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Cancer Biology

High expression of LUM independently predicts poor prognosis in gastric cancer: a bioinformatics study combining TCGA and GEO datasets

ORCID Icon, & ORCID Icon
Pages 1063-1072 | Received 08 Aug 2021, Accepted 27 Oct 2021, Published online: 17 Nov 2021

Figures & data

Figure 1. LUM differential expression in normal and tumor tissues. A: comparison of TCGA profile; B: comparison of GEO dataset

Figure 1. LUM differential expression in normal and tumor tissues. A: comparison of TCGA profile; B: comparison of GEO dataset

Figure 2. Validation of protein expression of LUM in normal tissue (A) and gastric cancer (B) using the Human Protein Atlas database.

Figure 2. Validation of protein expression of LUM in normal tissue (A) and gastric cancer (B) using the Human Protein Atlas database.

Figure 3. Association of LUM expression with clinical variates. A: age; B: gender; C: grade; D: distant metastasis; E: lymph node metastasis; F: clinical stage; G: depth of invasion

Figure 3. Association of LUM expression with clinical variates. A: age; B: gender; C: grade; D: distant metastasis; E: lymph node metastasis; F: clinical stage; G: depth of invasion

Table 1. Logistic regression between LUM expression and clinicopathologic parameters.

Figure 4. Receiver operating characteristic curve for LUM expression in normal and gastric cancer tissues.

Figure 4. Receiver operating characteristic curve for LUM expression in normal and gastric cancer tissues.

Figure 5. LUM expression and overall survival in gastric cancer patients in TCGA profile (A) and the GSE84437 dataset (B).

Figure 5. LUM expression and overall survival in gastric cancer patients in TCGA profile (A) and the GSE84437 dataset (B).

Table 2. Univariate and multivariate analysis of the correlation between LUM expression and overall survival in gastric cancer patients.

Table 3. Univariate and multivariate analysis of the correlation between LUM expression and overall survival in gastric cancer patients validated using the GSE8443 dataset.

Figure 6. Significantly enriched signaling pathways of GSEA. Genes involved in extracellular matrix-receptor interaction (A), focal adhesion (B), cancer (C), chemokine signaling (D), Toll-like receptor signaling (E) and WNT signaling (F) were significantly enriched in LUM-related gastric cancer.

Figure 6. Significantly enriched signaling pathways of GSEA. Genes involved in extracellular matrix-receptor interaction (A), focal adhesion (B), cancer (C), chemokine signaling (D), Toll-like receptor signaling (E) and WNT signaling (F) were significantly enriched in LUM-related gastric cancer.