Image_1_The Interaction Between lncRNA SNHG6 and hnRNPA1 Contributes to the Growth of Colorectal Cancer by Enhancing Aerobic Glycolysis Through the Regulation of Alternative Splicing of PKM.TIF

Background: Small nucleolar RNA host gene 6 (SNHG6) acts as a carcinogenic gene in colorectal cancer (CRC). However, previous studies on the mechanism by which long non-coding RNA (lncRNA) SNHG6 exerts its carcinogenic effect in CRC have not involved the direct interaction between SNHG6 and proteins, which is a very important carcinogenic mechanism of lncRNAs. Hence, our study conducted a comprehensive RNA-binding proteins–mass spectrometry (ChIRP–MS) analysis on SNHG6 to further explore its carcinogenic mechanism in CRC.Methods: Proteins that interact with SNHG6 were found using ChIRP–MS analysis and were used to construct the protein–protein interactive (PPI) network using STRING, while the core module of the PPI network was identified using the MCODE plugin in Cytoscape. Pathway enrichment analyses, using WebGestalt, were performed on proteins and RNAs that were found to be associated with the expression of SNHG6 or which directly interacted with SNHG6. Finally, CatRAPID, miRbase, and TargetScanHuman were used to identify the sites of interaction between SNHG6, heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1), and pyruvate kinase M (PKM) mRNA.Results: The expression of SNHG6 in CRC was found to be higher than that of normal tissues and was positively correlated with a poor prognosis (p Conclusion: SNHG6 was found to be able to target the mRNA of PKM as well as induce hnRNPA1 to specifically splice PKM mRNA, which increased the proportion of PKM2/PKM1, which may be an important carcinogenic mechanism in CRC that proceeds through the enhancement of aerobic glycolysis in CRC cells.</p

Data_Sheet_1_The Interaction Between lncRNA SNHG6 and hnRNPA1 Contributes to the Growth of Colorectal Cancer by Enhancing Aerobic Glycolysis Through the Regulation of Alternative Splicing of PKM.docx

Background: Small nucleolar RNA host gene 6 (SNHG6) acts as a carcinogenic gene in colorectal cancer (CRC). However, previous studies on the mechanism by which long non-coding RNA (lncRNA) SNHG6 exerts its carcinogenic effect in CRC have not involved the direct interaction between SNHG6 and proteins, which is a very important carcinogenic mechanism of lncRNAs. Hence, our study conducted a comprehensive RNA-binding proteins–mass spectrometry (ChIRP–MS) analysis on SNHG6 to further explore its carcinogenic mechanism in CRC.Methods: Proteins that interact with SNHG6 were found using ChIRP–MS analysis and were used to construct the protein–protein interactive (PPI) network using STRING, while the core module of the PPI network was identified using the MCODE plugin in Cytoscape. Pathway enrichment analyses, using WebGestalt, were performed on proteins and RNAs that were found to be associated with the expression of SNHG6 or which directly interacted with SNHG6. Finally, CatRAPID, miRbase, and TargetScanHuman were used to identify the sites of interaction between SNHG6, heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1), and pyruvate kinase M (PKM) mRNA.Results: The expression of SNHG6 in CRC was found to be higher than that of normal tissues and was positively correlated with a poor prognosis (p Conclusion: SNHG6 was found to be able to target the mRNA of PKM as well as induce hnRNPA1 to specifically splice PKM mRNA, which increased the proportion of PKM2/PKM1, which may be an important carcinogenic mechanism in CRC that proceeds through the enhancement of aerobic glycolysis in CRC cells.</p

MOESM1 of LncRNA SNHG6 promotes chemoresistance through ULK1-induced autophagy by sponging miR-26a-5p in colorectal cancer cells

Additional file 1: Figure S1. (a, b) RKO/5-FU cells had lower level of cell apoptosis and higher level of LC3-II. (c) RKO/5-FU cells had higher IC50 than RKO cells. (d) Graphs of cell apoptosis. ns P > 0.05, *P < 0.05, **P < 0.01, *** P < 0.001, ****P < 0.0001, data was shown as the mean ± SD

MOESM2 of LncRNA SNHG6 promotes chemoresistance through ULK1-induced autophagy by sponging miR-26a-5p in colorectal cancer cells

Additional file 2: Figure S2. (a) KEGG analysis showed ULK1 might be one of the downstream target genes of miR-26a-5p and related to mTOR signal pathway. (b) STRING analysis showed ULK1 interaction network. (c–e) qRT-PCR showed SNHG6 could inhibit miR-26a-5p but upregulate ULK. (f–h) qRT-PCR showed miR-26a-5P could inhibit ULK1 but have no effect on SNHG6 (i-k) qRT-PCR showed inhibiting miR-26a-5p in RKO-shSNHG6 cells could bring back ULK1. ns P > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, data was shown as the mean ± SD