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鉴定 MAGEC2/CT10 为三阴性乳腺癌中高钙诱导基因。

Identification of MAGEC2/CT10 as a High Calcium-Inducible Gene in Triple-Negative Breast Cancer.

机构信息

Department of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, School of Graduate Studies and Research, Meharry Medical College, Nashville, TN, United States.

Bioinformatics Core, School of Graduate Studies and Research, Meharry Medical College, Nashville, TN, United States.

出版信息

Front Endocrinol (Lausanne). 2022 Mar 10;13:816598. doi: 10.3389/fendo.2022.816598. eCollection 2022.

DOI:10.3389/fendo.2022.816598
PMID:35355564
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8959981/
Abstract

The expression of the melanoma/cancer-testis antigen MAGEC2/CT10 is restricted to germline cells, but like most cancer-testis antigens, it is frequently upregulated in advanced breast tumors and other malignant tumors. However, the physiological cues that trigger the expression of this gene during malignancy remain unknown. Given that malignant breast cancer is often associated with skeletal metastasis and co-morbidities such as cancer-induced hypercalcemia, we evaluated the effect of high Ca on the calcium-sensing receptor (CaSR) and potential mechanisms underlying the survival of triple-negative breast cancer (TNBC) cells at high Ca. We show that chronic exposure of TNBC cells to high Ca decreased the sensitivity of CaSR to Ca but stimulated tumor cell growth and migration. Furthermore, high extracellular Ca also stimulated the expression of early response genes such as FOS/FOSB and a unique set of genes associated with malignant tumors, including MAGEC2. We further show that the MAGEC2 proximal promoter is Ca inducible and that FOS/FOSB binds to this promoter in a Ca- dependent manner. Finally, downregulation of MAGEC2 strongly inhibited the growth of TNBC cells . These data suggest for the first time that MAGEC2 is a high Ca inducible gene and that aberrant expression of MAGEC2 in malignant TNBC tissues is at least in part mediated by an increase in circulating Ca the AP-1 transcription factor.

摘要

黑色素瘤/睾丸抗原 MAGEC2/CT10 的表达局限于生殖细胞，但与大多数睾丸抗原一样，它在晚期乳腺癌和其他恶性肿瘤中经常上调。然而，导致该基因在恶性肿瘤中表达的生理信号仍然未知。鉴于恶性乳腺癌常与骨转移和癌症引起的高钙血症等合并症相关，我们评估了高钙对钙敏感受体 (CaSR) 的影响，以及高钙环境下三阴性乳腺癌 (TNBC) 细胞存活的潜在机制。我们发现，TNBC 细胞长期暴露于高钙中会降低 CaSR 对钙的敏感性，但会刺激肿瘤细胞的生长和迁移。此外，高细胞外钙还会刺激早期反应基因（如 FOS/FOSB）和与恶性肿瘤相关的一组独特基因的表达，包括 MAGEC2。我们进一步表明，MAGEC2 的近端启动子可被 Ca 诱导，并且 FOS/FOSB 以 Ca 依赖性方式结合到该启动子上。最后，下调 MAGEC2 可强烈抑制 TNBC 细胞的生长。这些数据首次表明，MAGEC2 是一种高钙诱导基因，恶性 TNBC 组织中 MAGEC2 的异常表达至少部分是由循环 Ca 增加介导的，而这种增加是通过 AP-1 转录因子介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/8959981/1316e1782b80/fendo-13-816598-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/8959981/1316e1782b80/fendo-13-816598-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/8959981/5389c8ae3b79/fendo-13-816598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/8959981/36b3417cdf96/fendo-13-816598-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/8959981/f8edf1f46062/fendo-13-816598-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/8959981/22e3e29b80a3/fendo-13-816598-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/8959981/712281ced16a/fendo-13-816598-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/8959981/1331796facae/fendo-13-816598-g007.jpg
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