The microRNA‑200 family acts as an oncogene in colorectal cancer by inhibiting the tumor suppressor RASSF2
This study aimed to determine whether manipulation of the microRNA-200 (miR-200) family could influence colon adenocarcinoma cell behavior. The miR-200 family has a significant role in tumor suppression and functions as an oncogene. In vitro studies on gain and loss of function with small interferin...
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| Veröffentlicht in: | Oncology letters 2019-10, Vol.18 (4), p.3994-4007 |
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| creator | Carter, Jane V O'brien, Stephen J Burton, James F Oxford, Brent G Stephen, Vince Hallion, Jake Bishop, Campbell Galbraith, Norman J Eichenberger, Maurice R Sarojini, Harshini Hattab, Eyas Galandiuk, Susan |
| description | This study aimed to determine whether manipulation of the microRNA-200 (miR-200) family could influence colon adenocarcinoma cell behavior. The miR-200 family has a significant role in tumor suppression and functions as an oncogene. In vitro studies on gain and loss of function with small interfering RNA demonstrated that the miR-200 family could regulate RASSF2 expression. Knockdown of the miR-200 family in the HT-29 colon cancer cell line increased KRAS expression but decreased signaling in the MAPK/ERK signaling pathway through reduced ERK phosphorylation. Increased expression of the miR-200 family in the CCD-841 colon epithelium cell line increased KRAS expression and led to increased signaling in the MAPK/ERK signaling pathway but increased ERK phosphorylation. Functionally, knockdown of the miR-200 family led to decreased cell proliferation in the HT-29 cells; therefore, increased miR-200 family expression could increase cell proliferation in the CCD-841 cell line. The present study included a large paired miR array dataset (n=632), in which the miR-200 family was significantly found to be increased in colon cancer when compared with normal adjacent colon epithelium. In a miR-seq dataset (n=199), the study found that miR-200 family expression was increased in localized colon cancer compared with metastatic disease. Decreased expression was associated with poorer overall survival. The miR-200 family directly targeted RASSF2 and was inversely correlated with RASSF2 expression (n=199, all P |
| doi_str_mv | 10.3892/ol.2019.10753 |
| format | Article |
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The miR-200 family has a significant role in tumor suppression and functions as an oncogene. In vitro studies on gain and loss of function with small interfering RNA demonstrated that the miR-200 family could regulate RASSF2 expression. Knockdown of the miR-200 family in the HT-29 colon cancer cell line increased KRAS expression but decreased signaling in the MAPK/ERK signaling pathway through reduced ERK phosphorylation. Increased expression of the miR-200 family in the CCD-841 colon epithelium cell line increased KRAS expression and led to increased signaling in the MAPK/ERK signaling pathway but increased ERK phosphorylation. Functionally, knockdown of the miR-200 family led to decreased cell proliferation in the HT-29 cells; therefore, increased miR-200 family expression could increase cell proliferation in the CCD-841 cell line. The present study included a large paired miR array dataset (n=632), in which the miR-200 family was significantly found to be increased in colon cancer when compared with normal adjacent colon epithelium. In a miR-seq dataset (n=199), the study found that miR-200 family expression was increased in localized colon cancer compared with metastatic disease. Decreased expression was associated with poorer overall survival. The miR-200 family directly targeted RASSF2 and was inversely correlated with RASSF2 expression (n=199, all P<0.001). Despite the well-defined role of the miR-200 family in tumor suppression, the present findings demonstrated a novel function of the miR-200 family in tumor proliferation.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2019.10753</identifier><identifier>PMID: 31565080</identifier><language>eng</language><publisher>Athens: Spandidos Publications</publisher><subject>Adenocarcinoma ; Cancer genetics ; Cancer metastasis ; Cancer research ; Cancer treatment ; Cell growth ; Colorectal cancer ; Datasets ; Epithelium ; Family relations ; Genetic aspects ; Kinases ; MicroRNA ; MicroRNAs ; Novels ; Oncology ; RNA ; Tumors</subject><ispartof>Oncology letters, 2019-10, Vol.18 (4), p.3994-4007</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Carter et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-1c545b3988c2617df8c2497d6981813f0ff7a3ef4da99b0f77c906a7c68c94273</citedby><cites>FETCH-LOGICAL-c490t-1c545b3988c2617df8c2497d6981813f0ff7a3ef4da99b0f77c906a7c68c94273</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/PMC6759516/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6759516/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><creatorcontrib>Carter, Jane V</creatorcontrib><creatorcontrib>O'brien, Stephen J</creatorcontrib><creatorcontrib>Burton, James F</creatorcontrib><creatorcontrib>Oxford, Brent G</creatorcontrib><creatorcontrib>Stephen, Vince</creatorcontrib><creatorcontrib>Hallion, Jake</creatorcontrib><creatorcontrib>Bishop, Campbell</creatorcontrib><creatorcontrib>Galbraith, Norman J</creatorcontrib><creatorcontrib>Eichenberger, Maurice R</creatorcontrib><creatorcontrib>Sarojini, Harshini</creatorcontrib><creatorcontrib>Hattab, Eyas</creatorcontrib><creatorcontrib>Galandiuk, Susan</creatorcontrib><title>The microRNA‑200 family acts as an oncogene in colorectal cancer by inhibiting the tumor suppressor RASSF2</title><title>Oncology letters</title><description>This study aimed to determine whether manipulation of the microRNA-200 (miR-200) family could influence colon adenocarcinoma cell behavior. The miR-200 family has a significant role in tumor suppression and functions as an oncogene. In vitro studies on gain and loss of function with small interfering RNA demonstrated that the miR-200 family could regulate RASSF2 expression. Knockdown of the miR-200 family in the HT-29 colon cancer cell line increased KRAS expression but decreased signaling in the MAPK/ERK signaling pathway through reduced ERK phosphorylation. Increased expression of the miR-200 family in the CCD-841 colon epithelium cell line increased KRAS expression and led to increased signaling in the MAPK/ERK signaling pathway but increased ERK phosphorylation. Functionally, knockdown of the miR-200 family led to decreased cell proliferation in the HT-29 cells; therefore, increased miR-200 family expression could increase cell proliferation in the CCD-841 cell line. The present study included a large paired miR array dataset (n=632), in which the miR-200 family was significantly found to be increased in colon cancer when compared with normal adjacent colon epithelium. In a miR-seq dataset (n=199), the study found that miR-200 family expression was increased in localized colon cancer compared with metastatic disease. Decreased expression was associated with poorer overall survival. The miR-200 family directly targeted RASSF2 and was inversely correlated with RASSF2 expression (n=199, all P<0.001). Despite the well-defined role of the miR-200 family in tumor suppression, the present findings demonstrated a novel function of the miR-200 family in tumor proliferation.</description><subject>Adenocarcinoma</subject><subject>Cancer genetics</subject><subject>Cancer metastasis</subject><subject>Cancer research</subject><subject>Cancer treatment</subject><subject>Cell growth</subject><subject>Colorectal cancer</subject><subject>Datasets</subject><subject>Epithelium</subject><subject>Family relations</subject><subject>Genetic aspects</subject><subject>Kinases</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>Novels</subject><subject>Oncology</subject><subject>RNA</subject><subject>Tumors</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkt1qFTEQxxdRbKm99D4giDd7zMduPm6EQ7FWKAptvQ7ZbHI2JZsck6xw7nwFX9EnaU5bqkdMAjNMfvMfkpmmeY3ginCB30e_whCJFYKsJ8-aY8QEbhHk-PmTz7qj5jTnW1hXTxHn9GVzRFBPe8jhceNvJgNmp1O8-rL-_fMXhhBYNTu_A0qXDFQ9AcSg48YEA1wAOvqYjC7KA62CNgkMuxqf3OCKCxtQqmBZ5phAXrbbZHKu7tX6-vocv2peWOWzOX20J8238483Zxft5ddPn8_Wl63uBCwt0n3XD0RwrjFFbLTVdoKNVHDEEbHQWqaIsd2ohBigZUwLSBXTlGvRYUZOmg8PuttlmM2oTShJeblNblZpJ6Ny8vAmuElu4g9JWS96RKvAu0eBFL8vJhc5u6yN9yqYuGSJsRBdJ6iAFX3zD3oblxTq8-4pyJgQ5A-1Ud5IF2ysdfVeVK4prO3oENuXXf2Hqns0tUUxGOtq_CDh7V8Jk1G-TDn6pbgY8iHYPoC10TknY58-A0G5HyUZvdyPkrwfJXIHZFy4KA</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Carter, Jane V</creator><creator>O'brien, Stephen J</creator><creator>Burton, James F</creator><creator>Oxford, Brent G</creator><creator>Stephen, Vince</creator><creator>Hallion, Jake</creator><creator>Bishop, Campbell</creator><creator>Galbraith, Norman J</creator><creator>Eichenberger, Maurice R</creator><creator>Sarojini, Harshini</creator><creator>Hattab, Eyas</creator><creator>Galandiuk, Susan</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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The miR-200 family has a significant role in tumor suppression and functions as an oncogene. In vitro studies on gain and loss of function with small interfering RNA demonstrated that the miR-200 family could regulate RASSF2 expression. Knockdown of the miR-200 family in the HT-29 colon cancer cell line increased KRAS expression but decreased signaling in the MAPK/ERK signaling pathway through reduced ERK phosphorylation. Increased expression of the miR-200 family in the CCD-841 colon epithelium cell line increased KRAS expression and led to increased signaling in the MAPK/ERK signaling pathway but increased ERK phosphorylation. Functionally, knockdown of the miR-200 family led to decreased cell proliferation in the HT-29 cells; therefore, increased miR-200 family expression could increase cell proliferation in the CCD-841 cell line. The present study included a large paired miR array dataset (n=632), in which the miR-200 family was significantly found to be increased in colon cancer when compared with normal adjacent colon epithelium. In a miR-seq dataset (n=199), the study found that miR-200 family expression was increased in localized colon cancer compared with metastatic disease. Decreased expression was associated with poorer overall survival. The miR-200 family directly targeted RASSF2 and was inversely correlated with RASSF2 expression (n=199, all P<0.001). Despite the well-defined role of the miR-200 family in tumor suppression, the present findings demonstrated a novel function of the miR-200 family in tumor proliferation.</abstract><cop>Athens</cop><pub>Spandidos Publications</pub><pmid>31565080</pmid><doi>10.3892/ol.2019.10753</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1792-1074 |
| ispartof | Oncology letters, 2019-10, Vol.18 (4), p.3994-4007 |
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| source | Spandidos Publications Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Adenocarcinoma Cancer genetics Cancer metastasis Cancer research Cancer treatment Cell growth Colorectal cancer Datasets Epithelium Family relations Genetic aspects Kinases MicroRNA MicroRNAs Novels Oncology RNA Tumors |
| title | The microRNA‑200 family acts as an oncogene in colorectal cancer by inhibiting the tumor suppressor RASSF2 |
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