miR‐298 plays a pivotal role in colon cancer invasiveness by targeting PTEN
Evidence indicate that the miR‐298 dysregulation might associate with colorectal cancer (CRC) development. Herein, we evaluated the effect of miR‐298 dysregulation on colon cancer invasiveness. First, metabolic activity, cell cycle progression, apoptosis, and invasion of miR‐298 overexpressed/knocke...
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| Veröffentlicht in: | Journal of cellular physiology 2020-05, Vol.235 (5), p.4335-4350 |
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| description | Evidence indicate that the miR‐298 dysregulation might associate with colorectal cancer (CRC) development. Herein, we evaluated the effect of miR‐298 dysregulation on colon cancer invasiveness. First, metabolic activity, cell cycle progression, apoptosis, and invasion of miR‐298 overexpressed/knocked out colon cancer cells were examined and combined with their transcriptome analysis data for better visualization of miR‐298 intracellular signaling networks. Interaction between miR‐298 and its target was evaluated with luciferase assay and validated using western blot analysis. The proportion of abnormal miR‐298 level was investigated in tumor samples, matched normal adjacent tissues, and plasmas of 100 CRC patients, and also compared with 100 normal plasma samples. The Mann–Whitney U test was performed to assess miR‐298 differences among the studied groups, and the correlation between miR‐298 and the risk of CRC was shown by univariate and multivariate logistic regression. The data indicate that miR‐298 overexpression promoted proliferation and metastasis in CRC cells via targeting phosphatase and tensin homolog. Comparative analysis of CRC tumors, normal adjacent tissues, and plasmas indicated a significant miR‐298 upregulation in tumors and plasmas (1.72‐fold and 1.65‐fold, respectively; p |
| doi_str_mv | 10.1002/jcp.29310 |
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The aberrant level of miR‐298 increases the colon cancer cells proliferation and metastasis through downregulation of phosphatase and tensin homolog, and subsequent elevation of phosphorylated activation of Akt/ERK and Akt/mTOR/p70 S6K axis.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.29310</identifier><identifier>PMID: 31621072</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Adult ; Aged ; Apoptosis ; Cell Cycle ; Cell Line, Tumor ; Cell proliferation ; Cell Survival ; Colon ; Colon cancer ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Colorectal cancer ; Colorectal carcinoma ; Comparative analysis ; Confidence intervals ; Correlation analysis ; Evaluation ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic - physiology ; Homology ; Humans ; Intracellular signalling ; invasion ; Invasiveness ; Lymph nodes ; Male ; Metastases ; Metastasis ; MicroRNAs - genetics ; MicroRNAs - metabolism ; microRNA‐298 ; Middle Aged ; Multivariate analysis ; Neoplasm Invasiveness - genetics ; Plasmas (physics) ; PTEN ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; PTEN protein ; Regression analysis ; Sequence Analysis, RNA ; Statistical analysis ; Survival ; Tensin ; Therapeutic applications ; Tumors ; Up-Regulation</subject><ispartof>Journal of cellular physiology, 2020-05, Vol.235 (5), p.4335-4350</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><rights>2020 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3530-1b8ba5adc9bb286b2a26ef715277524f2bc274b064843615308a25f7095c1c583</citedby><cites>FETCH-LOGICAL-c3530-1b8ba5adc9bb286b2a26ef715277524f2bc274b064843615308a25f7095c1c583</cites><orcidid>0000-0001-6271-6731 ; 0000-0001-8914-004X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.29310$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.29310$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31621072$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arabsorkhi, Zahra</creatorcontrib><creatorcontrib>Gharib, Ehsan</creatorcontrib><creatorcontrib>Yaghmoorian Khojini, Javad</creatorcontrib><creatorcontrib>Farhadieh, Mohammad‐Erfan</creatorcontrib><creatorcontrib>Nazemalhosseini‐Mojarad, Ehsan</creatorcontrib><creatorcontrib>Zali, Mohammad Reza</creatorcontrib><title>miR‐298 plays a pivotal role in colon cancer invasiveness by targeting PTEN</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Evidence indicate that the miR‐298 dysregulation might associate with colorectal cancer (CRC) development. Herein, we evaluated the effect of miR‐298 dysregulation on colon cancer invasiveness. First, metabolic activity, cell cycle progression, apoptosis, and invasion of miR‐298 overexpressed/knocked out colon cancer cells were examined and combined with their transcriptome analysis data for better visualization of miR‐298 intracellular signaling networks. Interaction between miR‐298 and its target was evaluated with luciferase assay and validated using western blot analysis. The proportion of abnormal miR‐298 level was investigated in tumor samples, matched normal adjacent tissues, and plasmas of 100 CRC patients, and also compared with 100 normal plasma samples. The Mann–Whitney U test was performed to assess miR‐298 differences among the studied groups, and the correlation between miR‐298 and the risk of CRC was shown by univariate and multivariate logistic regression. The data indicate that miR‐298 overexpression promoted proliferation and metastasis in CRC cells via targeting phosphatase and tensin homolog. Comparative analysis of CRC tumors, normal adjacent tissues, and plasmas indicated a significant miR‐298 upregulation in tumors and plasmas (1.72‐fold and 1.65‐fold, respectively; p < .001). Also, the aberrant level of miR‐298 contributed with CRC tumor differentiation, TNM stage and lymph node metastasis (p < .001), and independently associated with poor survival of CRC patients (p < .029; hazard ratio: 1.292; 95% confidence interval: 0.339–2.184). Collectively, these data showed that abnormal level of miR‐298 correlated with cancer development and through that lowered the overall survival rate of CRC patients. Therefore, miR‐298 could be considered as a therapeutic target for CRC.
The aberrant level of miR‐298 increases the colon cancer cells proliferation and metastasis through downregulation of phosphatase and tensin homolog, and subsequent elevation of phosphorylated activation of Akt/ERK and Akt/mTOR/p70 S6K axis.</description><subject>Adult</subject><subject>Aged</subject><subject>Apoptosis</subject><subject>Cell Cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Survival</subject><subject>Colon</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Comparative analysis</subject><subject>Confidence intervals</subject><subject>Correlation analysis</subject><subject>Evaluation</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - physiology</subject><subject>Homology</subject><subject>Humans</subject><subject>Intracellular signalling</subject><subject>invasion</subject><subject>Invasiveness</subject><subject>Lymph nodes</subject><subject>Male</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>microRNA‐298</subject><subject>Middle Aged</subject><subject>Multivariate analysis</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Plasmas (physics)</subject><subject>PTEN</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>PTEN protein</subject><subject>Regression analysis</subject><subject>Sequence Analysis, RNA</subject><subject>Statistical analysis</subject><subject>Survival</subject><subject>Tensin</subject><subject>Therapeutic applications</subject><subject>Tumors</subject><subject>Up-Regulation</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10E1LwzAYB_AgipvTg19AAl700C0vTdscZcw3pg6Z55Jk6cjo2pq0k978CH5GP4mZnR4ELwkhv-fPwx-AU4yGGCEyWqlqSDjFaA_0MeJxEEaM7IO-_8MBZyHugSPnVgghzik9BD2KI4JRTPrgYW2eP98_CE9glYvWQQErsylrkUNb5hqaAqoyL_0pCqWtf2-EMxtdaOegbGEt7FLXpljC2XzyeAwOMpE7fbK7B-DlejIf3wbTp5u78dU0UJRRFGCZSMHEQnEpSRJJIkiksxgzEseMhBmRisShRFGYhDTCfiQRhGUx4kxhxRI6ABddbmXL10a7Ol0bp3Sei0KXjUsJ9bM8ChHz9PwPXZWNLfx2XjEacobZVl12StnSOauztLJmLWybYpRuO059x-l3x96e7RIbudaLX_lTqgejDryZXLf_J6X341kX-QWW04M2</recordid><startdate>202005</startdate><enddate>202005</enddate><creator>Arabsorkhi, Zahra</creator><creator>Gharib, Ehsan</creator><creator>Yaghmoorian Khojini, Javad</creator><creator>Farhadieh, Mohammad‐Erfan</creator><creator>Nazemalhosseini‐Mojarad, Ehsan</creator><creator>Zali, Mohammad Reza</creator><general>Wiley Subscription Services, 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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-6271-6731</orcidid><orcidid>https://orcid.org/0000-0001-8914-004X</orcidid></search><sort><creationdate>202005</creationdate><title>miR‐298 plays a pivotal role in colon cancer invasiveness by targeting PTEN</title><author>Arabsorkhi, Zahra ; Gharib, Ehsan ; Yaghmoorian Khojini, Javad ; Farhadieh, Mohammad‐Erfan ; Nazemalhosseini‐Mojarad, Ehsan ; Zali, Mohammad Reza</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3530-1b8ba5adc9bb286b2a26ef715277524f2bc274b064843615308a25f7095c1c583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Apoptosis</topic><topic>Cell Cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Survival</topic><topic>Colon</topic><topic>Colon cancer</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colonic Neoplasms - pathology</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Comparative analysis</topic><topic>Confidence intervals</topic><topic>Correlation analysis</topic><topic>Evaluation</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - physiology</topic><topic>Homology</topic><topic>Humans</topic><topic>Intracellular signalling</topic><topic>invasion</topic><topic>Invasiveness</topic><topic>Lymph nodes</topic><topic>Male</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>microRNA‐298</topic><topic>Middle Aged</topic><topic>Multivariate analysis</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Plasmas (physics)</topic><topic>PTEN</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>PTEN protein</topic><topic>Regression analysis</topic><topic>Sequence Analysis, RNA</topic><topic>Statistical analysis</topic><topic>Survival</topic><topic>Tensin</topic><topic>Therapeutic applications</topic><topic>Tumors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arabsorkhi, Zahra</creatorcontrib><creatorcontrib>Gharib, Ehsan</creatorcontrib><creatorcontrib>Yaghmoorian Khojini, Javad</creatorcontrib><creatorcontrib>Farhadieh, Mohammad‐Erfan</creatorcontrib><creatorcontrib>Nazemalhosseini‐Mojarad, Ehsan</creatorcontrib><creatorcontrib>Zali, Mohammad Reza</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arabsorkhi, Zahra</au><au>Gharib, Ehsan</au><au>Yaghmoorian Khojini, Javad</au><au>Farhadieh, Mohammad‐Erfan</au><au>Nazemalhosseini‐Mojarad, Ehsan</au><au>Zali, Mohammad Reza</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR‐298 plays a pivotal role in colon cancer invasiveness by targeting PTEN</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2020-05</date><risdate>2020</risdate><volume>235</volume><issue>5</issue><spage>4335</spage><epage>4350</epage><pages>4335-4350</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Evidence indicate that the miR‐298 dysregulation might associate with colorectal cancer (CRC) development. Herein, we evaluated the effect of miR‐298 dysregulation on colon cancer invasiveness. First, metabolic activity, cell cycle progression, apoptosis, and invasion of miR‐298 overexpressed/knocked out colon cancer cells were examined and combined with their transcriptome analysis data for better visualization of miR‐298 intracellular signaling networks. Interaction between miR‐298 and its target was evaluated with luciferase assay and validated using western blot analysis. The proportion of abnormal miR‐298 level was investigated in tumor samples, matched normal adjacent tissues, and plasmas of 100 CRC patients, and also compared with 100 normal plasma samples. The Mann–Whitney U test was performed to assess miR‐298 differences among the studied groups, and the correlation between miR‐298 and the risk of CRC was shown by univariate and multivariate logistic regression. The data indicate that miR‐298 overexpression promoted proliferation and metastasis in CRC cells via targeting phosphatase and tensin homolog. Comparative analysis of CRC tumors, normal adjacent tissues, and plasmas indicated a significant miR‐298 upregulation in tumors and plasmas (1.72‐fold and 1.65‐fold, respectively; p < .001). Also, the aberrant level of miR‐298 contributed with CRC tumor differentiation, TNM stage and lymph node metastasis (p < .001), and independently associated with poor survival of CRC patients (p < .029; hazard ratio: 1.292; 95% confidence interval: 0.339–2.184). Collectively, these data showed that abnormal level of miR‐298 correlated with cancer development and through that lowered the overall survival rate of CRC patients. Therefore, miR‐298 could be considered as a therapeutic target for CRC.
The aberrant level of miR‐298 increases the colon cancer cells proliferation and metastasis through downregulation of phosphatase and tensin homolog, and subsequent elevation of phosphorylated activation of Akt/ERK and Akt/mTOR/p70 S6K axis.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31621072</pmid><doi>10.1002/jcp.29310</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0001-6271-6731</orcidid><orcidid>https://orcid.org/0000-0001-8914-004X</orcidid></addata></record> |
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| subjects | Adult Aged Apoptosis Cell Cycle Cell Line, Tumor Cell proliferation Cell Survival Colon Colon cancer Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Colorectal cancer Colorectal carcinoma Comparative analysis Confidence intervals Correlation analysis Evaluation Female Gene expression Gene Expression Regulation, Neoplastic - physiology Homology Humans Intracellular signalling invasion Invasiveness Lymph nodes Male Metastases Metastasis MicroRNAs - genetics MicroRNAs - metabolism microRNA‐298 Middle Aged Multivariate analysis Neoplasm Invasiveness - genetics Plasmas (physics) PTEN PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism PTEN protein Regression analysis Sequence Analysis, RNA Statistical analysis Survival Tensin Therapeutic applications Tumors Up-Regulation |
| title | miR‐298 plays a pivotal role in colon cancer invasiveness by targeting PTEN |
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