Fig 2: Role of MPZL3 in cell proliferation and drug sensitivity among different breast cancer subtypes. Western blotting (A) was applied to detect MPZL3 expression after breast cancer cell lines were transfected with vector control and the MPZL3-overexpression plasmid. The cell proliferation ability (B) and colony formation (C, D) were assessed after breast cancer cell lines were transfected with vector control and the MPZL3-overexpression plasmid. (E–H) The drug sensitivity of fulvestrant, pyrotinib, and paclitaxel was measured in MCF7, SKBR3, and MDA-MB-231 cells after transfection with vector control and the MPZL3-overexpression plasmid. MPZL3, Myelin Protein Zero-like 3. (*p < 0.05, **p < 0.01, ***p < 0.001).

Fig 3: Association between MPZL3 and hallmarks across cancers. (A) Correlations of MPZL3 expression with HALLMARKS enrichment scores in 33 cancer types. (B) Enrichment analysis of hallmarks in the MPZL3 high- and low-expression groups. MPZL3, Myelin Protein Zero-like 3.

Fig 4: MPZL3 expression level in pan-cancer. (A) Comparison of MPZL3 expression in normal tissues in the GTEx database. (B) MPZL3 expression differed in tumor cell lines from the CCLE database. (C). MPZL3 expression differed in paired tumor and normal tissues of 27 cancer types from the TCGA and GTEx databases. (D) Correlations between the MPZL3 level and clinicopathological characteristics in BRCA. MPZL3, Myelin Protein Zero-like 3; GTEx, Genotype-Tissue Expression; CCLE, Cancer Cell Line Encyclopedia; TCGA, Cancer Genome Atlas; BRCA, breast invasive carcinoma. (*p < 0.05, **p < 0.01, ***p < 0.001).

Fig 5: MPZL3 mutation across cancers. (A, B) The mutation frequency and mutation count of MPZL3 in pan-cancer by the cBioPortal database.(C) Mutation diagram of MPZL3 in different cancer types across protein domains. (D) The different mutation landscapes in the MPZL3 high- and low-expression groups in BRCA. MPZL3, myelin protein zero-like 3; BRCA, breast invasive carcinoma.