Fig. 1: Screening for lncRNAs that may regulate G1/S transition.

A–B The cell cycle distribution and the expression pattern of cell cycle-related genes in serum starvation-stimulation models. SF cells were serum-deprived and then cultured in the 15% FBS-containing medium at the indicated time periods before FACS (A) or qPCR (B). The percentage of cells at the G1-phase is indicated for each sample (A). The time point for serum re-addition was set as 0 h. C Heat map of lncRNA expression profiles during cell cycle progression. For A–C, S⁺ indicates serum re-addition. D Pan-cancer analysis of SNHG17 expression based on TCGA data. The levels of SNHG17 in paired tumor (T) and non-tumor (N) tissues from 10 different cancer types are presented. LIHC, liver hepatocellular carcinoma; BLCA, bladder urothelial carcinoma; BRCA, breast invasive carcinoma; HNSC, head and neck squamous cell carcinoma; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; PRAD, prostate adenocarcinoma; STAD, stomach adenocarcinoma. E Kaplan–Meier analysis revealed a significant association between higher SNHG17 level and shorter recurrence-free survival or overall survival of HCC patients. The median SNHG17 level in all 364 HCC tissues, derived from TCGA, was chosen as the cut-off value to separate the high-SNHG17 group (n = 182) from the low-SNHG17 group (n = 182). F The level of SNHG17 was significantly increased in HCC tissues of our study cohort. The expression of SNHG17 was assessed by qPCR in 60 paired HCC (T) and adjacent non-tumor liver tissues (N). For B, error bars represent mean ± SEM from three independent experiments. P values were assessed by paired Student’s t test (D, F) or log-rank test (E). *, P < 0.05; **, P < 0.01; ***, P < 0.001.