Nc886, a non-coding RNA and suppressor of PKR, exerts an oncogenic function in thyroid cancer

Eun Kyung Lee, Seung Hyun Hong, Sooyong Shin, Hyun Sung Lee, Ju Seog Lee, Eun Jung Park, Sun Shim Choi, Jae Woong Min, Daeyoon Park, Jung Ah Hwang, Betty H. Johnson, Sung Ho Jeon, In Hoo Kim, Yeon Su Lee, Yong Sun Lee

    Research output: Contribution to journalArticle

    10 Citations (Scopus)

    Abstract

    nc886 is a recently identified cellular non-coding RNA and its depletion leads to acute cell death via PKR (Protein Kinase RNA-activated) activation. nc886 expression is increased in some malignancies, but silenced in others. However, the precise role of nc886/PKR is controversial: is it a tumor suppressor or an oncogene? In this study, we have clarified the role of nc886 in thyroid cancer by sequentially generating PKR knockout (KO) and PKR/nc886 double KO cell lines from Nthy-ori 3-1, a partially transformed thyroid cell line. Compared to the wildtype, PKR KO alone does not exhibit any significant phenotypic changes. However, nc886 KO cells are less proliferative, migratory, and invasive than their parental PKR KO cells. Importantly, the requirement of nc886 in tumor phenotypes is totally independent of PKR. In our microarray data, nc886 KO suppresses some genes whose elevated expression is associated with poor survival confirmed by data from total of 505 thyroid cancer patients in the Caner Genome Atlas project. Also, the nc886 expression level tends to be elevated and in more aggressively metastatic tumor specimens from thyroid cancer patients. In summary, we have discovered nc886's tumor-promoting role in thyroid cancer which has been concealed by the PKR-mediated acute cell death.

    Original languageEnglish (US)
    Pages (from-to)75000-75012
    Number of pages13
    JournalOncotarget
    Volume7
    Issue number46
    DOIs
    StatePublished - 2016

    Fingerprint

    eIF-2 Kinase
    Untranslated RNA
    Thyroid Neoplasms
    Neoplasms
    Cell Death
    Transformed Cell Line
    Atlases
    Oncogenes
    Thyroid Gland
    Genome
    Phenotype
    Cell Line
    Survival

    Keywords

    • nc886
    • Oncogene
    • Protein kinase R
    • Thyroid cancer

    ASJC Scopus subject areas

    • Oncology

    Cite this

    Lee, E. K., Hong, S. H., Shin, S., Lee, H. S., Lee, J. S., Park, E. J., ... Lee, Y. S. (2016). Nc886, a non-coding RNA and suppressor of PKR, exerts an oncogenic function in thyroid cancer. Oncotarget, 7(46), 75000-75012. https://doi.org/10.18632/oncotarget.11852

    Nc886, a non-coding RNA and suppressor of PKR, exerts an oncogenic function in thyroid cancer. / Lee, Eun Kyung; Hong, Seung Hyun; Shin, Sooyong; Lee, Hyun Sung; Lee, Ju Seog; Park, Eun Jung; Choi, Sun Shim; Min, Jae Woong; Park, Daeyoon; Hwang, Jung Ah; Johnson, Betty H.; Jeon, Sung Ho; Kim, In Hoo; Lee, Yeon Su; Lee, Yong Sun.

    In: Oncotarget, Vol. 7, No. 46, 2016, p. 75000-75012.

    Research output: Contribution to journalArticle

    Lee, EK, Hong, SH, Shin, S, Lee, HS, Lee, JS, Park, EJ, Choi, SS, Min, JW, Park, D, Hwang, JA, Johnson, BH, Jeon, SH, Kim, IH, Lee, YS & Lee, YS 2016, 'Nc886, a non-coding RNA and suppressor of PKR, exerts an oncogenic function in thyroid cancer', Oncotarget, vol. 7, no. 46, pp. 75000-75012. https://doi.org/10.18632/oncotarget.11852
    Lee, Eun Kyung ; Hong, Seung Hyun ; Shin, Sooyong ; Lee, Hyun Sung ; Lee, Ju Seog ; Park, Eun Jung ; Choi, Sun Shim ; Min, Jae Woong ; Park, Daeyoon ; Hwang, Jung Ah ; Johnson, Betty H. ; Jeon, Sung Ho ; Kim, In Hoo ; Lee, Yeon Su ; Lee, Yong Sun. / Nc886, a non-coding RNA and suppressor of PKR, exerts an oncogenic function in thyroid cancer. In: Oncotarget. 2016 ; Vol. 7, No. 46. pp. 75000-75012.
    @article{ca7f1140f28748bb95f4c00776eb51f8,
    title = "Nc886, a non-coding RNA and suppressor of PKR, exerts an oncogenic function in thyroid cancer",
    abstract = "nc886 is a recently identified cellular non-coding RNA and its depletion leads to acute cell death via PKR (Protein Kinase RNA-activated) activation. nc886 expression is increased in some malignancies, but silenced in others. However, the precise role of nc886/PKR is controversial: is it a tumor suppressor or an oncogene? In this study, we have clarified the role of nc886 in thyroid cancer by sequentially generating PKR knockout (KO) and PKR/nc886 double KO cell lines from Nthy-ori 3-1, a partially transformed thyroid cell line. Compared to the wildtype, PKR KO alone does not exhibit any significant phenotypic changes. However, nc886 KO cells are less proliferative, migratory, and invasive than their parental PKR KO cells. Importantly, the requirement of nc886 in tumor phenotypes is totally independent of PKR. In our microarray data, nc886 KO suppresses some genes whose elevated expression is associated with poor survival confirmed by data from total of 505 thyroid cancer patients in the Caner Genome Atlas project. Also, the nc886 expression level tends to be elevated and in more aggressively metastatic tumor specimens from thyroid cancer patients. In summary, we have discovered nc886's tumor-promoting role in thyroid cancer which has been concealed by the PKR-mediated acute cell death.",
    keywords = "nc886, Oncogene, Protein kinase R, Thyroid cancer",
    author = "Lee, {Eun Kyung} and Hong, {Seung Hyun} and Sooyong Shin and Lee, {Hyun Sung} and Lee, {Ju Seog} and Park, {Eun Jung} and Choi, {Sun Shim} and Min, {Jae Woong} and Daeyoon Park and Hwang, {Jung Ah} and Johnson, {Betty H.} and Jeon, {Sung Ho} and Kim, {In Hoo} and Lee, {Yeon Su} and Lee, {Yong Sun}",
    year = "2016",
    doi = "10.18632/oncotarget.11852",
    language = "English (US)",
    volume = "7",
    pages = "75000--75012",
    journal = "Oncotarget",
    issn = "1949-2553",
    publisher = "Impact Journals",
    number = "46",

    }

    TY - JOUR

    T1 - Nc886, a non-coding RNA and suppressor of PKR, exerts an oncogenic function in thyroid cancer

    AU - Lee, Eun Kyung

    AU - Hong, Seung Hyun

    AU - Shin, Sooyong

    AU - Lee, Hyun Sung

    AU - Lee, Ju Seog

    AU - Park, Eun Jung

    AU - Choi, Sun Shim

    AU - Min, Jae Woong

    AU - Park, Daeyoon

    AU - Hwang, Jung Ah

    AU - Johnson, Betty H.

    AU - Jeon, Sung Ho

    AU - Kim, In Hoo

    AU - Lee, Yeon Su

    AU - Lee, Yong Sun

    PY - 2016

    Y1 - 2016

    N2 - nc886 is a recently identified cellular non-coding RNA and its depletion leads to acute cell death via PKR (Protein Kinase RNA-activated) activation. nc886 expression is increased in some malignancies, but silenced in others. However, the precise role of nc886/PKR is controversial: is it a tumor suppressor or an oncogene? In this study, we have clarified the role of nc886 in thyroid cancer by sequentially generating PKR knockout (KO) and PKR/nc886 double KO cell lines from Nthy-ori 3-1, a partially transformed thyroid cell line. Compared to the wildtype, PKR KO alone does not exhibit any significant phenotypic changes. However, nc886 KO cells are less proliferative, migratory, and invasive than their parental PKR KO cells. Importantly, the requirement of nc886 in tumor phenotypes is totally independent of PKR. In our microarray data, nc886 KO suppresses some genes whose elevated expression is associated with poor survival confirmed by data from total of 505 thyroid cancer patients in the Caner Genome Atlas project. Also, the nc886 expression level tends to be elevated and in more aggressively metastatic tumor specimens from thyroid cancer patients. In summary, we have discovered nc886's tumor-promoting role in thyroid cancer which has been concealed by the PKR-mediated acute cell death.

    AB - nc886 is a recently identified cellular non-coding RNA and its depletion leads to acute cell death via PKR (Protein Kinase RNA-activated) activation. nc886 expression is increased in some malignancies, but silenced in others. However, the precise role of nc886/PKR is controversial: is it a tumor suppressor or an oncogene? In this study, we have clarified the role of nc886 in thyroid cancer by sequentially generating PKR knockout (KO) and PKR/nc886 double KO cell lines from Nthy-ori 3-1, a partially transformed thyroid cell line. Compared to the wildtype, PKR KO alone does not exhibit any significant phenotypic changes. However, nc886 KO cells are less proliferative, migratory, and invasive than their parental PKR KO cells. Importantly, the requirement of nc886 in tumor phenotypes is totally independent of PKR. In our microarray data, nc886 KO suppresses some genes whose elevated expression is associated with poor survival confirmed by data from total of 505 thyroid cancer patients in the Caner Genome Atlas project. Also, the nc886 expression level tends to be elevated and in more aggressively metastatic tumor specimens from thyroid cancer patients. In summary, we have discovered nc886's tumor-promoting role in thyroid cancer which has been concealed by the PKR-mediated acute cell death.

    KW - nc886

    KW - Oncogene

    KW - Protein kinase R

    KW - Thyroid cancer

    UR - http://www.scopus.com/inward/record.url?scp=84996995766&partnerID=8YFLogxK

    UR - http://www.scopus.com/inward/citedby.url?scp=84996995766&partnerID=8YFLogxK

    U2 - 10.18632/oncotarget.11852

    DO - 10.18632/oncotarget.11852

    M3 - Article

    VL - 7

    SP - 75000

    EP - 75012

    JO - Oncotarget

    JF - Oncotarget

    SN - 1949-2553

    IS - 46

    ER -