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Ribosomal protein RPL5 regulates colon cancer cell proliferation and migration through MAPK/ERK signaling pathway
Abnormal expression of ribosomal proteins has an important regulatory effect on the progression of cancer. RPL5 is involved in the progression of various malignancies, however, the role of RPL5 in colon cancer remains is still unclear. Data from TCGA and GTEx databases were used to analyze the RPL5...
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Published in: | BMC cell biology 2022-11, Vol.23 (1), p.1-48, Article 48 |
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description | Abnormal expression of ribosomal proteins has an important regulatory effect on the progression of cancer. RPL5 is involved in the progression of various malignancies, however, the role of RPL5 in colon cancer remains is still unclear. Data from TCGA and GTEx databases were used to analyze the RPL5 expression in pan-cancer. The expression level of RPL5 in clinical colon cancer tissue samples and human colon cancer cell lines was detected by western blotting; siRNA targeting RPL5 was designed, and its interference efficiency was verified by western blotting and RT-qPCR; CCK8 assay, clone formation assay, cell cycle assay, and cell scratch assay were used to observe the effect of RPL5 on colon cancer cell proliferation and migration; the changes of proteins related to MAPK/ERK signaling pathway were also detected using western blotting. The expression level of RPL5 in colon cancer tissues and cell lines was significantly higher than that in adjacent tissues and NCM460 cells, respectively, and its expression level was higher in HCT116 cells and RKO cells. Knockdown of RPL5 significantly inhibited the proliferation and migration of HCT16 and RKO cells, and arrested the cell cycle in G0/G1 phase. Mechanistic studies revealed that the expression of p-MEK1/2, p-ERK, c-Myc were down-regulated, and the expression of FOXO3 was up-regulated after down-regulation of RPL5, ERK activator (TBHQ) could partially reverse the above-mentioned effects caused by siRPL5. Moreover, TBHQ could partially reverse the inhibitory effect of siRPL5 on the proliferation and migration of colon cancer cells. Collectively, RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway. RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway, which may serve as a novel therapeutic target for cancers in which MAPK/ERK signaling is a dominant feature. |
doi_str_mv | 10.1186/s12860-022-00448-z |
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RPL5 is involved in the progression of various malignancies, however, the role of RPL5 in colon cancer remains is still unclear. Data from TCGA and GTEx databases were used to analyze the RPL5 expression in pan-cancer. The expression level of RPL5 in clinical colon cancer tissue samples and human colon cancer cell lines was detected by western blotting; siRNA targeting RPL5 was designed, and its interference efficiency was verified by western blotting and RT-qPCR; CCK8 assay, clone formation assay, cell cycle assay, and cell scratch assay were used to observe the effect of RPL5 on colon cancer cell proliferation and migration; the changes of proteins related to MAPK/ERK signaling pathway were also detected using western blotting. The expression level of RPL5 in colon cancer tissues and cell lines was significantly higher than that in adjacent tissues and NCM460 cells, respectively, and its expression level was higher in HCT116 cells and RKO cells. Knockdown of RPL5 significantly inhibited the proliferation and migration of HCT16 and RKO cells, and arrested the cell cycle in G0/G1 phase. Mechanistic studies revealed that the expression of p-MEK1/2, p-ERK, c-Myc were down-regulated, and the expression of FOXO3 was up-regulated after down-regulation of RPL5, ERK activator (TBHQ) could partially reverse the above-mentioned effects caused by siRPL5. Moreover, TBHQ could partially reverse the inhibitory effect of siRPL5 on the proliferation and migration of colon cancer cells. Collectively, RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway. RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway, which may serve as a novel therapeutic target for cancers in which MAPK/ERK signaling is a dominant feature.</description><identifier>ISSN: 2661-8850</identifier><identifier>EISSN: 2661-8850</identifier><identifier>EISSN: 1471-2121</identifier><identifier>DOI: 10.1186/s12860-022-00448-z</identifier><language>eng</language><publisher>London: BioMed Central Ltd</publisher><subject>c-Myc protein ; Cell adhesion & migration ; Cell cycle ; Cell growth ; Cell migration ; Cell proliferation ; Colon cancer ; Colorectal cancer ; Development and progression ; Extracellular signal-regulated kinase ; FOXO3 protein ; G1 phase ; Gene expression ; Health aspects ; Malignancy ; Manufacturers ; MAP kinase ; MAPK/ERK signaling pathway ; Medical prognosis ; Migration ; Mitogen-activated protein kinases ; Myc protein ; Physiological aspects ; Proliferation ; Protein synthesis ; Proteins ; Ribosomal protein RPL5 ; Ribosomal proteins ; Signal transduction ; siRNA ; t-Butylhydroquinone ; Therapeutic targets ; Tumor cell lines ; Tumors ; Variance analysis ; Western blotting ; Wound healing</subject><ispartof>BMC cell biology, 2022-11, Vol.23 (1), p.1-48, Article 48</ispartof><rights>COPYRIGHT 2022 BioMed Central Ltd.</rights><rights>2022. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c574t-f274f78479083837398e2b2af046e9119b3dc19cef9bcf143604f38cdcd0ae753</citedby><cites>FETCH-LOGICAL-c574t-f274f78479083837398e2b2af046e9119b3dc19cef9bcf143604f38cdcd0ae753</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9670436/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9670436/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,36992,53769,53771</link.rule.ids></links><search><creatorcontrib>Zhang, Huahua</creatorcontrib><creatorcontrib>Liu, Junli</creatorcontrib><creatorcontrib>Dang, Qingqing</creatorcontrib><creatorcontrib>Wang, Xueru</creatorcontrib><creatorcontrib>Chen, Jie</creatorcontrib><creatorcontrib>Lin, Xiaoyin</creatorcontrib><creatorcontrib>Yang, Na</creatorcontrib><creatorcontrib>Du, Juan</creatorcontrib><creatorcontrib>Shi, Haiyan</creatorcontrib><creatorcontrib>Liu, Yong</creatorcontrib><creatorcontrib>Han, Jiming</creatorcontrib><title>Ribosomal protein RPL5 regulates colon cancer cell proliferation and migration through MAPK/ERK signaling pathway</title><title>BMC cell biology</title><description>Abnormal expression of ribosomal proteins has an important regulatory effect on the progression of cancer. RPL5 is involved in the progression of various malignancies, however, the role of RPL5 in colon cancer remains is still unclear. Data from TCGA and GTEx databases were used to analyze the RPL5 expression in pan-cancer. The expression level of RPL5 in clinical colon cancer tissue samples and human colon cancer cell lines was detected by western blotting; siRNA targeting RPL5 was designed, and its interference efficiency was verified by western blotting and RT-qPCR; CCK8 assay, clone formation assay, cell cycle assay, and cell scratch assay were used to observe the effect of RPL5 on colon cancer cell proliferation and migration; the changes of proteins related to MAPK/ERK signaling pathway were also detected using western blotting. The expression level of RPL5 in colon cancer tissues and cell lines was significantly higher than that in adjacent tissues and NCM460 cells, respectively, and its expression level was higher in HCT116 cells and RKO cells. Knockdown of RPL5 significantly inhibited the proliferation and migration of HCT16 and RKO cells, and arrested the cell cycle in G0/G1 phase. Mechanistic studies revealed that the expression of p-MEK1/2, p-ERK, c-Myc were down-regulated, and the expression of FOXO3 was up-regulated after down-regulation of RPL5, ERK activator (TBHQ) could partially reverse the above-mentioned effects caused by siRPL5. Moreover, TBHQ could partially reverse the inhibitory effect of siRPL5 on the proliferation and migration of colon cancer cells. Collectively, RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway. RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway, which may serve as a novel therapeutic target for cancers in which MAPK/ERK signaling is a dominant feature.</description><subject>c-Myc protein</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Development and progression</subject><subject>Extracellular signal-regulated kinase</subject><subject>FOXO3 protein</subject><subject>G1 phase</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>Malignancy</subject><subject>Manufacturers</subject><subject>MAP kinase</subject><subject>MAPK/ERK signaling pathway</subject><subject>Medical prognosis</subject><subject>Migration</subject><subject>Mitogen-activated protein kinases</subject><subject>Myc protein</subject><subject>Physiological aspects</subject><subject>Proliferation</subject><subject>Protein synthesis</subject><subject>Proteins</subject><subject>Ribosomal protein RPL5</subject><subject>Ribosomal proteins</subject><subject>Signal transduction</subject><subject>siRNA</subject><subject>t-Butylhydroquinone</subject><subject>Therapeutic targets</subject><subject>Tumor cell lines</subject><subject>Tumors</subject><subject>Variance analysis</subject><subject>Western blotting</subject><subject>Wound healing</subject><issn>2661-8850</issn><issn>2661-8850</issn><issn>1471-2121</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkk1vEzEQhlcIJKrSP8BpJS5w2NZfsb0XpKhqIWoQVYCz5XjHG0e769T2Au2vx8lGqEHIB9szz7wev5qieIvRJcaSX0VMJEcVIqRCiDFZPb0ozgjnuJJyhl4-O78uLmLcIoQIpnWNyVnxsHJrH32vu3IXfAI3lKv75awM0I6dThBL4zs_lEYPBkJpoDuAnbMQdHI5o4em7F17vKVN8GO7Kb_M7--ublZ3ZXTtoDs3tOVOp80v_fimeGV1F-HiuJ8XP25vvl9_rpZfPy2u58vKzARLlSWCWSGZqJGkkgpaSyBroi1iHGqM6zVtDK4N2HptLGaUI2apNI1pkAYxo-fFYtJtvN6qXXC9Do_Ka6cOAR9apUNypgNFJGuwMQy4tayuiRZCChCYE2spCJ61Pk5au3HdQ2NgSEF3J6KnmcFtVOt_qpoLlFvLAu-PAsE_jBCT6l3cm6kH8GNURFDBOENk3_e7f9CtH0P2cKIExRQ_o1qdP-AG6_O7Zi-q5oJwKXF2LlOX_6HyaqB3xg9gXY6fFHw4KchMgt-p1WOMavFtdcqSiTXBxxjA_vUDI7UfTDUNpsqDqQ6DqZ7oHxFE1PI</recordid><startdate>20221116</startdate><enddate>20221116</enddate><creator>Zhang, Huahua</creator><creator>Liu, 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Wang, Xueru ; Chen, Jie ; Lin, Xiaoyin ; Yang, Na ; Du, Juan ; Shi, Haiyan ; Liu, Yong ; Han, Jiming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c574t-f274f78479083837398e2b2af046e9119b3dc19cef9bcf143604f38cdcd0ae753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>c-Myc protein</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Colon cancer</topic><topic>Colorectal cancer</topic><topic>Development and progression</topic><topic>Extracellular signal-regulated kinase</topic><topic>FOXO3 protein</topic><topic>G1 phase</topic><topic>Gene expression</topic><topic>Health aspects</topic><topic>Malignancy</topic><topic>Manufacturers</topic><topic>MAP kinase</topic><topic>MAPK/ERK signaling pathway</topic><topic>Medical prognosis</topic><topic>Migration</topic><topic>Mitogen-activated protein kinases</topic><topic>Myc protein</topic><topic>Physiological aspects</topic><topic>Proliferation</topic><topic>Protein synthesis</topic><topic>Proteins</topic><topic>Ribosomal protein RPL5</topic><topic>Ribosomal proteins</topic><topic>Signal transduction</topic><topic>siRNA</topic><topic>t-Butylhydroquinone</topic><topic>Therapeutic targets</topic><topic>Tumor cell lines</topic><topic>Tumors</topic><topic>Variance analysis</topic><topic>Western blotting</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Huahua</creatorcontrib><creatorcontrib>Liu, Junli</creatorcontrib><creatorcontrib>Dang, Qingqing</creatorcontrib><creatorcontrib>Wang, Xueru</creatorcontrib><creatorcontrib>Chen, Jie</creatorcontrib><creatorcontrib>Lin, Xiaoyin</creatorcontrib><creatorcontrib>Yang, Na</creatorcontrib><creatorcontrib>Du, 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Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>BMC cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Huahua</au><au>Liu, Junli</au><au>Dang, Qingqing</au><au>Wang, Xueru</au><au>Chen, Jie</au><au>Lin, Xiaoyin</au><au>Yang, Na</au><au>Du, Juan</au><au>Shi, Haiyan</au><au>Liu, Yong</au><au>Han, Jiming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ribosomal protein RPL5 regulates colon cancer cell proliferation and migration through MAPK/ERK signaling pathway</atitle><jtitle>BMC cell biology</jtitle><date>2022-11-16</date><risdate>2022</risdate><volume>23</volume><issue>1</issue><spage>1</spage><epage>48</epage><pages>1-48</pages><artnum>48</artnum><issn>2661-8850</issn><eissn>2661-8850</eissn><eissn>1471-2121</eissn><abstract>Abnormal expression of ribosomal proteins has an important regulatory effect on the progression of cancer. RPL5 is involved in the progression of various malignancies, however, the role of RPL5 in colon cancer remains is still unclear. Data from TCGA and GTEx databases were used to analyze the RPL5 expression in pan-cancer. The expression level of RPL5 in clinical colon cancer tissue samples and human colon cancer cell lines was detected by western blotting; siRNA targeting RPL5 was designed, and its interference efficiency was verified by western blotting and RT-qPCR; CCK8 assay, clone formation assay, cell cycle assay, and cell scratch assay were used to observe the effect of RPL5 on colon cancer cell proliferation and migration; the changes of proteins related to MAPK/ERK signaling pathway were also detected using western blotting. The expression level of RPL5 in colon cancer tissues and cell lines was significantly higher than that in adjacent tissues and NCM460 cells, respectively, and its expression level was higher in HCT116 cells and RKO cells. Knockdown of RPL5 significantly inhibited the proliferation and migration of HCT16 and RKO cells, and arrested the cell cycle in G0/G1 phase. Mechanistic studies revealed that the expression of p-MEK1/2, p-ERK, c-Myc were down-regulated, and the expression of FOXO3 was up-regulated after down-regulation of RPL5, ERK activator (TBHQ) could partially reverse the above-mentioned effects caused by siRPL5. Moreover, TBHQ could partially reverse the inhibitory effect of siRPL5 on the proliferation and migration of colon cancer cells. Collectively, RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway. RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway, which may serve as a novel therapeutic target for cancers in which MAPK/ERK signaling is a dominant feature.</abstract><cop>London</cop><pub>BioMed Central Ltd</pub><doi>10.1186/s12860-022-00448-z</doi><oa>free_for_read</oa></addata></record> |
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subjects | c-Myc protein Cell adhesion & migration Cell cycle Cell growth Cell migration Cell proliferation Colon cancer Colorectal cancer Development and progression Extracellular signal-regulated kinase FOXO3 protein G1 phase Gene expression Health aspects Malignancy Manufacturers MAP kinase MAPK/ERK signaling pathway Medical prognosis Migration Mitogen-activated protein kinases Myc protein Physiological aspects Proliferation Protein synthesis Proteins Ribosomal protein RPL5 Ribosomal proteins Signal transduction siRNA t-Butylhydroquinone Therapeutic targets Tumor cell lines Tumors Variance analysis Western blotting Wound healing |
title | Ribosomal protein RPL5 regulates colon cancer cell proliferation and migration through MAPK/ERK signaling pathway |
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