Figures index

From

Colorectal Cancer Remains A Formidable Global Health Challenge

Mariam Abulgith, Salhah Alshihri, Hassan Al mnamis, Ohud Asiri, Nourah Shaio, Fatimah Alqisi

American Journal of Medical and Biological Research. 2024, 12(2), 49-60 doi:10.12691/ajmbr-12-2-3
  • Figure 1. Flowchart for comprehensive analysis of prognostic model based on recurrence related genes in colorectal cancer
  • Figure 2. Identification of key genes for recurrence in colorectal cancer. (A) Volcano plot and (B) heatmap showing differentially expressed genes between recurrent and non-recurrent colorectal cancer patients in the GSE17536 dataset; (C) Principal Component Analysis (PCA); (D-F) Enrichment analysis of upregulated genes: (D) KEGG pathway, (E) GO-BP, and (F) Hallmark gene set; (G-I) Enrichment analysis of downregulated genes: (G) KEGG pathway, (H) GO-BP, and (I) Hallmark gene set
  • Figure 3. Construction of a diagnostic model for colorectal cancer recurrence. (A-B) Lasso regression for constructing the diagnostic model of colorectal cancer recurrence; (C) Differential analysis of RRGS values between recurrent and non-recurrent groups; (D) ROC analysis of RRGS for diagnosing colorectal cancer recurrence; (E) RRGS, survival status, and expression levels of the eleven genes in the GSE17536 cohort; (F) The impact of RRGS on patients' overall survival (OS) in the GSE17536 cohort; (G) Time-dependent ROC analysis of RRGS; (H) The impact of RRGS on patients' disease-free survival (DFS) in the GSE17536 cohort; (I) RRGS, survival status, and expression levels of the eleven genes in the TCGA cohort; (J) The impact of RRGS on patients' overall survival (OS) in the TCGA cohort
  • Figure 4. Correlation analysis of risk score with clinical characteristics of colorectal cancer. (A) Analysis of RRGS expression differences based on gender, tumor type, TMN staging, and overall stage using TCGA cohort; (B) Gene mutation analysis in RRGS-High and RRGS-Low subgroups; (C) GSVA analysis of the correlation between RRGS and different signaling pathways; (D) Correlation analysis of seven signaling pathways positively associated with RRGS in the TCGA cohort; (E) Correlation analysis of seven signaling pathways positively associated with RRGS in the GSE17536 cohort. NS, p>0.05; ***, p<0.001
  • Figure 5. Relationship between RRGS and the immune microenvironment. (A) Results of differential immune cell infiltration between RRGS-High and RRGS-Low subgroups assessed by CIBERSORT and ESTIMATE; (B) The relative cell abundances of macrophages between the two groups are calculated using xCELL and CIBERSORT. *, p<0.05; ***, p<0.001
  • Figure 6. Prognostic analysis of RRGS in colorectal cancer patients undergoing chemotherapy. (A-C) Differential expression analysis of RRGS in colorectal cancer patients with chemotherapy from the GSE40967 dataset, based on (A) stage, (B) T classification, and (C) M classification; (D-E) The impact of RRGS on patients' overall survival (OS) and disease-free survival (DFS) in the GSE40967 cohort. NS, p>0.05; *, p<0.05
  • Figure 7. High expression of STC1 in colorectal cancer tissue is associated with poor prognosis. (A-I) The expression of STC1 between cancer tissues and adjacent non-cancerous tissues in (A) GSE18105, (B) GSE21510, (C) GSE25071, (D) GSE39582, (E) GSE41258, (F) GSE62321, (G) GSE71187, (H) GSE87211, and (I) TCGA cohort. (J-O) OS analysis of STC1 in the (J) TCGA, (K) GSE71187, (L) GSE41258, (M) GSE39582, (N) GSE17537, and (O) GSE17536 cohort. (P-R) RFS analysis in the (P) GSE17536, (Q) GSE29621, and (R) GSE103479 cohort. (S-V) DFS analysis of STC1 in the (S) GSE161158, (T) GSE38832, (U) TCGA, and (V) GSE17536 cohort. (W-X) STC1 protein expression in (W) colorectal cancer tissues and (X) adjacent normal tissues from the THPA database. *, p<0.05; **, p<0.01; ***, p<0.001
  • Figure 8. Knockdown of STC1 inhibits the in vitro proliferation and metastasis capabilities of colorectal cancer cells. (A) RT-PCR detection of STC1 expression after knockdown in HCT-116 cells; (B) CCK8 assay for changes in proliferation ability after STC1 knockdown in HCT-116 cells; (C-D) Effect of STC1 knockdown on migration and invasion abilities of HCT-116 cells (C) migration and (D) invasion; (E) RT-PCR detection of STC1 expression after knockdown in DLD1 cells; (F) CCK8 assay for changes in proliferation ability after STC1 knockdown in DLD1 cells; (G-H) Effect of STC1 knockdown on migration and invasion abilities of DLD1 cells (G) migration and (H) invasion.**, p<0.01; ***, p<0.001
  • Figure 9. Knockdown of STC1 inhibits the proliferation and metastasis capabilities of colorectal cancer cells in zebrafish. Effect of STC1 knockdown on in vivo proliferation and metastasis capabilities of HCT-116 cells in zebrafish (A) proliferation and (B) metastasis. NS, p>0.05; *, p<0.05; **, p<0.01