Evidence map›Paper›PMID 30286765›Full record

ArticleCell communication and signaling : CCS2018

Rhomboid domain-containing protein 1 promotes breast cancer progression by regulating the p-Akt and CDK2 levels.

Xin Zhang, Yuechao Zhao, Changjun Wang, Hongge Ju, Wenjie Liu, Xiaohui Zhang, Shiying Miao, Linfang Wang, Qiang Sun, Wei Song

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 16% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

20 citing papers in PubMed, 39 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Xin ZhangDepartment of Biochemistry and Molecular Biology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China.
Yuechao ZhaoDepartment of Biochemistry and Molecular Biology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China.
Changjun WangDepartment of Breast Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, 100730, China.
Hongge JuDepartment of Pathology, Baotou Medical College, Baotou, 014040, China.
Wenjie LiuDepartment of Biochemistry and Molecular Biology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China.
Xiaohui ZhangDepartment of Breast Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, 100730, China.
Shiying MiaoDepartment of Biochemistry and Molecular Biology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China.
Linfang WangDepartment of Biochemistry and Molecular Biology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China. wang.linfang@imicams.ac.cn.
Qiang SunDepartment of Breast Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, 100730, China. sunqiangpumch@sina.com.
Wei SongDepartment of Biochemistry and Molecular Biology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China. songwei@ibms.pumc.edu.cn.ORCID 0000-0003-2108-1164
Chinese Academy of Medical Sciences & Peking Union Medical College · CNWeifang Medical University · CNBaotou Medical College · CN

Funding

CAMS Initiative for Innovative Medicine 2016-I2M-1-001National Important Research Plan of China 2015CB943001National Natural Science Foundation of China 81372661National Natural Science Foundation of China 8167002793the State Key Laboratory Special fund from the Ministry of Science 2060204
6 · The paper itself

Abstract

backgroundOur previous work revealed that rhomboid domain-containing protein 1 (RHBDD1) participates in the modulation of cell growth and apoptosis in colorectal cancer cells. This study aimed to investigate the function of RHBDD1 in regulating breast cancer progression and its underlying molecular basis.

methodsImmunohistochemistry was performed to evaluate RHBDD1 expression in 116 breast cancer tissue and 39 adjacent normal tissue and expression of RHBDD1, phospho-Akt (p-Akt) and cyclin-dependent kinase 2 (CDK2) in the same 84 breast cancer specimens. RHBDD1-knock-out cells were established using breast cancer cell lines. In vitro studies were carried out to estimate the function of RHBDD1 in cell proliferation, migration and invasion. Fluorescence microscopy assay and flow cytometric analysis were used to measure apoptosis and cell cycle regulation. RNA sequencing and western blot analysis were used to investigate the molecular mechanisms of RHBDD1.

resultsRHBDD1 was highly up-regulated in breast cancer tissue compared with that in normal tissue and associated with pathological tumor (pT) stage, pathological tumor-node-metastasis (pTNM) stage and estrogen receptor (ER) expression. RHBDD1 up-regulation was associated with poor prognosis in several subtypes of breast cancer. Deletion of RHBDD1 promoted apoptosis and suppressed proliferation, migration and invasion in breast cancer cells. RHBDD1 deletion suppressed Akt activation and decreased CDK2 protein level via proteasome pathway, thus inhibited cell cycle progression and G1/S phase transition. Moreover, the protein level of RHBDD1, p-Akt and CDK2 was significantly positively correlated in breast cancer tissue.

conclusionsOur study reveals that RHBDD1 promotes breast cancer progression by regulating p-Akt and CDK2 protein levels, and might be a potential biomarker and prognostic indicator for breast cancer patients.

Indexed as

Disease ProgressionApoptosisBreast NeoplasmsCell MovementCell ProliferationCell SurvivalCyclin-Dependent Kinase 2Down-RegulationG2 Phase Cell Cycle CheckpointsGene DeletionHumansMCF-7 CellsM Phase Cell Cycle CheckpointsNeoplasm InvasivenessPhosphoproteinsProto-Oncogene Proteins c-aktCDK2 protein, humanCyclin-Dependent Kinase 2PhosphoproteinsProto-Oncogene Proteins c-aktRHBDD1 protein, humanSerine EndopeptidasesBreast cancerCDK2Cell cycle progressionG1/S phase transitionP-AktRHBDD1

Identifiers

PMID30286765
PMCPMC6172813
OpenAlexW2894742643

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.