Evidence map›Paper›PMID 37286891›Full record

ArticleBreast cancer research and treatment2023

Induction of SGK1 via glucocorticoid-influenced clinical outcome of triple-negative breast cancer patients.

Junjia Zhang, Yasuhiro Miki, Erina Iwabuchi, Junyao Xu, Ayako Kanai, Yasuaki Sagara, Yasuyo Ohi, Yoshiaki Rai, Rin Yamaguchi, Maki Tanaka and 3 more

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Article in Breast cancer research and treatment, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Role of KDM2B epigenetic factor in regulating calcium signaling in prostate cancer cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Junjia ZhangDepartment of Breast and Endocrine Surgical Oncology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Yasuhiro MikiDepartment of Nursing, Faculty of Medical Science and Welfare, Tohoku Bunka Gakuen University, Sendai, Japan. miki@patholo2.med.tohoku.ac.jp.ORCID http://orcid.org/0000-0003-3618-5652
Erina IwabuchiDepartment of Pathology and Histotechnology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Junyao XuThe Cancer Hospital of the University of Chinese Academy of Sciences Zhejiang Cancer Hospital, Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang, China.
Ayako KanaiDepartment of Breast Surgery, Hachinohe City Hospital, Aomori, Japan.
Yasuaki SagaraDepartment of Breast and Thyroid Surgical Oncology, Sagara Hospital, Kagoshima, Japan.
Yasuyo OhiDepartment of Pathology, Sagara Hospital, Kagoshima, Japan.
Yoshiaki RaiDepartment of Breast and Thyroid Surgical Oncology, Sagara Hospital, Kagoshima, Japan.
Rin YamaguchiDepartment of Pathology, Nagasaki University Hospital, Nagasaki, Japan.
Maki TanakaJCHO Kurume General Hospital, Fukuoka, Japan.
Takanori IshidaDepartment of Breast and Endocrine Surgical Oncology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Takashi SuzukiDepartment of Anatomic Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Hironobu SasanoDepartment of Anatomic Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTriple-negative breast cancer (TNBC) is a highly heterogeneous and aggressive breast malignancy. Glucocorticoid (GC)-glucocorticoid receptor (GR) pathway plays a pivotal role in the cellular responses to various stresses including chemotherapy. Serum- and glucocorticoid-induced kinase-1 (SGK1) is known as an important downstream effector molecule in the GR signaling pathway, we attempted to explore its clinicopathological and functional significance in TNBC in which GR is expressed.

methodsWe first immunolocalized GR and SGK1 and correlated the results with clinicopathological variables and clinical outcome in 131 TNBC patients. We also evaluated the effects of SGK1 on the cell proliferation and migration in TNBC cell lines with administration of dexamethasone (DEX) to further clarify the significance of SGK1.

resultsThe status of SGK1 in carcinoma cells was significantly associated with adverse clinical outcome in TNBC patients examined and was significantly associated with lymph node metastasis, pathological stage, and lymphatic invasion of the patients. In particular, SGK1 immunoreactivity was significantly associated with an increased risk of recurrence in GR-positive TNBC patients. Subsequent in vitro studies also demonstrated that DEX promoted TNBC cell migration and the silencing of gene expression did inhibit the cell proliferation and migration of TNBC cells under DEX treatment.

conclusionsTo the best of our knowledge, this is the first study to explore an association between SGK1 and clinicopathological variables and clinical outcome of TNBC patients. SGK1 status was significantly positively correlated with adverse clinical outcome of TNBC patients and promoted carcinoma cell proliferation and migration of carcinoma cells.

Indexed as

CarcinomaTriple Negative Breast NeoplasmsCell Line, TumorCell ProliferationFemaleGlucocorticoidsHumansReceptors, GlucocorticoidGlucocorticoidsReceptors, GlucocorticoidDexamethasoneGlucocorticoid receptorSGK1Triple-negative breast cancer

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.