Silencing long noncoding RNA colon cancer-associated transcript-1 upregulates microRNA-34a-5p to promote proliferation and differentiation of osteoblasts in osteoporosis
Long noncoding RNAs (lncRNAs) have been revealed to be related to multiple physiological and pathology processes such as development, carcinogenesis, and osteogenesis. It is reported that lncRNAs might exert function in osteoblast differentiation and bone formation. Here, we determined this study to...
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| Veröffentlicht in: | Cancer gene therapy 2021-11, Vol.28 (10-11), p.1150-1161 |
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| creator | Hu, Fangke Jiang, Chengying Bu, Guoyun Fu, Yiru Yu, Yanfang |
| description | Long noncoding RNAs (lncRNAs) have been revealed to be related to multiple physiological and pathology processes such as development, carcinogenesis, and osteogenesis. It is reported that lncRNAs might exert function in osteoblast differentiation and bone formation. Here, we determined this study to clarify whether lncRNA CCAT1 could regulate osteoblast proliferation and differentiation in ovariectomized rats with osteoporosis. The osteoporosis models were established by bilateral ovariectomy and treated with CCAT1 siRNAs to discuss the effect of CCAT1 on pathological changes and osteocyte apoptosis in ovariectomized rats with osteoporosis. The osteoblasts from ovariectomized rats were cultured in vitro, which were then treated with CCAT1 siRNAs to explore the role of CCAT1 in osteoblast proliferation and differentiation. Moreover, the relationships among CCAT1, miR-34a-5p, and SMURF2 were confirmed. CCAT1 and SMURF2 were amplified while miR-34a-5p expression was inhibited in bone tissues and osteoblasts of ovariectomized rats with osteoporosis. Inhibited CCAT1 improved pathology and restricted osteocyte apoptosis of bone tissues in ovariectomized rats with osteoporosis in vivo, and also enhanced differentiation, mineralization abilities, and proliferation, and suppressed apoptosis of osteoblasts from ovariectomized rats in vitro through upregulating miR-34a-5p expression. LncRNA CCAT1 could competitively bind with miR-34a-5p to prevent the degradation of its target gene SMURF2. Results of this research suggested that the CCAT1 inhibits the proliferation and differentiation of osteoblasts in rats with osteoporosis by binding to miR-34a-5p, providing novel biomarkers for osteoporosis treatment. |
| doi_str_mv | 10.1038/s41417-020-00264-7 |
| format | Article |
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It is reported that lncRNAs might exert function in osteoblast differentiation and bone formation. Here, we determined this study to clarify whether lncRNA CCAT1 could regulate osteoblast proliferation and differentiation in ovariectomized rats with osteoporosis. The osteoporosis models were established by bilateral ovariectomy and treated with CCAT1 siRNAs to discuss the effect of CCAT1 on pathological changes and osteocyte apoptosis in ovariectomized rats with osteoporosis. The osteoblasts from ovariectomized rats were cultured in vitro, which were then treated with CCAT1 siRNAs to explore the role of CCAT1 in osteoblast proliferation and differentiation. Moreover, the relationships among CCAT1, miR-34a-5p, and SMURF2 were confirmed. CCAT1 and SMURF2 were amplified while miR-34a-5p expression was inhibited in bone tissues and osteoblasts of ovariectomized rats with osteoporosis. Inhibited CCAT1 improved pathology and restricted osteocyte apoptosis of bone tissues in ovariectomized rats with osteoporosis in vivo, and also enhanced differentiation, mineralization abilities, and proliferation, and suppressed apoptosis of osteoblasts from ovariectomized rats in vitro through upregulating miR-34a-5p expression. LncRNA CCAT1 could competitively bind with miR-34a-5p to prevent the degradation of its target gene SMURF2. Results of this research suggested that the CCAT1 inhibits the proliferation and differentiation of osteoblasts in rats with osteoporosis by binding to miR-34a-5p, providing novel biomarkers for osteoporosis treatment.</description><identifier>ISSN: 0929-1903</identifier><identifier>EISSN: 1476-5500</identifier><identifier>DOI: 10.1038/s41417-020-00264-7</identifier><identifier>PMID: 33402731</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>13/31 ; 13/51 ; 38/109 ; 631/208/199 ; 631/80 ; Animals ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Bone growth ; Carcinogenesis ; Cell Differentiation ; Cell Proliferation ; Colon cancer ; Colorectal cancer ; Development and progression ; Disease Models, Animal ; Disease Progression ; Female ; Gene Expression ; Gene Therapy ; Genetic aspects ; Health aspects ; Humans ; Mineralization ; miRNA ; Non-coding RNA ; Osteoblastogenesis ; Osteoblasts ; Osteoblasts - metabolism ; Osteogenesis ; Osteoporosis ; Osteoporosis - genetics ; Osteoporosis - pathology ; Ovariectomy ; Pathology ; Physiological aspects ; Rats ; Rats, Sprague-Dawley ; RNA ; RNA, Long Noncoding - metabolism ; RNA-mediated interference ; siRNA ; Transcription ; Up-Regulation</subject><ispartof>Cancer gene therapy, 2021-11, Vol.28 (10-11), p.1150-1161</ispartof><rights>The Author(s), under exclusive licence to Springer Nature America, Inc. part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Nature America, Inc. part of Springer Nature.</rights><rights>COPYRIGHT 2021 Nature Publishing Group</rights><rights>The Author(s), under exclusive licence to Springer Nature America, Inc. part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c473t-31c5f1e6cf88263080ccde891bcc09b469461f359bedd43a90bb95c6f99f906f3</citedby><cites>FETCH-LOGICAL-c473t-31c5f1e6cf88263080ccde891bcc09b469461f359bedd43a90bb95c6f99f906f3</cites><orcidid>0000-0001-8022-516X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41417-020-00264-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41417-020-00264-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33402731$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Fangke</creatorcontrib><creatorcontrib>Jiang, Chengying</creatorcontrib><creatorcontrib>Bu, Guoyun</creatorcontrib><creatorcontrib>Fu, Yiru</creatorcontrib><creatorcontrib>Yu, Yanfang</creatorcontrib><title>Silencing long noncoding RNA colon cancer-associated transcript-1 upregulates microRNA-34a-5p to promote proliferation and differentiation of osteoblasts in osteoporosis</title><title>Cancer gene therapy</title><addtitle>Cancer Gene Ther</addtitle><addtitle>Cancer Gene Ther</addtitle><description>Long noncoding RNAs (lncRNAs) have been revealed to be related to multiple physiological and pathology processes such as development, carcinogenesis, and osteogenesis. It is reported that lncRNAs might exert function in osteoblast differentiation and bone formation. Here, we determined this study to clarify whether lncRNA CCAT1 could regulate osteoblast proliferation and differentiation in ovariectomized rats with osteoporosis. The osteoporosis models were established by bilateral ovariectomy and treated with CCAT1 siRNAs to discuss the effect of CCAT1 on pathological changes and osteocyte apoptosis in ovariectomized rats with osteoporosis. The osteoblasts from ovariectomized rats were cultured in vitro, which were then treated with CCAT1 siRNAs to explore the role of CCAT1 in osteoblast proliferation and differentiation. Moreover, the relationships among CCAT1, miR-34a-5p, and SMURF2 were confirmed. CCAT1 and SMURF2 were amplified while miR-34a-5p expression was inhibited in bone tissues and osteoblasts of ovariectomized rats with osteoporosis. Inhibited CCAT1 improved pathology and restricted osteocyte apoptosis of bone tissues in ovariectomized rats with osteoporosis in vivo, and also enhanced differentiation, mineralization abilities, and proliferation, and suppressed apoptosis of osteoblasts from ovariectomized rats in vitro through upregulating miR-34a-5p expression. LncRNA CCAT1 could competitively bind with miR-34a-5p to prevent the degradation of its target gene SMURF2. Results of this research suggested that the CCAT1 inhibits the proliferation and differentiation of osteoblasts in rats with osteoporosis by binding to miR-34a-5p, providing novel biomarkers for osteoporosis treatment.</description><subject>13/31</subject><subject>13/51</subject><subject>38/109</subject><subject>631/208/199</subject><subject>631/80</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bone growth</subject><subject>Carcinogenesis</subject><subject>Cell Differentiation</subject><subject>Cell Proliferation</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Development and progression</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Therapy</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Mineralization</subject><subject>miRNA</subject><subject>Non-coding RNA</subject><subject>Osteoblastogenesis</subject><subject>Osteoblasts</subject><subject>Osteoblasts - 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It is reported that lncRNAs might exert function in osteoblast differentiation and bone formation. Here, we determined this study to clarify whether lncRNA CCAT1 could regulate osteoblast proliferation and differentiation in ovariectomized rats with osteoporosis. The osteoporosis models were established by bilateral ovariectomy and treated with CCAT1 siRNAs to discuss the effect of CCAT1 on pathological changes and osteocyte apoptosis in ovariectomized rats with osteoporosis. The osteoblasts from ovariectomized rats were cultured in vitro, which were then treated with CCAT1 siRNAs to explore the role of CCAT1 in osteoblast proliferation and differentiation. Moreover, the relationships among CCAT1, miR-34a-5p, and SMURF2 were confirmed. CCAT1 and SMURF2 were amplified while miR-34a-5p expression was inhibited in bone tissues and osteoblasts of ovariectomized rats with osteoporosis. Inhibited CCAT1 improved pathology and restricted osteocyte apoptosis of bone tissues in ovariectomized rats with osteoporosis in vivo, and also enhanced differentiation, mineralization abilities, and proliferation, and suppressed apoptosis of osteoblasts from ovariectomized rats in vitro through upregulating miR-34a-5p expression. LncRNA CCAT1 could competitively bind with miR-34a-5p to prevent the degradation of its target gene SMURF2. Results of this research suggested that the CCAT1 inhibits the proliferation and differentiation of osteoblasts in rats with osteoporosis by binding to miR-34a-5p, providing novel biomarkers for osteoporosis treatment.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>33402731</pmid><doi>10.1038/s41417-020-00264-7</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-8022-516X</orcidid></addata></record> |
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| subjects | 13/31 13/51 38/109 631/208/199 631/80 Animals Apoptosis Biomedical and Life Sciences Biomedicine Bone growth Carcinogenesis Cell Differentiation Cell Proliferation Colon cancer Colorectal cancer Development and progression Disease Models, Animal Disease Progression Female Gene Expression Gene Therapy Genetic aspects Health aspects Humans Mineralization miRNA Non-coding RNA Osteoblastogenesis Osteoblasts Osteoblasts - metabolism Osteogenesis Osteoporosis Osteoporosis - genetics Osteoporosis - pathology Ovariectomy Pathology Physiological aspects Rats Rats, Sprague-Dawley RNA RNA, Long Noncoding - metabolism RNA-mediated interference siRNA Transcription Up-Regulation |
| title | Silencing long noncoding RNA colon cancer-associated transcript-1 upregulates microRNA-34a-5p to promote proliferation and differentiation of osteoblasts in osteoporosis |
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