Cancer stem‑like cells with increased expression of NY‑ESO‑1 initiate breast cancer metastasis
- Mai‑Ying Liu
- Hang Su
- Hua‑Lan Huang
- Jing‑Qi Chen
Published online on: August 1, 2019
Copyright: © Liu et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
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Breast cancer stem‑like cells (BCSLCs) with a CD44+/CD24‑/low phenotype initiate the invasion and metastasis of breast cancer. The expression of New York oesophageal squamous cell carcinoma 1 (NY‑ESO‑1), one of the most immunogenic cancer‑testicular antigens, is largely restricted to cancer and germ cells/placental trophoblasts, with little to no expression in normal adult somatic cells. Currently, few studies have reported the expression or function of NY‑ESO‑1 in BCSLCs. In the present study, immunohistochemistry indicated enhanced expression levels of NY‑ESO‑1/CD44 (P<0.01) and decreased expression levels of CD24 (P<0.01) in metastatic breast cancer tissues (MBCT) compared with non‑MBCT. Additionally, the co‑localization of CD44, CD24 and NY‑ESO‑1 in tissue samples was determined using immunofluorescence analysis. The results revealed that the expression of NY‑ESO‑1/CD44/CD24 was associated with breast cancer metastasis. Moreover, Spearman's rank correlation analysis indicated that CD44/CD24 expression was significantly correlated with that of NY‑ESO‑1. In the present study, mammosphere culture, a valuable method of BCSLC enrichment, was used to enrich MCF‑7 and SK‑BR‑3 BCSLCs; immunofluorescence, western blotting and flow cytometry demonstrated increased expression levels of NY‑ESO‑1 and CD44, and low expression levels of CD24 in BCSLCs. Furthermore, the cell migration and invasion assays verified that BCSLCs with an increased NY‑ESO‑1 expression level exhibited greater invasive and migratory capacity compared with parental breast cancer cells. In addition to previously reported findings from the Oncomine database, it was ascertained that CD44+/CD24‑/low BCSLCs with an increased level of NY‑ESO‑1 expression initiated the invasion and metastasis of breast cancer; therefore, NY‑ESO‑1 may serve as a novel target for metastatic breast cancer immunotherapy.