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MicroRNA and cancer – focus on apoptosis
• Introduction • miR biogenesis • miR and Cancer • miR and Apoptosis ‐ The pro‐apoptotic miRs targeting the BCL2 family of genes ‐ The anti‐apoptotic miR‐21 targets PTEN and PDCD4 ‐ miR‐210 decreases proapoptotic signalling in a hypoxic environment ‐ Let‐7/miR‐98 family and possible co‐opera...
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Published in: | Journal of cellular and molecular medicine 2009-01, Vol.13 (1), p.12-23 |
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description | •
Introduction
•
miR biogenesis
•
miR and Cancer
•
miR and Apoptosis
‐
The pro‐apoptotic miRs targeting the BCL2 family of genes
‐
The anti‐apoptotic miR‐21 targets PTEN and PDCD4
‐
miR‐210 decreases proapoptotic signalling in a hypoxic environment
‐
Let‐7/miR‐98 family and possible co‐operation with miR‐21
‐
miR‐17–92 cluster highlights the complexity of miR regulatory networks
‐
miR‐224, the double‐edged sword
‐
Other miRs implicated in apoptosis
•
Conclusion
MicroRNAs (miRs) are small non‐coding RNAs regulating gene expression at the post‐transcriptional and/or translational levels. miRs play important roles in diverse biological processes, including development, cell differentiation, proliferation and apoptosis. Recent evidence has shown that miR loci frequently map to cancer‐associated genomic regions and deregulated miR expression profiles are associated with many cancer types, implicating miRs in crucial processes that lead to tumourigenesis. Here, we review the current findings about miRs and tumourigenesis, focusing on their involvement in the apoptosis pathway. A significant observation is that greater than one‐quarter of all known human miRs were reported to be deregulated in at least one cancer type. The expression of a subset of miRs (e.g. miR‐21 and miR‐155) was found to be consistently up‐regulated, whereas another subset of miRs (e.g.miR‐143 and miR‐145) was consistently down‐regulated across different cancer types suggesting their involvement in regulating common cellular processes whose deregulation may lead to tumourigenesis. Several miRs were implicated to play roles in cell proliferation and apoptosis. Some miRs, such as miR‐29b and miR‐15–16, influence only the apoptotic pathway, whereas others including let‐7/miR‐98 and miR‐17–92 may play roles in both the apoptotic and cell‐proliferation pathways. In conclusion, although our current understanding of the functions of miRs is still fragmentary, taken together, this review highlights the complex and intricate roles that miRs play in the regulation of cellular processes. Perturbation of the expression of miRs may thus lead to tumourigenesis. |
doi_str_mv | 10.1111/j.1582-4934.2008.00510.x |
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Introduction
•
miR biogenesis
•
miR and Cancer
•
miR and Apoptosis
‐
The pro‐apoptotic miRs targeting the BCL2 family of genes
‐
The anti‐apoptotic miR‐21 targets PTEN and PDCD4
‐
miR‐210 decreases proapoptotic signalling in a hypoxic environment
‐
Let‐7/miR‐98 family and possible co‐operation with miR‐21
‐
miR‐17–92 cluster highlights the complexity of miR regulatory networks
‐
miR‐224, the double‐edged sword
‐
Other miRs implicated in apoptosis
•
Conclusion
MicroRNAs (miRs) are small non‐coding RNAs regulating gene expression at the post‐transcriptional and/or translational levels. miRs play important roles in diverse biological processes, including development, cell differentiation, proliferation and apoptosis. Recent evidence has shown that miR loci frequently map to cancer‐associated genomic regions and deregulated miR expression profiles are associated with many cancer types, implicating miRs in crucial processes that lead to tumourigenesis. Here, we review the current findings about miRs and tumourigenesis, focusing on their involvement in the apoptosis pathway. A significant observation is that greater than one‐quarter of all known human miRs were reported to be deregulated in at least one cancer type. The expression of a subset of miRs (e.g. miR‐21 and miR‐155) was found to be consistently up‐regulated, whereas another subset of miRs (e.g.miR‐143 and miR‐145) was consistently down‐regulated across different cancer types suggesting their involvement in regulating common cellular processes whose deregulation may lead to tumourigenesis. Several miRs were implicated to play roles in cell proliferation and apoptosis. Some miRs, such as miR‐29b and miR‐15–16, influence only the apoptotic pathway, whereas others including let‐7/miR‐98 and miR‐17–92 may play roles in both the apoptotic and cell‐proliferation pathways. In conclusion, although our current understanding of the functions of miRs is still fragmentary, taken together, this review highlights the complex and intricate roles that miRs play in the regulation of cellular processes. Perturbation of the expression of miRs may thus lead to tumourigenesis.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/j.1582-4934.2008.00510.x</identifier><identifier>PMID: 19175697</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Apoptosis ; Apoptosis - physiology ; Apoptosis Regulatory Proteins - genetics ; Apoptosis Regulatory Proteins - metabolism ; Bcl-2 protein ; Cancer ; Cell death ; Cell differentiation ; Cell growth ; Cell proliferation ; Cells ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes ; Hematology ; Humans ; Hypoxia ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Neoplasms - genetics ; Oncology ; Post-transcription ; Prostate ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; PTEN protein ; Reviews ; Ribonucleic acid ; RNA ; RNA polymerase ; RNA-Binding Proteins - genetics ; RNA-Binding Proteins - metabolism ; Signal transduction ; Signal Transduction - physiology ; Thyroid gland ; Tumorigenesis ; Tumors ; tumourigenesis ; Urogenital system</subject><ispartof>Journal of cellular and molecular medicine, 2009-01, Vol.13 (1), p.12-23</ispartof><rights>2009 The Authors Journal compilation © 2009 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd</rights><rights>Copyright Blackwell Publishing Ltd. Jan 2009</rights><rights>2009. This work is published under https://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>2009 The Authors Journal compilation © 2009 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5930-dc3ac58d04d5e5a77aa3e8d904117c1f0f17186366491548b24923b05327c2ba3</citedby><cites>FETCH-LOGICAL-c5930-dc3ac58d04d5e5a77aa3e8d904117c1f0f17186366491548b24923b05327c2ba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/3074762817/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/3074762817?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,11541,25731,27901,27902,36989,36990,44566,46027,46451,53766,53768,74869</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1582-4934.2008.00510.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19175697$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yu</creatorcontrib><creatorcontrib>Lee, Caroline G. L.</creatorcontrib><title>MicroRNA and cancer – focus on apoptosis</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>•
Introduction
•
miR biogenesis
•
miR and Cancer
•
miR and Apoptosis
‐
The pro‐apoptotic miRs targeting the BCL2 family of genes
‐
The anti‐apoptotic miR‐21 targets PTEN and PDCD4
‐
miR‐210 decreases proapoptotic signalling in a hypoxic environment
‐
Let‐7/miR‐98 family and possible co‐operation with miR‐21
‐
miR‐17–92 cluster highlights the complexity of miR regulatory networks
‐
miR‐224, the double‐edged sword
‐
Other miRs implicated in apoptosis
•
Conclusion
MicroRNAs (miRs) are small non‐coding RNAs regulating gene expression at the post‐transcriptional and/or translational levels. miRs play important roles in diverse biological processes, including development, cell differentiation, proliferation and apoptosis. Recent evidence has shown that miR loci frequently map to cancer‐associated genomic regions and deregulated miR expression profiles are associated with many cancer types, implicating miRs in crucial processes that lead to tumourigenesis. Here, we review the current findings about miRs and tumourigenesis, focusing on their involvement in the apoptosis pathway. A significant observation is that greater than one‐quarter of all known human miRs were reported to be deregulated in at least one cancer type. The expression of a subset of miRs (e.g. miR‐21 and miR‐155) was found to be consistently up‐regulated, whereas another subset of miRs (e.g.miR‐143 and miR‐145) was consistently down‐regulated across different cancer types suggesting their involvement in regulating common cellular processes whose deregulation may lead to tumourigenesis. Several miRs were implicated to play roles in cell proliferation and apoptosis. Some miRs, such as miR‐29b and miR‐15–16, influence only the apoptotic pathway, whereas others including let‐7/miR‐98 and miR‐17–92 may play roles in both the apoptotic and cell‐proliferation pathways. In conclusion, although our current understanding of the functions of miRs is still fragmentary, taken together, this review highlights the complex and intricate roles that miRs play in the regulation of cellular processes. Perturbation of the expression of miRs may thus lead to tumourigenesis.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Bcl-2 protein</subject><subject>Cancer</subject><subject>Cell death</subject><subject>Cell differentiation</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cells</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Hematology</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Neoplasms - genetics</subject><subject>Oncology</subject><subject>Post-transcription</subject><subject>Prostate</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>PTEN protein</subject><subject>Reviews</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA polymerase</subject><subject>RNA-Binding Proteins - genetics</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - physiology</subject><subject>Thyroid gland</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>tumourigenesis</subject><subject>Urogenital system</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNqNkc1qGzEUhUVJaX6aVyhDAl0E7F7p6neRQDBJf4hbKM1ayBpNMmY8ckaeJtnlHfqGfZJqapO2gUK00YXz3YOODiEFhTHN5918TIVmI26QjxmAHgOIrN29IDuPwtZmphr1NtlNaQ6AkqJ5RbapoUpIo3bI0bT2Xfz6-bRwbVl41_rQFT8ffhRV9H0qYlu4ZVyuYqrTa_Kyck0K-5t7j1yen32bfBhdfHn_cXJ6MfLCIIxKj84LXQIvRRBOKecw6NIAp1R5WkFFFdUSpeSGCq5njBuGMxDIlGczh3vkZO277GeLUPrQrjrX2GVXL1x3b6Or7b9KW1_bq_jdomYIiNng7cagizd9SCu7qJMPTePaEPtkpdQSGKgMHj4B57Hv2hzOIiiuJNN0oA7-R7EcRXGUJkN6DeXfTKkL1eN7KdihMzu3Qx12qMYOndnfndm7vPrm77x_FjclZeB4DdzWTbh_trH9NJlO84S_AIBtovM</recordid><startdate>200901</startdate><enddate>200901</enddate><creator>Wang, Yu</creator><creator>Lee, Caroline G. L.</creator><general>Blackwell Publishing Ltd</general><general>John Wiley & Sons, Inc</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>K9.</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200901</creationdate><title>MicroRNA and cancer – focus on apoptosis</title><author>Wang, Yu ; Lee, Caroline G. L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5930-dc3ac58d04d5e5a77aa3e8d904117c1f0f17186366491548b24923b05327c2ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Bcl-2 protein</topic><topic>Cancer</topic><topic>Cell death</topic><topic>Cell differentiation</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Cells</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Hematology</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Neoplasms - genetics</topic><topic>Oncology</topic><topic>Post-transcription</topic><topic>Prostate</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>PTEN protein</topic><topic>Reviews</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA polymerase</topic><topic>RNA-Binding Proteins - genetics</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - physiology</topic><topic>Thyroid gland</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><topic>tumourigenesis</topic><topic>Urogenital system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yu</creatorcontrib><creatorcontrib>Lee, Caroline G. L.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content (ProQuest)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Wang, Yu</au><au>Lee, Caroline G. L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA and cancer – focus on apoptosis</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2009-01</date><risdate>2009</risdate><volume>13</volume><issue>1</issue><spage>12</spage><epage>23</epage><pages>12-23</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>•
Introduction
•
miR biogenesis
•
miR and Cancer
•
miR and Apoptosis
‐
The pro‐apoptotic miRs targeting the BCL2 family of genes
‐
The anti‐apoptotic miR‐21 targets PTEN and PDCD4
‐
miR‐210 decreases proapoptotic signalling in a hypoxic environment
‐
Let‐7/miR‐98 family and possible co‐operation with miR‐21
‐
miR‐17–92 cluster highlights the complexity of miR regulatory networks
‐
miR‐224, the double‐edged sword
‐
Other miRs implicated in apoptosis
•
Conclusion
MicroRNAs (miRs) are small non‐coding RNAs regulating gene expression at the post‐transcriptional and/or translational levels. miRs play important roles in diverse biological processes, including development, cell differentiation, proliferation and apoptosis. Recent evidence has shown that miR loci frequently map to cancer‐associated genomic regions and deregulated miR expression profiles are associated with many cancer types, implicating miRs in crucial processes that lead to tumourigenesis. Here, we review the current findings about miRs and tumourigenesis, focusing on their involvement in the apoptosis pathway. A significant observation is that greater than one‐quarter of all known human miRs were reported to be deregulated in at least one cancer type. The expression of a subset of miRs (e.g. miR‐21 and miR‐155) was found to be consistently up‐regulated, whereas another subset of miRs (e.g.miR‐143 and miR‐145) was consistently down‐regulated across different cancer types suggesting their involvement in regulating common cellular processes whose deregulation may lead to tumourigenesis. Several miRs were implicated to play roles in cell proliferation and apoptosis. Some miRs, such as miR‐29b and miR‐15–16, influence only the apoptotic pathway, whereas others including let‐7/miR‐98 and miR‐17–92 may play roles in both the apoptotic and cell‐proliferation pathways. In conclusion, although our current understanding of the functions of miRs is still fragmentary, taken together, this review highlights the complex and intricate roles that miRs play in the regulation of cellular processes. Perturbation of the expression of miRs may thus lead to tumourigenesis.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>19175697</pmid><doi>10.1111/j.1582-4934.2008.00510.x</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Apoptosis Apoptosis - physiology Apoptosis Regulatory Proteins - genetics Apoptosis Regulatory Proteins - metabolism Bcl-2 protein Cancer Cell death Cell differentiation Cell growth Cell proliferation Cells Gene expression Gene Expression Profiling Gene Expression Regulation, Neoplastic Genes Hematology Humans Hypoxia MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Neoplasms - genetics Oncology Post-transcription Prostate Proteins Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism PTEN protein Reviews Ribonucleic acid RNA RNA polymerase RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Signal transduction Signal Transduction - physiology Thyroid gland Tumorigenesis Tumors tumourigenesis Urogenital system |
title | MicroRNA and cancer – focus on apoptosis |
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