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Background: Pancreatic cancer stem cells are crucial for tumorigenesis and cancer metastasis. Presently, long non-coding RNAs were found to be associated with Pancreatic Ductal Adenocarcinoma stemness characteristics but the underlying mechanism is largely known. Here, we aim to explore the function of LINC00909 in regulating pancreatic cancer stemness and cancer metastasis. Methods: The expression level and clinical characteristics of LINC00909 were verified in 80-paired normal pancreas and Pancreatic Ductal Adenocarcinoma tissues from Guangdong Provincial People's Hospital cohort by in situ hybridization. RNA sequencing of PANC-1 cells with empty vector or vector encoding LINC00909 was experimented for subsequent bioinformatics analysis. The effect of LINC00909 in cancer stemness and metastasis was examined by in vitro and in vivo experiments. The interaction between LINC00909 with SMAD4 and the pluripotency factors were studied. Results: LINC00909 was generally upregulated in pancreatic cancer tissues and was associated with inferior clinicopathologic features and outcome. Over-expression of LINC00909 enhanced the expression of pluripotency factors and cancer stem cells phenotype, while knock-down of LINC00909 decreased the expression of pluripotency factors and cancer stem cells phenotype. Moreover, LINC00909 inversely regulated SMAD4 expression, knock-down of SMAD4 rescued the effect of LINC00909-deletion inhibition on pluripotency factors and cancer stem cells phenotype. These indicated the effect of LINC00909 on pluripotency factors and CSC phenotype was dependent on SMAD4 and MAPK/JNK signaling pathway, another downstream pathway of SMAD4 was also activated by LINC00909. Specifically, LINC00909 was localized in the cytoplasm in pancreatic cancer cells and decreased the stability the SMAD4 mRNA. Finally, we found over-expression of LINC00909 not only accelerated tumor growth in subcutaneous mice models, but also facilitated tumorigenicity and spleen metastasis in orthotopic mice models. Conclusion: We demonstrate LINC00909 inhibits SMAD4 expression at the post-transcriptional level, which up-regulates the expression of pluripotency factors and activates the MAPK/JNK signaling pathway, leading to enrichment of cancer stem cells and cancer metastasis in pancreatic cancer. [ABSTRACT FROM AUTHOR]

The sustainability of biogas production from straws is limited by the collection, transportation, storage, and pretreatment of feedstocks. To address these constraints, this study investigated briquetting as a pretreatment strategy for rice straw (RS) to increase bioenergy generation. The results indicated that briquetted RS yielded 205.4 mL/g VS of methane, which was 11.7% higher compared to that produced by the untreated RS. The economic analysis revealed that the briquetting process had positive effects with a payback time of 3.4 y and an internal rate of return of 23.4%. It also reduced feedstock transportation and storage costs by 42.6%. Adding a NaOH treatment to the briquetting process increased methane production by 26.4% compared to untreated RS. However, the integration of briquetting with NaOH treatment might be an unprofitable method for processing RS. This became apparent when examining the production cost, which stood at 1.13 $/kg biomethane with an internal rate of return of 16.2%, representing an 8.7% increase and a 7.2% decrease, respectively, compared to the mono briquetting method. These results revealed that briquetting as a source pretreatment strategy can improve the productivity of straw biogas plants, thereby advancing the industry towards cleaner production. [Display omitted] • Briquetting, a source pretreatment strategy, improved straw biogas production. • The briquetting strategy integrates the collection and pretreatment of rice straw. • The proposed strategy reduced straw transportation and storage costs by 42.6%. • Adding an NaOH treatment reduced the profitability of a straw biogas plant. [ABSTRACT FROM AUTHOR]