Evidence map›Paper›PMID 32270348›Full record

ArticleMedical oncology (Northwood, London, England)2020

Cellular apoptosis susceptibility protein (CAS) suppresses the proliferation of breast cancer cells by upregulated cyp24a1.

Mei Ye, Ruigang Han, Jianwu Shi, Xunda Wang, Allan Z Zhao, Fanghong Li, Hao Chen

Abstract read
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In one paragraph

Article in Medical oncology (Northwood, London, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

4 citing papers in PubMed, 6 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

7 authors at 3 institutions in 1 country.

Mei YeSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Ruigang HanReproductive Medicine Center of The 306th Hospital of PLA, Beijing, China.
Jianwu ShiInstitute of Reproductive Medicine, Medical School of Nantong University, Nantong University, Nantong, China.
Xunda WangSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Allan Z ZhaoSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Fanghong LiSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China. fli@gdut.edu.cn.
Hao ChenSchool of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China. chenhao@ntu.edu.cn.ORCID http://orcid.org/0000-0001-8319-8101
Guangdong University of Technology · CNNantong University · CNPLA 306 Hospital · CN

Funding

National Key Research and Development Program of China 2018YFC1003602National Natural Science Foundation of China 81671432National Natural Science Foundation of China 81871202the startup R&D funding of Nantong University 03083011
6 · The paper itself

Abstract

Breast cancer is the most common cancer in women. Although several studies demonstrated cellular apoptosis susceptibility protein (CAS) involved in the development of breast cancer, the underlying mechanisms of CAS regulating cell processes in the breast cancer remain elusive. In the present study, we explored the possible mechanism of CAS in contributing to the cell proliferation in the breast cancer cell line MCF-7. Knockdown of CAS led to the reduction of cell viability and proliferation. Furthermore, cell cycle was arrested in G0/G1 phase after knocking down CAS with the decrease of cyclinD1. In addition, RNA-seq analysis for the CAS knockdown cells demonstrated that total eleven genes were significantly altered (Fold changes > 2). Of note, the expression of cyp24a1 was dramatically increased in the shCAS cells compared to that of shNC cells as well as confirmed by quantitative real-time polymerase chain reaction (qPCR). These observations clarified the previous conflicting results on the cell fates of the breast cells regulated by CAS and provide new insight into the role of CAS in the development of breast cancer.

Indexed as

Breast NeoplasmsCell CycleCell ProliferationCell SurvivalCellular Apoptosis Susceptibility ProteinDatabases, GeneticFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsPrognosisVitamin D3 24-HydroxylaseCellular Apoptosis Susceptibility ProteinCYP24A1 protein, humanVitamin D3 24-HydroxylaseBreast cancerCASCell proliferation

Identifiers

PMID32270348
OpenAlexW3015723337

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.