IGHG1 Regulates Prostate Cancer Growth via the MEK/ERK/c-Myc Pathway.

Jing Chu,Zhihai Deng,Weifeng Zhong,Yutong Li,Qun Xie,Zhenlin Zhang,Heyuan Zhang,Bin Pan

doi:10.1155/2019/7201562

Abstract

Increasing evidence indicates that immunoglobulins are important for the regulation of various cancers including prostate cancer (PCa). However, the underlying mechanisms of IgG regulated PCa development remain to be further explored. Here, we demonstrated that IgG1 heavy chain (IGHG1) was increased in tissues from PCa patients. Inhibition of IGHG1 by antibody blocking or genetic knockdown suppressed cell growth and induced cell cycle arrest and ultimate apoptosis. Expression levels of c-Myc were positively correlated with the levels of IGHG1. Furthermore, MEK/ERK/c-Myc pathway lied downstream of IGHG1 in cultured prostate cancer cells. Inhibition of IGHG1 restrained the tumor growth in nude mice and inactivated MEK/ERK/c-Myc pathway both in vitro and in vivo. These findings suggest that IGHG1 play a crucial role during the development of prostate cancer and inhibition of IGHG1 may be a potential therapy in the treatment of PCa.

Highlights

Prostate cancer (PCa), the second leading cause of cancerrelated death of man, is one of the most common cancers of urinary system [1]
We found that IGHG1 was upregulated in clinical prostate cancer tissue from PCa patients and downregulation of IGHG1 reduced the growth and proliferation of PCa cells
In order to further determine the role of IGHG1, we firstly searched the Oncomine database for gene expressions in prostate cancer

Summary

Introduction

Prostate cancer (PCa), the second leading cause of cancerrelated death of man, is one of the most common cancers of urinary system [1]. Metastasis induces the morbidity and mortality of PCa patients [2, 3]. Hormone therapy is one the most common treatments of PCa. Restricted androgen level shrinks cancer volume and delays the development of tumors. Hormone therapy only results in a medium survival time of around 12 months in patients with metastatic PCa [4]. Further elucidation of PCa development of molecular mechanisms and exploration of new therapeutic targets and reliable biomarkers for detection of metastatic potential are of specific importance

Methods

Results

Conclusion