IGHG1 promotes malignant progression in breast cancer cells through the regulation of AKT and VEGF signaling

Authors

  • Yong Zhang Department of Surgery, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China
  • Xueying Fang Department of Oncology, Beijing Puxiang Traditional Chinese Medicine Cancer Hospital, Beijing, China
  • Yan Sun Department of Surgery, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China https://orcid.org/0000-0002-5727-9562

DOI:

https://doi.org/10.17305/bb.2022.8508

Keywords:

Breast cancer, vascular endothelial growth factor (VEGF), AKT, immunoglobulin heavy constant chain gamma 1 (IGHG1)

Abstract

Immunoglobulin heavy constant chain gamma 1 (IGHG1) is highly expressed in a variety of cancers and is considered an emerging prognostic marker. Overexpression of IGHG1 in breast cancer tissues has also been demonstrated, but an in-depth analysis of its role in disease progression has not been explored. In this study, we used a range of molecular and cell-based assays to show that increased expression of IGHG1 in breast cancer cells activates AKT and vascular endothelial growth factor (VEGF) signaling, leading to enhanced cell proliferation, invasion, and angiogenesis. We further showed that IGHG1-silencing can suppress the neoplastic characteristics of breast cancer cells in vitro and suppresses tumor growth in nude mice. These data reveal a key role of IGHG1 in the malignant progression of breast cancer cells and highlight its potential as a prognostic marker and therapeutic target to control metastasis and angiogenesis in malignant breast tissue.

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IGHG1 promotes malignant progression in breast cancer cells through the regulation of AKT and VEGF signaling

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Published

03-07-2023

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Section

Molecular Biology

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How to Cite

1.
IGHG1 promotes malignant progression in breast cancer cells through the regulation of AKT and VEGF signaling. Biomol Biomed [Internet]. 2023 Jul. 3 [cited 2024 Jun. 15];23(4):616–623. Available from: https://www.bjbms.org/ojs/index.php/bjbms/article/view/8508