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Small breast epithelial mucin promotes the invasion and metastasis of breast cancer cells via promoting epithelial?to?mesenchymal transition.

ABSTRACT: The aim of the present study was to observe the influence of the small breast epithelial mucin (MUCL1) (also known as SBEM) gene on migration and invasion ability of breast cancer cells and to explore the potentially involved mechanism. SBEM?interference plasmid and SBEM?overexpressing plasmid were constructed. SBEM?knockdown or SBEM??overexpressing MCF?7 and MDA?MB?231 breast cancer cells were established by lentivirus?mediated stable transfection method. The scratch wound?healing assay and Transwell chamber experiment were used to detect the influence of the SBEM gene on the migration and invasion abilities of MCF?7 and MDA?MB?231 cells. Real?time PCR (polymerase chain reaction) and western blotting were used to detect the expression of epithelial?to?mesenchymal transition (EMT)?related markers and regulators. The cell morphology was observed after transfection. The SBEM?knockdown or SBEM?overexpressing MCF?7 and MDA?MB?231 cells were established successfully. The migration and invasion abilities were decreased after SBEM was downregulated, and were increased after SBEM was overexpressed both in MCF?7 and MDA?MB?231 cell lines. The mRNA and protein expressions of N?cadherin, Twist and vimentin were elevated following SBEM overexpression, while the expression of E?cadherin and claudin?1 were found to be decreased following SBEM overexpression. In conclusion, SBEM has the potential to promote migration and invasion ability of breast cancer cells via promoting epithelial?to?mesenchymal transition.

SUBMITTER: Li QH

PROVIDER: S-EPMC7336452 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Small breast epithelial mucin promotes the invasion and metastasis of breast cancer cells via promoting epithelial‑to‑mesenchymal transition.

Li Qiu-Hua QH Liu Zhao-Zhe ZZ Ge Ya-Νan YΝ Liu Xing X Xie Xiao-Dong XD Zheng Zhen-Dong ZD Ma Yue-Hai YH Liu Bin B

Oncology reports 20200609 2

The aim of the present study was to observe the influence of the small breast epithelial mucin (MUCL1) (also known as SBEM) gene on migration and invasion ability of breast cancer cells and to explore the potentially involved mechanism. SBEM‑interference plasmid and SBEM‑overexpressing plasmid were constructed. SBEM‑knockdown or SBEM‑overexpressing MCF‑7 and MDA‑MB‑231 breast cancer cells were established by lentivirus‑mediated stable transfection method. The scratch wound‑healing assay and Tra ...[more]

PMID: 32627029

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Project description:BACKGROUND:Activins belong to the transforming growth factor-? (TGF-?) superfamily of cytokines. Although the role of TGF-? in cancer progression has been highly advocated, the role of activin signaling in cancer is not well known. However, overexpression of activin-A has been observed in several cancers. AIMS:The gene expression profile indicated higher expression of Activin-A in breast tumors. Hence the aim of this study was to evaluate the status and role of Activin signaling pathway in these tumors. METHODS:Microarray analysis was performed to reveal gene expression changes in breast tumors. The results were validated by quantitative PCR and immunohistochemical analysis in two independent sets of normal and tumor samples. Further, correlation of activin expression with survival and distant metastasis was performed to evaluate its possible role in tumor progression. We used recombinant activin-A, inhibitors, overexpression, and knockdown strategies both in vitro and in vivo, to understand the mechanism underlying the protumorigenic role of this signaling pathway. RESULTS:We report that activin-A signaling is hyperactivated in breast cancers as indicated by higher activin-A, phosphoSMAD2, and phosphoSMAD3 levels in advanced breast cancers. Bone morphogenetic proteins and molecules involved in this signaling pathway were downregulated, suggesting its suppression in breast cancers. Activin-A expression correlates inversely with survival and metastasis in advanced breast cancers. Further, activin-A promotes anchorage-independent growth, epithelial-mesenchymal transition, invasion, angiogenesis, and stemness of breast cancer cells. We show that activin-A-induced phenotype is mediated by SMAD signaling pathway. In addition, activin-A expression affects the tumor-forming ability and metastatic colonization of cancer cells in nude mice. CONCLUSIONS:These results suggest that activin-A has a critical role in breast cancer progression and, hence, targeting this pathway can be a valuable strategy in treating breast cancer patients.

Dataset Information

Small breast epithelial mucin promotes the invasion and metastasis of breast cancer cells via promoting epithelial?to?mesenchymal transition.

Publications

Small breast epithelial mucin promotes the invasion and metastasis of breast cancer cells via promoting epithelial‑to‑mesenchymal transition.

Similar Datasets

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