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We employed RNA sequencing analysis to reveal dysregulated lncRNAs in lung cancer utilizing 461 lung adenocarcinomas and 156 normal lung tissues from 3 separate cohorts. We found that  LINC00152  was highly overexpressed in lung tumors as compared to their adjacent normal tissues. Patients with high  LINC00152  expression demonstrate a significantly poorer survival than those with low expression. We verified the diagnostic/prognostic potential of  LINC00152  expression in an independent cohort of lung tumor tissues using quantitative RT-PCR. After knockdown of  LINC00152  using siRNAs in lung cancer cell lines, both cell proliferation and colony formation were decreased. Cell fractionation and qRT-PCR analysis indicated that  LINC00152  is found mainly in the cytoplasm. Treatment with Trichostatin A in cell lines having low  LINC00152  expression indicated that histone acetylation may be one mechanism underlying  LINC00152  overexpression in NSCLC. Western blot analyses indicated that p38a, STAT1, STAT3, CREB1, CCNE1 and c-MYC proteins were decreased after  LINC00152  siRNA treatment. Our study indicates  LINC00152  plays an important role in lung tumor growth and is potentially a diagnostic/prognostic marker. Further characterization of  LINC00152  in regulating its target proteins may provide a novel therapeutic target of lung cancer.

Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer