vitro assays demonstrated that the knockdown of RRP15 inhibited the growth, colony-forming ability and invasive ability of the CC cells whereas its overexpression enhanced the above oncogenic function. Moreover, subcutaneous tumors in nude mice showed that RRP15 knockdown inhibited the CC growth while its overexpression enhanced their growth. Additionally, the knockdown of RRP15 inhibited the epithelial-mesenchymal transition (EMT), whereas overexpression of RRP15 promoted the EMT process in CC. Collectively, inhibition of RRP15 suppressed tumor growth, invasion and EMT of CC, and might be considered a promising therapeutic target for treating CC.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms24043528</identifier><identifier>PMID: 36834940</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Apoptosis ; Biosynthesis ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation - genetics ; Colon cancer ; Colonic Neoplasms - genetics ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Colorectal cancer ; DNA damage ; Epithelial-Mesenchymal Transition - genetics ; Gene Expression Regulation, Neoplastic ; Homology ; Humans ; Liver cancer ; Medical prognosis ; Melanoma ; Mesenchyme ; Mice ; Mice, Nude ; Patients ; Plasmids ; Protein synthesis ; Proteins ; Ribosomal Proteins - metabolism ; RNA processing ; RNA Processing, Post-Transcriptional ; RNA, Ribosomal ; rRNA ; Senescence ; Survival ; Therapeutic targets ; Tumorigenesis ; Tumors</subject><ispartof>International journal of molecular sciences, 2023-02, Vol.24 (4), p.3528</ispartof><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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Thus, this present study aims to determine RRP15 expression and biological function in CC. The results demonstrated a strong expression of RRP15 in CC compared to normal colon specimens, which was correlated with poorer overall survival (OS) and disease-free survival (DFS) of the patients. Among the nine investigated CC cell lines, RRP15 demonstrated the highest and lowest expression in HCT15 and HCT116 cells, respectively. In vitro assays demonstrated that the knockdown of RRP15 inhibited the growth, colony-forming ability and invasive ability of the CC cells whereas its overexpression enhanced the above oncogenic function. Moreover, subcutaneous tumors in nude mice showed that RRP15 knockdown inhibited the CC growth while its overexpression enhanced their growth. Additionally, the knockdown of RRP15 inhibited the epithelial-mesenchymal transition (EMT), whereas overexpression of RRP15 promoted the EMT process in CC. Collectively, inhibition of RRP15 suppressed tumor growth, invasion and EMT of CC, and might be considered a promising therapeutic target for treating CC.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biosynthesis</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colorectal cancer</subject><subject>DNA damage</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Homology</subject><subject>Humans</subject><subject>Liver cancer</subject><subject>Medical prognosis</subject><subject>Melanoma</subject><subject>Mesenchyme</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Patients</subject><subject>Plasmids</subject><subject>Protein synthesis</subject><subject>Proteins</subject><subject>Ribosomal Proteins - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deng, Zirong</au><au>Xu, Yun</au><au>Cai, Yuchen</au><au>Lin, Weiling</au><au>Zhang, Libei</au><au>Jiang, Aoqing</au><au>Zhou, Yuhang</au><au>Zhao, Rui</au><au>Zhao, Heyan</au><au>Liu, Zhaoguo</au><au>Yan, Tingdong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of Ribosomal RNA Processing 15 Homolog (RRP15) Suppressed Tumor Growth, Invasion and Epithelial to Mesenchymal Transition (EMT) of Colon Cancer</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2023-02-09</date><risdate>2023</risdate><volume>24</volume><issue>4</issue><spage>3528</spage><pages>3528-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Although ribosomal RNA processing 15 Homolog (RRP15) has been implicated in the occurrence of various cancers and is considered a potential target for cancer treatment, its significance in colon cancer (CC) is unclear. Thus, this present study aims to determine RRP15 expression and biological function in CC. The results demonstrated a strong expression of RRP15 in CC compared to normal colon specimens, which was correlated with poorer overall survival (OS) and disease-free survival (DFS) of the patients. Among the nine investigated CC cell lines, RRP15 demonstrated the highest and lowest expression in HCT15 and HCT116 cells, respectively. In vitro assays demonstrated that the knockdown of RRP15 inhibited the growth, colony-forming ability and invasive ability of the CC cells whereas its overexpression enhanced the above oncogenic function. Moreover, subcutaneous tumors in nude mice showed that RRP15 knockdown inhibited the CC growth while its overexpression enhanced their growth. Additionally, the knockdown of RRP15 inhibited the epithelial-mesenchymal transition (EMT), whereas overexpression of RRP15 promoted the EMT process in CC. 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subjects | Animals Apoptosis Biosynthesis Cell cycle Cell growth Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics Colon cancer Colonic Neoplasms - genetics Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Colorectal cancer DNA damage Epithelial-Mesenchymal Transition - genetics Gene Expression Regulation, Neoplastic Homology Humans Liver cancer Medical prognosis Melanoma Mesenchyme Mice Mice, Nude Patients Plasmids Protein synthesis Proteins Ribosomal Proteins - metabolism RNA processing RNA Processing, Post-Transcriptional RNA, Ribosomal rRNA Senescence Survival Therapeutic targets Tumorigenesis Tumors |
title | Inhibition of Ribosomal RNA Processing 15 Homolog (RRP15) Suppressed Tumor Growth, Invasion and Epithelial to Mesenchymal Transition (EMT) of Colon Cancer |
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