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Low serum gastrin associated with ER+ breast cancer development via inactivation of CCKBR/ERK/P65 signaling

Overview of attention for article published in BMC Cancer, August 2018
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Title
Low serum gastrin associated with ER+ breast cancer development via inactivation of CCKBR/ERK/P65 signaling
Published in
BMC Cancer, August 2018
DOI 10.1186/s12885-018-4717-7
Pubmed ID
Authors

Li-Li Meng, Jing-Long Wang, Shu-Ping Xu, Li-Dong Zu, Zhao-Wen Yan, Jian-Bing Zhang, Ya-Qin Han, Guo-Hui Fu

Abstract

Gastrin is an important gastrointestinal hormone produced primarily by G-cells in the antrum of the stomach. It normally regulates gastric acid secretion and is implicated in a number of human disease states, but how its function affects breast cancer (BC) development is not documented. The current study investigated the suppressive effects of gastrin on BC and its underlying mechanisms. Serum levels of gastrin were measured by enzyme-linked immunosorbent assay (ELISA) and correlation between gastrin level and development of BC was analyzed by chi-square test. Inhibitory effects of gastrin on BC were investigated by CCK-8 assay and nude mice models. Expressions of CCKBR/ERK/P65 in BC patients were determined through immunohistochemistry (IHC) and Western blot. Survival analysis was performed using the log-rank test. The results indicated that the serum level of gastrin in BC patients was lower compared with normal control. Cellular and molecular experiments indicated that reduction of gastrin is associated with inactivation of cholecystokinin B receptor (CCKBR)/ERK/P65 signaling in BC cells which is corresponding to molecular type of estrogen receptor (ER) positive BC. Furthermore, we found that low expression of gastrin/CCKBR/ERK /P65 was correlated to worse prognosis in BC patients. Gastrin or ERK/P65 activators inhibited ER+ BC through CCKBR-mediated activation of ERK/P65. Moreover, combination treatment with gastrin and tamoxifen more efficiently inhibited ER+ BC than tamoxifen alone. We concluded that low serum gastrin is related to increased risk of ER+ BC development. The results also established that CCKBR/ERK/P65 signaling function is generally tumor suppressive in ER+ BC, indicating therapies should focus on restoring, not inhibiting, CCKBR/ERK/P65 pathway activity.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 9 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 9 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 33%
Student > Bachelor 2 22%
Librarian 1 11%
Student > Master 1 11%
Unknown 2 22%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 2 22%
Pharmacology, Toxicology and Pharmaceutical Science 1 11%
Social Sciences 1 11%
Medicine and Dentistry 1 11%
Chemistry 1 11%
Other 1 11%
Unknown 2 22%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 August 2018.
All research outputs
#21,264,673
of 23,881,329 outputs
Outputs from BMC Cancer
#6,689
of 8,483 outputs
Outputs of similar age
#266,426
of 303,241 outputs
Outputs of similar age from BMC Cancer
#111
of 139 outputs
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So far Altmetric has tracked 8,483 research outputs from this source. They receive a mean Attention Score of 4.4. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 139 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.