nc886, a non-coding RNA and suppressor of PKR, exerts an oncogenic function in thyroid cancer

Eun Kyung Lee1, Seung-Hyun Hong2, Sooyong Shin3,4

  • 1Center for Thyroid Cancer, National Cancer Center, Goyang, 410-769, Korea.

Oncotarget
|September 11, 2016
PubMed

Insights

Non-coding RNA nc886 promotes thyroid cancer progression independently of PKR. nc886 enhances cell proliferation, migration, and invasion, acting as an oncogene in this context.

Area of Science:

  • Molecular Biology
  • Oncology
  • RNA Biology

Background:

  • nc886 is a non-coding RNA involved in cell death via Protein Kinase RNA-activated (PKR) activation.
  • nc886 expression varies in malignancies, with its role as a tumor suppressor or oncogene being debated.
  • The specific function of nc886 in thyroid cancer remains unclear.

Purpose of the Study:

  • To elucidate the role of nc886 in thyroid cancer progression.
  • To determine if nc886's function is dependent on PKR in thyroid cancer cells.

Main Methods:

  • Generated PKR knockout (KO) and PKR/nc886 double KO thyroid cell lines from Nthy-ori 3-1.
  • Assessed cell proliferation, migration, and invasion in generated cell lines.
  • Analyzed microarray data and correlated nc886 expression with patient survival and metastasis data from The Cancer Genome Atlas (TCGA).

Main Results:

  • nc886 knockout (KO) cells exhibited reduced proliferation, migration, and invasion compared to parental PKR KO cells.
  • nc886's contribution to tumor phenotypes was independent of PKR.
  • nc886 KO suppressed genes linked to poor survival in thyroid cancer patients.
  • Elevated nc886 expression correlated with more aggressive metastatic tumors in thyroid cancer patients.

Conclusions:

  • nc886 acts as a tumor promoter in thyroid cancer.
  • nc886's oncogenic role is masked by PKR-mediated cell death.
  • nc886 represents a potential therapeutic target in thyroid cancer.

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