Search

Additional file 5: Table S3. Correlation between LINRIS expression and clinicopathological features in 118 CRC patients.

Additional file 2: Table S2. The sequences of siRNAs or shRNAs used in this article.

Additional file 3. Supplementary methods.

Additional file 13: Table S6. Correlation between LINRIS/IGF2BP2 expression and clinicopathological features in 220 CRC patients.

Additional file 10: Figure S5, related to Fig. 5. In vivo experiments elucidated the effect of the inhibition of LINRIS in CRC. (A) qPCR detection shows the relative RNA levels of LINRIS in tumors in two PDX experiments. Error bars, SD of four independent experiments. *P

Additional file 4: Figure S1, related to Fig. 1. Identification of LINRIS as an oncogenic lncRNA in CRC. (A) Volcano plots of downregulated and upregulated lncRNA, including LINRIS, based on RNA-seq. (B) LINRIS was highly expressed in CRC tissues (T, n = 21) compared with the expression in normal colon tissues (N). *P

Figure S2. Mean plasma concentration–time curve of ascorbic acid after fixed-rate infusions at 0.6, 0.8, 1.0 g/min to cancer patients. After i.v. administration, the plasma concentrations of ascorbic acid rose gradually and peaked at 3 h. Cmax, and AUC values of ascorbic acid display dose-dependent increases. Ascorbic acid concentrations in the high-dose groups remained at 10–20 mmol/L for more than 4 h and showed no accumulation in the body during the administrations. (PDF 20 kb)

Additional file 7: Figure S2, related to Fig. 2. LINRIS was associated with IGF2BP2 in CRC. (A) The protein score graph of the 18 proteins identified by the RNA pull-down and LC-MS. (B) The emPAI graph of the 18 proteins identified by RNA pull-down assays and LC-MS. (C) Protein cover graph of the 18 proteins identified by RNA pull-down assays and LC-MS. (D) Immunofluorescence assays identifying the subcellular location of IGF2BP2 in the indicated cells. Bar scale: 50 μm. (E) Computational secondary structure of LINRIS predicted with RNAfold. (F) In vitro-synthesized full-length (FL) and 450–640 nt fragments of LINRIS were incubated with protein lysates from HCT116 cells. RNA pull-down and Western blotting assays were then performed. The data shown represent three independent experiments. (G) qPCR detection of LINRIS levels in 11 CRC cell lines. The data are shown as the mean ± SD; n = 3 independent experiments, two-tailed Student’s t-test, *P

Table S1. Pharmacokinetic values. The volumes of distribution and clearance were similar to those parameters in the fixed infusion time group. When the recommended subsequent dose was administered, the plasma concentrations of AA were maintained at 10â 20â mmol/L for more than 4â h. (DOCX 17 kb)

Figure S1. Evaluation of the ascorbic acid dose proportionality in part 1 of the study. The mean AA Cmax and AUC are presented vs increasing doses of AA (measured after the first administered dose of AA) on day 1 and day 3. AUC 0â 9: area under the plasma concentration-time curve from time zero to hour 9; Cmax: maximum plasma concentration. (PDF 21 kb)

Additional file 6: Table S4. Effect of factors on OS in the CRC patients in the univariate and multivariate Cox regression model.

Additional file 8: Figure S3, related to Fig. 3. LINRIS is involved in the autophagic degradation of IGF2BP2. (A) Western blotting shows the levels of IGF2BP2 in the indicated cells with the knockdown of LINRIS after treatment with or without 3-MA (10 mg/ml) for 24 h. GAPDH was used as the loading control. (B) Confocal microscopy of HCT116 cells treated with or without EBSS for 3 h. Scale bar, 50 μm. (C) Western blotting shows the knockout of ATG5 in DLD-1 cells with sgRNA (sg-ATG5) compared with that in control cells. GAPDH was used as the loading control. (D) DLD-1 cells with the knockout of ATG5 and control cells were transfected with shRNAs specific for LINRIS. Cell lysates were analyzed by immunoblotting with GAPDH as the loading control.

Additional file 12: Table S5. Correlation between IGF2BP2 expression and clinicopathological features in 220 CRC patients.