e23136 Background: We have reported the usefulness of Family with sequence similarity 83, member B (FAM83B) as a novel biomarker for diagnosis and prognosis of lung squamous cell carcinoma. FAM83B expresses not only in lung cancer but also in several types of solid cancer. More recently, novel finding showing FAM83B involve to tumor growth, oncogenesis, and resistance of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) in breast cancer cell lines has been shown. EGFR signaling pathway also plays an important role in lung adenocarcinoma, therefore, we hypothesize that FAM83B associates with tumor proliferation in lung adenocarcinoma (ADC), results in resistance to EGFR-TKI and in a novel therapeutic target in a part of lung ADC. Here we show that correlation between FAM83B expression and clinicopathological features. Methods: This study was conducted with approval of ethics committee in our institute, and informed consent was obtained from all the participants. We identified 216 participants underwent for primary lung ADC between 2008 and 2015. Paired tumor and corresponding normal tissue samples obtained from patients were subjected. FAM83B mRNA expression were examined by cDNA microarray, and analyzed relationship between the level of FAM83B and clinicopathological variables including survival analysis. Further, FAM83B knock down study was performed in several types of cancer cell lines (H1975, HLC-1, H2347) to validate whether FAM83B involve to cell proliferation. Results: FAM83B highly expressed in male (p = 0.007), or smoker (p = 0.007), or EGFR wild type tumor (p<0.001). Multivariate analyses also showed that EGFR wild type-tumor correlate with FAM83B expression. In survival analysis, multivariate analysis showed FAM83B correlated with poor outcome in both disease free survival and overall survival (p = 0.011 and p = 0.001), especially stratified by EGFR wild type-tumor (p = 0.017, p = 0.008). Gene silencing with FAM83B siRNA showed growth suppression of HLC-1 and H1975 cell lines. Conclusions: FAM83B could involve to tumor proliferation of lung ADC in part, and expected to be the novel therapeutic target of EGFR wild type-ADC.
LncRNA FAM83A-AS1 facilitates tumor proliferation and the migration via the HIF-1α/ glycolysis axis in lung adenocarcinoma
