Evidence map›Paper›PMID 31485632›Full record

ArticleOncology reports2019

MTMR3 is upregulated in patients with breast cancer and regulates proliferation, cell cycle progression and autophagy in breast cancer cells.

Zhan Wang, Min Zhang, Rong Shan, Yu-Jie Wang, Juan Chen, Juan Huang, Lun-Quan Sun, Wei-Bing Zhou

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

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  9. Cancers · 2020
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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

8 authors at 2 institutions in 1 country.

Zhan WangDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Min ZhangDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Rong ShanDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Yu-Jie WangDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Juan ChenDepartment of Pharmacy, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Juan HuangHunan Province Clinic Meditech Research Center for Breast Cancer, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Lun-Quan SunCenter for Molecular Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Wei-Bing ZhouDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a member of the myotubularin family, myotubularin related protein 3 (MTMR3) has been demonstrated to participate in tumor development, including oral and colon cancer. However, little is known about its functional roles in breast cancer. In the present study, the expression of MTMR3 in breast cancer was evaluated by immunohistochemical staining of tumor tissues from 172 patients. Online data was then used for survival analysis from the PROGgeneV2 database. In vitro, MTMR3 expression was silenced in MDA‑MB‑231 cells via lentiviral shRNA transduction. MTT, colony formation and flow cytometry assays were performed in the control and MTMR3‑silenced cells to evaluate the cell growth, proliferation and cell cycle phase distribution, respectively. Western blotting was used to evaluate the protein expression levels of autophagy‑related markers. The results demonstrated that the expression of MTMR3 in breast cancer tissues was significantly increased compared with adjacent normal tissues. MTMR3 was highly expressed in triple‑negative breast cancer and was associated with disease recurrence. MTMR3 knockdown in MDA‑MB‑231 cells inhibited cell proliferation and induced cell cycle arrest and autophagy. The present results indicated that MTMR3 may have an important role in promoting the progression of breast cancer, and its inhibition may serve as a promising therapeutic target for breast cancer treatment.

Indexed as

Up-RegulationAutophagyBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsNeoplasm MetastasisNeoplasm Recurrence, LocalNeoplasm StagingPrognosisProtein Tyrosine Phosphatases, Non-ReceptorSurvival AnalysisMTMR3 protein, humanProtein Tyrosine Phosphatases, Non-Receptor

Identifiers

PMID31485632
PMCPMC6775797
OpenAlexW2969803599

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.