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Heterogeneity of CEACAM5 in breast cancer.

ABSTRACT: CEACAM5 is overexpressed in many primary breast carcinomas. However, the exact role of CEACAM5 in breast cancer tumorigenesis remains unresolved. Here, we examined a repository of 110 cryopreserved primary breast carcinomas by immunohistochemistry to assess the distribution of CEACAM5 in tumor subtypes. The majority of estrogen receptor-positive and HER2-overexpressing tumors were CEACAM5-positive, whereas most of Triple-negative tumors were negative. Assessing sample sets of paired primary breast cancers and corresponding lymph node lesions from a total of 59 patients revealed a high correlation between primary tumor and lymph node with regard to CEACAM5-status. However, a notable subset of sample sets demonstrated intratumoral heterogeneity in the primary tumor, the metastatic lesion or both, suggesting that both CEACAM5-positive and -negative cells can play a role in tumor dissemination. When examining the consequence of expression of CEACAM5 in breast cancer cell lines in culture assays we found that CEACAM5-expressing cells were less invasive. In survival analysis, using cohort studies of breast cancer, expression of CEACAM5 predicted different clinical outcomes depending on molecular subtypes. Altogether, our analysis suggests that CEACAM5 plays a context-dependent role in breast cancer that warrants further investigation.

SUBMITTER: Bechmann MB

PROVIDER: S-EPMC7597409 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Heterogeneity of CEACAM5 in breast cancer.

Bechmann Marc B MB Brydholm Andreas V AV Codony Victoria L VL Kim Jiyoung J Villadsen René R

Oncotarget 20201027 43

CEACAM5 is overexpressed in many primary breast carcinomas. However, the exact role of CEACAM5 in breast cancer tumorigenesis remains unresolved. Here, we examined a repository of 110 cryopreserved primary breast carcinomas by immunohistochemistry to assess the distribution of CEACAM5 in tumor subtypes. The majority of estrogen receptor-positive and HER2-overexpressing tumors were CEACAM5-positive, whereas most of Triple-negative tumors were negative. Assessing sample sets of paired primary brea ...[more]

PMID: 33196697

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Project description:ObjectiveTo explore the heterogeneity of pancreatic cancer and new methods for tumor cell molecular subtyping and identify the signature genes in pancreatic cancer progression.MethodsBased on the single-cell sequencing data of 16 pancreatic cancer tissues from the GSE155698 dataset, the single pancreatic cancer cells were classified according to EPCAM gene expression after preliminary clustering, re-clustering, and subgrouping to identify the signature genes, followed by pathway enrichment analysis and pseudo-time analysis. The key genes identified were validated using the clinical and tissue gene and protein expression data from 179 pancreatic cancer patients and 171 healthy controls. The impact of CEACAM5, LGALS1, and CENPF on proliferation, migration and invasion of pancreatic cancer cells were analyzed.ResultsAnalysis of 48 570 cells from 16 pancreatic cancer samples revealed a total of 22 clusters, including 5 clusters of pancreatic cancer cells, which were classified into Subtype 1, Subtype 2, and Subtype 3, each exhibiting distinct gene expression patterns and functions. The signature genes were enriched in negatively regulated protein metabolic processes, ferroptosis, and antigen processing and presentation-related pathways in Subtype 1 pancreatic cancer cells; in peptide synthesis processes, translation, and ribosome-related pathways in Subtype 2; and in ATP metabolic processes, glycolysis/gluconeogenesis, and cell cyclerelated pathways in Subtype 3. Subtypes 2 and 3 were potentially derived from Subtype 1, and Subtype 3 possibly represented the final developmental stage of pancreatic cancer cells. The key signature genes (CEACAM5, LGALS1, and CENPF) also exhibited different expression patterns in the developmental trajectory and showed high expressions in pancreatic cancer in association with poor prognoses. In pancreatic cancer cells, downregulation of CEACAM5, LGALS1, and CENPF significantly inhibited the proliferation, migration, and invasion abilities of the cells (P<0.05).ConclusionPancreatic cancer cells exhibit significant heterogeneity, and CEACAM5, LGALS1, and CENPF gene expressions, which affect pancreatic cancer cell proliferation, invasion, and metastasis, can be used to identify distinct molecular subtypes during tumor cell development.

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Heterogeneity of CEACAM5 in breast cancer.

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Heterogeneity of CEACAM5 in breast cancer.

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