Fig 1: Validation of the predictive efficacy of the signature for predicting recurrence of laryngeal cancer in the verification set. (A) Heat maps visualizing the differences expression patterns of these eight genes including RCN1, LAT2, DAPK2, DNAJA2, FUZ, LASP1, IBSP and HOOK2 between high- and low- risk score group. Red expresses up-regulation and blue indicates down-regulation. (B) Ranking of risk scores among all laryngeal cancer patients. (C) Distribution of recurrence time among all laryngeal cancer patients. Red dots express recurrence laryngeal cancer samples and blue dots represent non-recurrence samples. The dotted line indicates the optimal cutoff value of risk score. The left side of the line represents low-risk patients, while the right side represents high-risk patients. (D) Recurrence-free survival between high- and low- risk score groups. (E) ROC curve for predicting the patients’ 1-year recurrence. (F) ROC curves for predicting the patients’ 3 and 5-year recurrence.
Fig 2: Validation of the genes in the prognostic signature. (A–I) Western blot for detection of the protein expression of (B) RCN1, (C) DNAJA2, (D) LASP1, (E) IBSP, (F) LAT2, (G) FUZ, (H) HOOK2, and (I) DAPK2 in laryngeal cancer and normal tissues. (J–Q) RT-qPCR for detecting the mRNA expression of (J) RCN1, (K) DNAJA2, (L) LASP1, (M) IBSP, (N) LAT2, (O) FUZ, (P) HOOK2, and (Q) DAPK2 in laryngeal cancer and normal tissues. Ns, not significant; *P < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.
Fig 3: miR-29a-3p reverses the effects of H19 on OS cells. miR-29a-3p expression was elevated in (A) MG-63 and (B) Saos-2 cells transfected with H19 siRNA. LASP1 mRNA and protein expression levels were decreased by inhibition of H19 and restored by miR-29a-3p inh in (C and E) MG-63 and (D and F) Saos-2 cells. Data are expressed as the mean ± SEM (n=3). *P<0.05, **P<0.01 and ***P<0.001 vs. NC + inh-NC. miR, microRNA; si, small interfering; LASP1, LIM and SH3 domain protein 1; inh, inhibitor; NC, negative control.
Fig 4: Lasp-1 and ERK1/2 expression levels in tumors and adjacent normal colorectal mucosa tissues. The mRNA expression of (A) Lasp-1 and (B) ERK1/2 was examined in 20 pairs of colorectal cancer and adjacent normal tissues using the reverse transcription-quantitative polymerase chain reaction. ***P<0.001. (C) Lasp-1, ERK1/2 and p-ERK1/2 protein expression was examined in representative samples using western blot analysis. (D) Quantitative densitometric analysis of the western blotting data (n=20; *P<0.05 vs. N). Lasp-1, LIM and SH3 protein 1; ERK, extracellular-signal-regulated kinase; p-, phospho-; N, normal group; T, tumor group.
Fig 5: Effects of Lasp-1 in cellular proliferation, induction of apoptotic cell death and cell cycle progression in colorectal carcinoma cells. Cells were transfected with Lasp-1 siRNA or NC siRNA. (A) Cellular proliferation was determined using the Cell Counting Kit-8 assay (n=3; *P<0.05 vs. NC; #P<0.05 vs. siRNA). (B) Cellular apoptosis and (C) cell cycle progression were detected using flow cytometric analysis. Lasp-1, LIM and SH3 protein 1; NC, negative control; siRNA, small interfering RNA; PI, propidium iodide; FITC, fluorescein isothiocyanate.
Supplier Page from Abcam for Anti-LASP1 antibody [EPR11221]