Background:The role of long non-coding RNAs (lncRNAs) in senescence is little known. Results: Senescence-associated lncRNA (SALNR) expression is reduced during senescence. SALNR delays oncogene-induced senescence through suppressing NF90 nucleolus translocation. Conclusion: lncRNA SALNR plays an important role in senescence. Significance: We profiled lncRNAs in senescence and provided novel insights into the role of lncRNAs in senescence.

A previous study has demonstrated that adiponectin (APN) could promote preadipocyte differentiation, and the present study further explored its mechanism. 3T3-L1 cells were infected with adenovirus holding human adiponectin gene apM1 and mouse neuronatin (Nnat) shRNA and initiated differentiation while coculturing with mature adipocytes stimulated with LPS. After 8 days, preadipocyte differentiation was observed by Oil Red O staining. Real-time quantitative PCR was used to evaluate mRNA expression levels of monocyte chemoattractant protein-1 (MCP-1), interleukin- (IL-) 6, IL-8, and tumor necrosis factor α (TNF-α). The levels of reactive oxygen species (ROS), total antioxidant capacity (T-AOC), malondialdehyde (MDA), and superoxide dismutase (SOD) in 3T3-L1 cells were detected. Western blotting was done to quantify the protein expression levels of Nnat, peroxisome proliferator-activated receptor (PPAR) γ, p65, and inhibitor of nuclear factor κB (IκB) α. Results demonstrated that APN overexpression markedly increased preadipocyte differentiation; inhibited gene expression of MCP-1, IL-6, IL-8, and TNF-α; reduced ROS and MDA release; increased T-AOC and SOD levels; upregulated Nnat, PPAR γ, and IκB α protein expressions; and downregulated p65 protein expression under LPS stimulation. However, the effects of APN were markedly attenuated when Nnat expression was knocked down. Taken together, the present study provided evidences that the effects of APN on promoting preadipocyte differentiation under inflammatory conditions via anti-inflammation and antioxidative stress may be regulated by the PPAR γ/Nnat/NF-κB signaling pathway.

Background: Actin cytoskeleton is connected with the processes of cell proliferation and migration in colorectal cancer (CRC). However, it is unknown how to accomplish these adjustments in CRC by actin cytoskeleton genes (ACGs) and here we investigated the role of hub prognosis-related ACGs-Diaphanous-related formin 3 (DIAPH3) in CRC, as a potential, novel target. Methods: The ACGs gene set from the Kyoto Encyclopedia of Genes and Genomes (KEGG) was used to group CRC patients and select prognosis-related ACGs by univariate and multivariate Cox regression for constructing prognostic model. Next, we tested hub prognosis-related ACGs-DIAPH3 expression in CRC and clarified the role of DIAPH3 by shRNA constructs in KM12 and SW480. Activation of EGFR was analyzed by western blot and immunofluorescence. Results: The results showed that actin cytoskeleton function is a significant prognostic factor for CRC patients and related to clinicopathological characteristics such as T stage and lymph node metastasis. A prognostic model constructed by four prognosis-related ACGs has a moderate intensity to 1-year Survival (AUC = 0.71). And hub prognosis-related ACGs DIAPH3 is downregulated in CRC. Knockdown of DIAPH3 could promote the proliferation and migration capacity of CRC. In addition, DIAPH3-silenced cells increase EGFR phosphorylation by inhibiting EGFR transportation to lysosome. Conclusions: ACGs play a significant role in tumor invasion and have the potential to predict the prognosis of CRC. Prognosis-related ACGs DIAPH3 might be a new prognostic biomarker and DIAPH3 could inhibit CRC progression through maintaining EGFR degradation.