Cell migration inducing hyaluronidase 1 (CEMIP) activates STAT3 pathway to facilitate cell proliferation and migration in breast cancer

Abstract

Purpose

This paper aims to assess the role of CEMIP in human breast cancer, and explore the potential mechanisms of CEMIP in the progression of breast cancer.

Methods

We examined the expression levels of CEMIP in breast cancer tissues and cell lines by quantitative PCR and immunohistochemical assays. The effects of CEMIP on the proliferation, migration and invasion of breast cancer cells were determined through colony formation assay, flow cytometry (FCM) assay, wound healing assay and transwell assay, respectively. Additionally, the downstream targets of CEMIP were examined by Immunoblot assays.

Results

CEMIP expression was upregulated in both breast cancer tissues and cell lines. Patients with higher CEMIP expression displayed shorter survival time than those with lower expression. In addition, CEMIP knockdown inhibited breast cancer cell proliferation, migration, and invasion in vitro. Our data further confirmed that CEMIP promoted the proliferation and migration of breast cancer cells via GRP78-STAT3 axis.

Conclusion

Our data demonstrated the role of CEMIP in breast cancer was associated with STAT3 signaling pathway. Therefore, CEMIP might act as a possible therapeutic target for breast cancer.

Keywords:

• Breast cancer
• CEMIP
• GRP78
• migration
• proliferation
• STAT3 signaling pathway

Author contributions

LHL conceived and designed the experiments, YC analyzed and interpreted the results of the experiments, JFZ performed the experiments.

Ethics approval and consent to participate

The study was approved by the Ethics Committee of the Affiliated Hospital of Putian University (Approval no.201921). Formal consent was obtained from all patients.

Informed consent

Written informed consent was obtained from a legally authorized representative(s) for anonymous patient information to be published in this article.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

All data generated or analyzed during this study are included in this published article.