LncRNA-SNHG16 promotes proliferation and migration of acute myeloid leukemia cells via PTEN/PI3K/AKT axis through suppressing CELF2 protein
The silence of lncRNA small nucleolar RNA host gene 16 ( SNHG16 ) suppressed acute lymphoblastic leukemia (ALL) cell proliferation and migration, whereas its role in acute myeloid leukemia (AML) still lacks clarity. This study showed that SNHG16 was upregulated in AML patients and cells. And SNHG16...
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| creator | Shi, Min Yang, Ruili Lin, Jing Wei, Qi Chen, Lei Gong, Weifeng Li, Yang Guo, Xiaobo |
| description | The silence of lncRNA small nucleolar RNA host gene 16 (
SNHG16
) suppressed acute lymphoblastic leukemia (ALL) cell proliferation and migration, whereas its role in acute myeloid leukemia (AML) still lacks clarity. This study showed that
SNHG16
was upregulated in AML patients and cells. And
SNHG16
overexpression remarkably enhanced the proliferation and migration capacities of HL60 and AML-193 cells, while
SNHG16
knockdown acted the opposite way. Subsequently, we revealed that
SNHG16
directly bound to CELF2 (CUGBP Elav-like family member 2) protein, and caused CELF2 mRNA unstably and proteins reducing. CELF2 was decreased both in AML patients and cells. CELF2 overexpression or interference weakened the effect of overexpressing or silencing
SNHG16
on proliferation and migration. Moreover, the transfection of pcDNA-CELF2 elevated PTEN (phosphatase and tensin homolog) activity and hindered the phosphoinositide 3-kinase (PI3K)/AKT signaling. And
SNHG16
reduced PTEN activity and promoted the PI3K/AKT pathway activation by restraining CELF2. Furthermore, GDC-0941 (a specific inhibitor of the PI3K/AKT pathway) impeded the effect of
SNHG16
increase, and bpV(pic) (a specific PTEN inhibitor) declined the effect of
SNHG16
decrease on cell proliferation and migration. Taken together, the present study indicated that
SNHG16
promoted proliferation and migration of AML cells via PTEN/PI3K/AKT axis through suppressing CELF2 protein. |
| doi_str_mv | 10.1007/s12038-020-00127-1 |
| format | Article |
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SNHG16
) suppressed acute lymphoblastic leukemia (ALL) cell proliferation and migration, whereas its role in acute myeloid leukemia (AML) still lacks clarity. This study showed that
SNHG16
was upregulated in AML patients and cells. And
SNHG16
overexpression remarkably enhanced the proliferation and migration capacities of HL60 and AML-193 cells, while
SNHG16
knockdown acted the opposite way. Subsequently, we revealed that
SNHG16
directly bound to CELF2 (CUGBP Elav-like family member 2) protein, and caused CELF2 mRNA unstably and proteins reducing. CELF2 was decreased both in AML patients and cells. CELF2 overexpression or interference weakened the effect of overexpressing or silencing
SNHG16
on proliferation and migration. Moreover, the transfection of pcDNA-CELF2 elevated PTEN (phosphatase and tensin homolog) activity and hindered the phosphoinositide 3-kinase (PI3K)/AKT signaling. And
SNHG16
reduced PTEN activity and promoted the PI3K/AKT pathway activation by restraining CELF2. Furthermore, GDC-0941 (a specific inhibitor of the PI3K/AKT pathway) impeded the effect of
SNHG16
increase, and bpV(pic) (a specific PTEN inhibitor) declined the effect of
SNHG16
decrease on cell proliferation and migration. Taken together, the present study indicated that
SNHG16
promoted proliferation and migration of AML cells via PTEN/PI3K/AKT axis through suppressing CELF2 protein.</description><identifier>ISSN: 0250-5991</identifier><identifier>EISSN: 0973-7138</identifier><identifier>DOI: 10.1007/s12038-020-00127-1</identifier><identifier>PMID: 33576342</identifier><language>eng</language><publisher>New Delhi: Springer India</publisher><subject>1-Phosphatidylinositol 3-kinase ; Acute lymphoblastic leukemia ; Acute myeloid leukemia ; AKT protein ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell growth ; Cell migration ; Cell proliferation ; Cells ; Homology ; Inhibitors ; Kinases ; Leukemia ; Life Sciences ; Lymphatic leukemia ; Microbiology ; mRNA ; Myeloid leukemia ; Nucleic acids ; Nucleoli ; Phosphatase ; Plant Sciences ; Proliferation ; Proteins ; PTEN protein ; RNA ; snoRNA ; Tensin ; Transfection ; Zoology</subject><ispartof>Journal of biosciences, 2021-12, Vol.46 (1), Article 4</ispartof><rights>Indian Academy of Sciences 2021</rights><rights>Indian Academy of Sciences 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-65a6bc773128a89dadd2537719cb359d3692394dc90b6ec1fcdf4e3a6b822ebd3</citedby><cites>FETCH-LOGICAL-c375t-65a6bc773128a89dadd2537719cb359d3692394dc90b6ec1fcdf4e3a6b822ebd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12038-020-00127-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12038-020-00127-1$$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/33576342$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Min</creatorcontrib><creatorcontrib>Yang, Ruili</creatorcontrib><creatorcontrib>Lin, Jing</creatorcontrib><creatorcontrib>Wei, Qi</creatorcontrib><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Gong, Weifeng</creatorcontrib><creatorcontrib>Li, Yang</creatorcontrib><creatorcontrib>Guo, Xiaobo</creatorcontrib><title>LncRNA-SNHG16 promotes proliferation and migration of acute myeloid leukemia cells via PTEN/PI3K/AKT axis through suppressing CELF2 protein</title><title>Journal of biosciences</title><addtitle>J Biosci</addtitle><addtitle>J Biosci</addtitle><description>The silence of lncRNA small nucleolar RNA host gene 16 (
SNHG16
) suppressed acute lymphoblastic leukemia (ALL) cell proliferation and migration, whereas its role in acute myeloid leukemia (AML) still lacks clarity. This study showed that
SNHG16
was upregulated in AML patients and cells. And
SNHG16
overexpression remarkably enhanced the proliferation and migration capacities of HL60 and AML-193 cells, while
SNHG16
knockdown acted the opposite way. Subsequently, we revealed that
SNHG16
directly bound to CELF2 (CUGBP Elav-like family member 2) protein, and caused CELF2 mRNA unstably and proteins reducing. CELF2 was decreased both in AML patients and cells. CELF2 overexpression or interference weakened the effect of overexpressing or silencing
SNHG16
on proliferation and migration. Moreover, the transfection of pcDNA-CELF2 elevated PTEN (phosphatase and tensin homolog) activity and hindered the phosphoinositide 3-kinase (PI3K)/AKT signaling. And
SNHG16
reduced PTEN activity and promoted the PI3K/AKT pathway activation by restraining CELF2. Furthermore, GDC-0941 (a specific inhibitor of the PI3K/AKT pathway) impeded the effect of
SNHG16
increase, and bpV(pic) (a specific PTEN inhibitor) declined the effect of
SNHG16
decrease on cell proliferation and migration. Taken together, the present study indicated that
SNHG16
promoted proliferation and migration of AML cells via PTEN/PI3K/AKT axis through suppressing CELF2 protein.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Acute lymphoblastic leukemia</subject><subject>Acute myeloid leukemia</subject><subject>AKT protein</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Cells</subject><subject>Homology</subject><subject>Inhibitors</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Life Sciences</subject><subject>Lymphatic leukemia</subject><subject>Microbiology</subject><subject>mRNA</subject><subject>Myeloid leukemia</subject><subject>Nucleic acids</subject><subject>Nucleoli</subject><subject>Phosphatase</subject><subject>Plant Sciences</subject><subject>Proliferation</subject><subject>Proteins</subject><subject>PTEN protein</subject><subject>RNA</subject><subject>snoRNA</subject><subject>Tensin</subject><subject>Transfection</subject><subject>Zoology</subject><issn>0250-5991</issn><issn>0973-7138</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kUtvEzEUhS0EoqXwB1ggS2zYmPgxHo-XUZQ-1ChUENaWx76Tuswj2DOI_gb-NB4SQGLByse637nnSgeh14y-Z5SqRWKciopQTgmljCvCnqBzqpUgionqadZcUiK1ZmfoRUoPGdKFoM_RmRBSlaLg5-jHpncft0vyaXt9xUp8iEM3jJBm0YYGoh3D0GPbe9yF_ek3NNi6aQTcPUI7BI9bmL5AFyx20LYJf8vqbrfeLu5uxO1iebvD9ntIeLyPw7S_x2k6HCKkFPo9Xq03l3wOGyH0L9GzxrYJXp3eC_T5cr1bXZPNh6ub1XJDnFByJKW0Ze2UEoxXttLees-lUIppVwupvSg1F7rwTtO6BMca55sCRDZVnEPtxQV6d9ybc79OkEbThTSfbnsYpmR4UWkuecXLjL79B30Yptjn62ZK6oJTOlP8SLk4pBShMYcYOhsfDaNmrsocqzK5KvOrKsOy6c1p9VR34P9YfneTAXEEUh71e4h_s_-z9iduuJ4s</recordid><startdate>20211201</startdate><enddate>20211201</enddate><creator>Shi, 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promotes proliferation and migration of acute myeloid leukemia cells via PTEN/PI3K/AKT axis through suppressing CELF2 protein</title><author>Shi, Min ; Yang, Ruili ; Lin, Jing ; Wei, Qi ; Chen, Lei ; Gong, Weifeng ; Li, Yang ; Guo, Xiaobo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-65a6bc773128a89dadd2537719cb359d3692394dc90b6ec1fcdf4e3a6b822ebd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Acute lymphoblastic leukemia</topic><topic>Acute myeloid leukemia</topic><topic>AKT protein</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Cells</topic><topic>Homology</topic><topic>Inhibitors</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Life Sciences</topic><topic>Lymphatic leukemia</topic><topic>Microbiology</topic><topic>mRNA</topic><topic>Myeloid leukemia</topic><topic>Nucleic acids</topic><topic>Nucleoli</topic><topic>Phosphatase</topic><topic>Plant Sciences</topic><topic>Proliferation</topic><topic>Proteins</topic><topic>PTEN protein</topic><topic>RNA</topic><topic>snoRNA</topic><topic>Tensin</topic><topic>Transfection</topic><topic>Zoology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Min</creatorcontrib><creatorcontrib>Yang, Ruili</creatorcontrib><creatorcontrib>Lin, Jing</creatorcontrib><creatorcontrib>Wei, Qi</creatorcontrib><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Gong, Weifeng</creatorcontrib><creatorcontrib>Li, Yang</creatorcontrib><creatorcontrib>Guo, Xiaobo</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology 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Xiaobo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA-SNHG16 promotes proliferation and migration of acute myeloid leukemia cells via PTEN/PI3K/AKT axis through suppressing CELF2 protein</atitle><jtitle>Journal of biosciences</jtitle><stitle>J Biosci</stitle><addtitle>J Biosci</addtitle><date>2021-12-01</date><risdate>2021</risdate><volume>46</volume><issue>1</issue><artnum>4</artnum><issn>0250-5991</issn><eissn>0973-7138</eissn><abstract>The silence of lncRNA small nucleolar RNA host gene 16 (
SNHG16
) suppressed acute lymphoblastic leukemia (ALL) cell proliferation and migration, whereas its role in acute myeloid leukemia (AML) still lacks clarity. This study showed that
SNHG16
was upregulated in AML patients and cells. And
SNHG16
overexpression remarkably enhanced the proliferation and migration capacities of HL60 and AML-193 cells, while
SNHG16
knockdown acted the opposite way. Subsequently, we revealed that
SNHG16
directly bound to CELF2 (CUGBP Elav-like family member 2) protein, and caused CELF2 mRNA unstably and proteins reducing. CELF2 was decreased both in AML patients and cells. CELF2 overexpression or interference weakened the effect of overexpressing or silencing
SNHG16
on proliferation and migration. Moreover, the transfection of pcDNA-CELF2 elevated PTEN (phosphatase and tensin homolog) activity and hindered the phosphoinositide 3-kinase (PI3K)/AKT signaling. And
SNHG16
reduced PTEN activity and promoted the PI3K/AKT pathway activation by restraining CELF2. Furthermore, GDC-0941 (a specific inhibitor of the PI3K/AKT pathway) impeded the effect of
SNHG16
increase, and bpV(pic) (a specific PTEN inhibitor) declined the effect of
SNHG16
decrease on cell proliferation and migration. Taken together, the present study indicated that
SNHG16
promoted proliferation and migration of AML cells via PTEN/PI3K/AKT axis through suppressing CELF2 protein.</abstract><cop>New Delhi</cop><pub>Springer India</pub><pmid>33576342</pmid><doi>10.1007/s12038-020-00127-1</doi></addata></record> |
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| source | Indian Academy of Sciences; SpringerLink Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | 1-Phosphatidylinositol 3-kinase Acute lymphoblastic leukemia Acute myeloid leukemia AKT protein Biomedical and Life Sciences Biomedicine Cell Biology Cell growth Cell migration Cell proliferation Cells Homology Inhibitors Kinases Leukemia Life Sciences Lymphatic leukemia Microbiology mRNA Myeloid leukemia Nucleic acids Nucleoli Phosphatase Plant Sciences Proliferation Proteins PTEN protein RNA snoRNA Tensin Transfection Zoology |
| title | LncRNA-SNHG16 promotes proliferation and migration of acute myeloid leukemia cells via PTEN/PI3K/AKT axis through suppressing CELF2 protein |
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