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LncRNA CTC-497E21.4 promotes the progression of gastric cancer via modulating miR-22/NET1 axis through RhoA signaling pathway
Background Long non-coding RNAs (lncRNAs) have emerged as important roles in gastric cancer (GC). However, the role of the dysregulated lncRNAs in GC remained large unknown. We investigated the clinical significance, biological function and mechanism of CTC-497E21.4 in GC. Methods Firstly, RTFQ-PCR...
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| Published in: | Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association 2020-03, Vol.23 (2), p.228-240 |
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| container_title | Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association |
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| creator | Zong, Wei Feng, Wei Jiang, Yun Cao, Yaning Ke, Yuchen Shi, Xin Ju, Shaoqing Cong, Hui Wang, Xudong Cui, Ming Jing, Rongrong |
| description | Background
Long non-coding RNAs (lncRNAs) have emerged as important roles in gastric cancer (GC). However, the role of the dysregulated lncRNAs in GC remained large unknown. We investigated the clinical significance, biological function and mechanism of CTC-497E21.4 in GC.
Methods
Firstly, RTFQ-PCR was used to detect the expression of CTC-497E21.4 in GC. Furthermore, knockdown of CTC-497E21.4 was conducted to assess the effect of CTC-497E21.4 in vitro and vivo. Subcellular localization of CTC-497E21.4 was determined by nuclear plasmolysis PCR and FISH. We also predicted CTC-497E21.4 binding miRNAs and downstream target genes and evaluated its regulation of miR-22 by acting as a ceRNA.
Result
CTC-497E21.4 was upregulated in GC tissues and GC cell lines (
P
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| doi_str_mv | 10.1007/s10120-019-00998-w |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2281109526</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2358710100</sourcerecordid><originalsourceid>FETCH-LOGICAL-c470t-d664eef3a776042c9241554741cc842a22cd6690c75478d1a7c447c2627c88e13</originalsourceid><addsrcrecordid>eNp9kc1OGzEURi0EAkp5ARaVJTZsDPd6POPxMopCWykCKUrXlnGcidHMOLVnmrLou9dpgEpddOW_c79r-xByhXCLAPIuISAHBqgYgFI12x2RcxRFxYoCyuO3OVd4Rj6k9AyApcLqlJwVKEpUip-TX_PeLh4mdLqcMqHkjOOtoNsYujC4RIeN2y-a6FLyoadhTRuThugttaa3LtIf3tAurMbWDL5vaOcXjPO7h9kSqfnp9wkxjM2GLjZhQpNvetPuua0ZNjvz8pGcrE2b3OXreEG-3c-W0y9s_vj563QyZ1ZIGNiqqoRz68JIWYHgVnGBZSmkQGtrwQ3nNiMKrMyb9QqNtEJIyysubV07LC7IzSE3P-b76NKgO5-sa1vTuzAmzXmNCKrkVUav_0GfwxjztTNVlLXMfw6QKX6gbAwpRbfW2-g7E180gt7L0Qc5OsvRf-ToXS769Bo9PnVu9V7yZiMDxQFI-ahvXPzb-z-xvwH-rJd3</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2358710100</pqid></control><display><type>article</type><title>LncRNA CTC-497E21.4 promotes the progression of gastric cancer via modulating miR-22/NET1 axis through RhoA signaling pathway</title><source>Springer Nature</source><creator>Zong, Wei ; Feng, Wei ; Jiang, Yun ; Cao, Yaning ; Ke, Yuchen ; Shi, Xin ; Ju, Shaoqing ; Cong, Hui ; Wang, Xudong ; Cui, Ming ; Jing, Rongrong</creator><creatorcontrib>Zong, Wei ; Feng, Wei ; Jiang, Yun ; Cao, Yaning ; Ke, Yuchen ; Shi, Xin ; Ju, Shaoqing ; Cong, Hui ; Wang, Xudong ; Cui, Ming ; Jing, Rongrong</creatorcontrib><description>Background
Long non-coding RNAs (lncRNAs) have emerged as important roles in gastric cancer (GC). However, the role of the dysregulated lncRNAs in GC remained large unknown. We investigated the clinical significance, biological function and mechanism of CTC-497E21.4 in GC.
Methods
Firstly, RTFQ-PCR was used to detect the expression of CTC-497E21.4 in GC. Furthermore, knockdown of CTC-497E21.4 was conducted to assess the effect of CTC-497E21.4 in vitro and vivo. Subcellular localization of CTC-497E21.4 was determined by nuclear plasmolysis PCR and FISH. We also predicted CTC-497E21.4 binding miRNAs and downstream target genes and evaluated its regulation of miR-22 by acting as a ceRNA.
Result
CTC-497E21.4 was upregulated in GC tissues and GC cell lines (
P
< 0.05), and the expression was associated with depth of invasion, lymph node metastasis, and neurological invasion. Besides, knockdown of CTC-497E21.4 inhibited cell proliferation, invasion and promoted cell cycle arrest in vitro and inhibited tumorigenesis in vivo. Mechanistic investigations indicated that CTC-497E21.4 acted as a ceRNA for miR-22 and regulated NET1 expression. CTC-497E21.4/miR-22-3p/NET1 participated in the RhoA signaling pathway in the GC progression.
Conclusion
CTC-497E21.4 competed with miR-22 to regulate the expression of NET1 and regulated the malignant progression of GC through RhoA signaling pathway.</description><identifier>ISSN: 1436-3291</identifier><identifier>EISSN: 1436-3305</identifier><identifier>DOI: 10.1007/s10120-019-00998-w</identifier><identifier>PMID: 31451992</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Abdominal Surgery ; Animals ; Apoptosis ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Cancer Research ; Case-Control Studies ; Cell Cycle ; Cell Proliferation ; Disease Progression ; Female ; Follow-Up Studies ; Gastric cancer ; Gastroenterology ; Gene Expression Regulation, Neoplastic ; Gene regulation ; Humans ; Kinases ; Localization ; Lymph nodes ; Lymphatic Metastasis ; Male ; Medicine ; Medicine & Public Health ; Metastases ; Mice ; Mice, Nude ; MicroRNAs - genetics ; Middle Aged ; Neoplasm Invasiveness ; Non-coding RNA ; Oncogene Proteins - genetics ; Oncogene Proteins - metabolism ; Oncology ; Original Article ; Plasmolysis ; Prognosis ; rhoA GTP-Binding Protein - genetics ; rhoA GTP-Binding Protein - metabolism ; RhoA protein ; RNA, Long Noncoding - genetics ; Signal Transduction ; Stomach Neoplasms - genetics ; Stomach Neoplasms - metabolism ; Stomach Neoplasms - pathology ; Surgical Oncology ; Survival Rate ; Tumor Cells, Cultured ; Tumorigenesis ; Xenograft Model Antitumor Assays</subject><ispartof>Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2020-03, Vol.23 (2), p.228-240</ispartof><rights>The International Gastric Cancer Association and The Japanese Gastric Cancer Association 2019</rights><rights>The International Gastric Cancer Association and The Japanese Gastric Cancer Association 2019.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-d664eef3a776042c9241554741cc842a22cd6690c75478d1a7c447c2627c88e13</citedby><cites>FETCH-LOGICAL-c470t-d664eef3a776042c9241554741cc842a22cd6690c75478d1a7c447c2627c88e13</cites><orcidid>0000-0002-3750-6916</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31451992$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zong, Wei</creatorcontrib><creatorcontrib>Feng, Wei</creatorcontrib><creatorcontrib>Jiang, Yun</creatorcontrib><creatorcontrib>Cao, Yaning</creatorcontrib><creatorcontrib>Ke, Yuchen</creatorcontrib><creatorcontrib>Shi, Xin</creatorcontrib><creatorcontrib>Ju, Shaoqing</creatorcontrib><creatorcontrib>Cong, Hui</creatorcontrib><creatorcontrib>Wang, Xudong</creatorcontrib><creatorcontrib>Cui, Ming</creatorcontrib><creatorcontrib>Jing, Rongrong</creatorcontrib><title>LncRNA CTC-497E21.4 promotes the progression of gastric cancer via modulating miR-22/NET1 axis through RhoA signaling pathway</title><title>Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association</title><addtitle>Gastric Cancer</addtitle><addtitle>Gastric Cancer</addtitle><description>Background
Long non-coding RNAs (lncRNAs) have emerged as important roles in gastric cancer (GC). However, the role of the dysregulated lncRNAs in GC remained large unknown. We investigated the clinical significance, biological function and mechanism of CTC-497E21.4 in GC.
Methods
Firstly, RTFQ-PCR was used to detect the expression of CTC-497E21.4 in GC. Furthermore, knockdown of CTC-497E21.4 was conducted to assess the effect of CTC-497E21.4 in vitro and vivo. Subcellular localization of CTC-497E21.4 was determined by nuclear plasmolysis PCR and FISH. We also predicted CTC-497E21.4 binding miRNAs and downstream target genes and evaluated its regulation of miR-22 by acting as a ceRNA.
Result
CTC-497E21.4 was upregulated in GC tissues and GC cell lines (
P
< 0.05), and the expression was associated with depth of invasion, lymph node metastasis, and neurological invasion. Besides, knockdown of CTC-497E21.4 inhibited cell proliferation, invasion and promoted cell cycle arrest in vitro and inhibited tumorigenesis in vivo. Mechanistic investigations indicated that CTC-497E21.4 acted as a ceRNA for miR-22 and regulated NET1 expression. CTC-497E21.4/miR-22-3p/NET1 participated in the RhoA signaling pathway in the GC progression.
Conclusion
CTC-497E21.4 competed with miR-22 to regulate the expression of NET1 and regulated the malignant progression of GC through RhoA signaling pathway.</description><subject>Abdominal Surgery</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Cancer Research</subject><subject>Case-Control Studies</subject><subject>Cell Cycle</subject><subject>Cell Proliferation</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Gastric cancer</subject><subject>Gastroenterology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene regulation</subject><subject>Humans</subject><subject>Kinases</subject><subject>Localization</subject><subject>Lymph nodes</subject><subject>Lymphatic Metastasis</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness</subject><subject>Non-coding RNA</subject><subject>Oncogene Proteins - genetics</subject><subject>Oncogene Proteins - metabolism</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Plasmolysis</subject><subject>Prognosis</subject><subject>rhoA GTP-Binding Protein - genetics</subject><subject>rhoA GTP-Binding Protein - metabolism</subject><subject>RhoA protein</subject><subject>RNA, Long Noncoding - genetics</subject><subject>Signal Transduction</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach Neoplasms - pathology</subject><subject>Surgical Oncology</subject><subject>Survival Rate</subject><subject>Tumor Cells, Cultured</subject><subject>Tumorigenesis</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1436-3291</issn><issn>1436-3305</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp9kc1OGzEURi0EAkp5ARaVJTZsDPd6POPxMopCWykCKUrXlnGcidHMOLVnmrLou9dpgEpddOW_c79r-xByhXCLAPIuISAHBqgYgFI12x2RcxRFxYoCyuO3OVd4Rj6k9AyApcLqlJwVKEpUip-TX_PeLh4mdLqcMqHkjOOtoNsYujC4RIeN2y-a6FLyoadhTRuThugttaa3LtIf3tAurMbWDL5vaOcXjPO7h9kSqfnp9wkxjM2GLjZhQpNvetPuua0ZNjvz8pGcrE2b3OXreEG-3c-W0y9s_vj563QyZ1ZIGNiqqoRz68JIWYHgVnGBZSmkQGtrwQ3nNiMKrMyb9QqNtEJIyysubV07LC7IzSE3P-b76NKgO5-sa1vTuzAmzXmNCKrkVUav_0GfwxjztTNVlLXMfw6QKX6gbAwpRbfW2-g7E180gt7L0Qc5OsvRf-ToXS769Bo9PnVu9V7yZiMDxQFI-ahvXPzb-z-xvwH-rJd3</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Zong, Wei</creator><creator>Feng, Wei</creator><creator>Jiang, Yun</creator><creator>Cao, Yaning</creator><creator>Ke, Yuchen</creator><creator>Shi, Xin</creator><creator>Ju, Shaoqing</creator><creator>Cong, Hui</creator><creator>Wang, Xudong</creator><creator>Cui, Ming</creator><creator>Jing, Rongrong</creator><general>Springer Singapore</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3750-6916</orcidid></search><sort><creationdate>20200301</creationdate><title>LncRNA CTC-497E21.4 promotes the progression of gastric cancer via modulating miR-22/NET1 axis through RhoA signaling pathway</title><author>Zong, Wei ; Feng, Wei ; Jiang, Yun ; Cao, Yaning ; Ke, Yuchen ; Shi, Xin ; Ju, Shaoqing ; Cong, Hui ; Wang, Xudong ; Cui, Ming ; Jing, Rongrong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-d664eef3a776042c9241554741cc842a22cd6690c75478d1a7c447c2627c88e13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Abdominal Surgery</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Cancer Research</topic><topic>Case-Control Studies</topic><topic>Cell Cycle</topic><topic>Cell Proliferation</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Gastric cancer</topic><topic>Gastroenterology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene regulation</topic><topic>Humans</topic><topic>Kinases</topic><topic>Localization</topic><topic>Lymph nodes</topic><topic>Lymphatic Metastasis</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness</topic><topic>Non-coding RNA</topic><topic>Oncogene Proteins - genetics</topic><topic>Oncogene Proteins - metabolism</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Plasmolysis</topic><topic>Prognosis</topic><topic>rhoA GTP-Binding Protein - genetics</topic><topic>rhoA GTP-Binding Protein - metabolism</topic><topic>RhoA protein</topic><topic>RNA, Long Noncoding - genetics</topic><topic>Signal Transduction</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach Neoplasms - pathology</topic><topic>Surgical Oncology</topic><topic>Survival Rate</topic><topic>Tumor Cells, Cultured</topic><topic>Tumorigenesis</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zong, Wei</creatorcontrib><creatorcontrib>Feng, Wei</creatorcontrib><creatorcontrib>Jiang, Yun</creatorcontrib><creatorcontrib>Cao, Yaning</creatorcontrib><creatorcontrib>Ke, Yuchen</creatorcontrib><creatorcontrib>Shi, Xin</creatorcontrib><creatorcontrib>Ju, Shaoqing</creatorcontrib><creatorcontrib>Cong, Hui</creatorcontrib><creatorcontrib>Wang, Xudong</creatorcontrib><creatorcontrib>Cui, Ming</creatorcontrib><creatorcontrib>Jing, Rongrong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zong, Wei</au><au>Feng, Wei</au><au>Jiang, Yun</au><au>Cao, Yaning</au><au>Ke, Yuchen</au><au>Shi, Xin</au><au>Ju, Shaoqing</au><au>Cong, Hui</au><au>Wang, Xudong</au><au>Cui, Ming</au><au>Jing, Rongrong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA CTC-497E21.4 promotes the progression of gastric cancer via modulating miR-22/NET1 axis through RhoA signaling pathway</atitle><jtitle>Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association</jtitle><stitle>Gastric Cancer</stitle><addtitle>Gastric Cancer</addtitle><date>2020-03-01</date><risdate>2020</risdate><volume>23</volume><issue>2</issue><spage>228</spage><epage>240</epage><pages>228-240</pages><issn>1436-3291</issn><eissn>1436-3305</eissn><abstract>Background
Long non-coding RNAs (lncRNAs) have emerged as important roles in gastric cancer (GC). However, the role of the dysregulated lncRNAs in GC remained large unknown. We investigated the clinical significance, biological function and mechanism of CTC-497E21.4 in GC.
Methods
Firstly, RTFQ-PCR was used to detect the expression of CTC-497E21.4 in GC. Furthermore, knockdown of CTC-497E21.4 was conducted to assess the effect of CTC-497E21.4 in vitro and vivo. Subcellular localization of CTC-497E21.4 was determined by nuclear plasmolysis PCR and FISH. We also predicted CTC-497E21.4 binding miRNAs and downstream target genes and evaluated its regulation of miR-22 by acting as a ceRNA.
Result
CTC-497E21.4 was upregulated in GC tissues and GC cell lines (
P
< 0.05), and the expression was associated with depth of invasion, lymph node metastasis, and neurological invasion. Besides, knockdown of CTC-497E21.4 inhibited cell proliferation, invasion and promoted cell cycle arrest in vitro and inhibited tumorigenesis in vivo. Mechanistic investigations indicated that CTC-497E21.4 acted as a ceRNA for miR-22 and regulated NET1 expression. CTC-497E21.4/miR-22-3p/NET1 participated in the RhoA signaling pathway in the GC progression.
Conclusion
CTC-497E21.4 competed with miR-22 to regulate the expression of NET1 and regulated the malignant progression of GC through RhoA signaling pathway.</abstract><cop>Singapore</cop><pub>Springer Singapore</pub><pmid>31451992</pmid><doi>10.1007/s10120-019-00998-w</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-3750-6916</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Abdominal Surgery Animals Apoptosis Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Cancer Research Case-Control Studies Cell Cycle Cell Proliferation Disease Progression Female Follow-Up Studies Gastric cancer Gastroenterology Gene Expression Regulation, Neoplastic Gene regulation Humans Kinases Localization Lymph nodes Lymphatic Metastasis Male Medicine Medicine & Public Health Metastases Mice Mice, Nude MicroRNAs - genetics Middle Aged Neoplasm Invasiveness Non-coding RNA Oncogene Proteins - genetics Oncogene Proteins - metabolism Oncology Original Article Plasmolysis Prognosis rhoA GTP-Binding Protein - genetics rhoA GTP-Binding Protein - metabolism RhoA protein RNA, Long Noncoding - genetics Signal Transduction Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Surgical Oncology Survival Rate Tumor Cells, Cultured Tumorigenesis Xenograft Model Antitumor Assays |
| title | LncRNA CTC-497E21.4 promotes the progression of gastric cancer via modulating miR-22/NET1 axis through RhoA signaling pathway |
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