tRF-Leu-CAG promotes cell proliferation and cell cycle in non-small cell lung cancer.

tRNA-derived RNA fragments (tRFs), non-coding single-stranded RNAs with 14-35 nt in length, were found to play important roles in gene regulation, even in carcinogenesis. In this study, we investigated the expression of tRF-Leu-CAG in human non-small cell lung cancer (NSCLC) and its function in the cell proliferation and cell cycle of NSCLC. The expression level of tRF-Leu-CAG was detected in NSCLC tissues, cell lines, and sera. tRF-Leu-CAG RNA levels were higher in NSCLC tumor tissues than in normal tissues, and also upregulated in NSCLC cell lines. A significant relationship was observed between stage progression and tRF-Leu-CAG in NSCLC sera. We found that in H1299 cells, inhibition of tRF-Leu-CAG suppressed cell proliferation and impeded cell cycle. AURKA was also repressed with the knockdown of tRF-Leu-CAG. Thus, our study revealed that tRF-Leu-CAG may be involved in regulating AURKA and could be a new diagnostic marker and potential therapeutic target in NSCLC.

Shao Y ，Sun Q ，Liu X ，Wang P ，Wu R ，Ma Z ... -  《-》

Oncogenic tRNA-derived fragment tRF-Leu-CAG promotes tumorigenesis of lung cancer via targeting TCEA3 and increasing autophagy.

Wu F ，Chai B ，Qi P ，Han Y ，Gu Z ，Pan W ，Zhang H ，Wang X ，Liu X ，Zou H ，Liang C ，Li Y ，Fang W ，Ma Z ... -  《-》

High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer.

Lv J ，Qiu M ，Xia W ，Liu C ，Xu Y ，Wang J ，Leng X ，Huang S ，Zhu R ，Zhao M ，Ji F ，Xu L ，Xu K ，Yin R ... -  《JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH》

Highly expressed long non-coding RNA CRNDE promotes cell proliferation through PI3K/AKT signalling in non-small cell lung carcinoma.

Recently, numerous studies have revealed that long non-coding RNAs (lncRNAs) play complex roles in various lung diseases, while the colorectal neoplasia differentially expressed (CRNDE) functions in non-small cell lung carcinomas (NSCLC) remain largely unknown. In the present study, we investigate the role and mechanism of CRNDE in the progression of NSCLC. The mRNA level of CRNDE in NSCLC patients and cells was detected by qRT-PCR. The influence of CRNDE silencing or over-expression on NSCLC cell proliferation and growth were assessed by MTT and flow cytometry, respectively. We also investigated the effect of abnormal CRNDE expression on cyclins and PI3K/AKT pathway. Furthermore, si-CRNDE NSCLC cell lines were injected subcutaneously into nude mice to explore tumour formation in vivo. The expression of CRNDE was significantly upregulated in NSCLC patients and cells. In addition, both loss and gain function assays revealed that CRNDE promoted NSCLC cell proliferation and growth both in vitro and in vivo. Moreover, CRNDE regulated the cell cycle transition from G0 /G1 stage to S stage and modulated the expression of CDK4, CDK6 and CCNE1. We further illustrated that CRNDE activated PI3K/AKT signalling in NSCLC cell lines. In conclusion, CRNDE was highly expressed in NSCLC malignant tissues and the heightened CRNDE strongly promoted NSCLC cell proliferation and growth through activating PI3K/AKT signalling; our results shed a light on utilizing CRNDE as a potential novel therapeutic target for the treatment of NSCLC.

Liu XX ，Xiong HP ，Huang JS ，Qi K ，Xu JJ ... -  《-》

Highly expressed lncRNA LOC730101 promotes lung cancer cell growth through Wnt canonical pathway.

Many long non-coding RNA (lncRNA) has recently been reported to be dysregulated and involved in the progression of non-small-cell lung cancer. However, the biological role of LOC730101 in NSCLC carcinogenesis remains unclear. In the present study, we found that LOC730101 was up-regulated in TCGA and GEO database, so were in NSCLC tissues and cell lines. Overexpression of LOC730101 prompted the proliferation of NSCLC both in vitro and in vivo while Silencing observed opposite phenomenon. Furthermore, we found that LOC730101 enhances the activity of Wnt/β-catenin signaling to promote the progression of cell cycle and ultimate promotes cell proliferation and growth. Therefore, our study may provide a better understanding of the pathogenesis of NSCLC and indicates that LOC730101 may be a potential therapeutic target in NSCLC.

Liu L ，Zhang Y ，Cao W 《-》