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Lung cancer is a molecularly-heterogenous disease and the leading cause of cancer mortality. The molecular basis for this heterogeneity remains incompletely understood. In the past few years, long non-coding RNAs (lncRNAs) have emerged as novel mechanisms in mediating cancer biology, although most lncRNAs are still undiscovered. LINC00152 has been identified as highly associated with the tumorigenesis and development in gastric cancer, colon cancer and hepatocellular carcinoma, however, the expression level and its oncogenic roles in lung cancer remains unknown. In the present study, we employed next generation RNA sequencing analysis to reveal dysregulated lncRNAs in lung cancer utilizing datasets of 461 lung adenocarcinomas (LUAD) and 156 normal lung tissues from 3 separate institutions. We found that LINC00152 was 4-fold (p 0.8 in these 3 data sets. Patients with high LINC00152 expression have significantly poorer survival than those with low expression (log-rank test, p = 0.003). We verified this diagnostic/prognostic potential in an independent cohort of lung tumor tissues by quantitative RT-PCR. Cell proliferation and colony formation ability were decreased after knockdown of LINC00152 using siRNAs in lung cancer cell lines. The expression of LINC00152 was found primarily in the cytoplasm by qRT-PCR analysis. Trichostatin A treatment indicated that histone acetylation could be one of the mechanisms underlying LINC00152 overexpression in NSCLC and cell-based analyses showed p38 signaling was mainly affected by LINC00152 in vitro. Taken together, our study suggests that LINC00152 is involved in lung tumor growth, may have potential as diagnostic/prognostic marker and that further characterization of this lncRNA as a novel therapeutic target for lung cancer is warranted. Note: This abstract was not presented at the meeting. Citation Format: Shumei Feng, Jie Zhang, Wenmei Su, Shengbin Bai, Lei Xiao, Zhuwen Wang, Jules Lin, Rishindra Reddy, Andrew Chang, David Beer, Guoan Chen. LINC00152 regulates cell proliferation via p38 signaling and overexpression predicts poor patient survival in lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3444. doi:10.1158/1538-7445.AM2017-3444