Evidence map›Paper›PMID 35789980›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2022

BMI1 promotes the proliferation and inhibits autophagy of breast cancer cells by activating COPZ1.

Shuming Chen, He Li, Siyu Chen, Bing Wang, Kaixiang Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
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

5 authors at 2 institutions in 1 country.

Shuming Chen *Department of General Surgery, 900 Hospital of the Joint Logistics Supports Force, Fuzhou, 350025, Fujian, China.
He Li *Department of General Surgery, 900 Hospital of the Joint Logistics Supports Force, Fuzhou, 350025, Fujian, China.
Siyu ChenDepartment of Oncology, 900 Hospital of the Joint Logistics Supports Force, No.156 West Second Ring North Road, Gulou District, Fuzhou, 350025, Fujian, China.
Bing WangDepartment of General Surgery, 900 Hospital of the Joint Logistics Supports Force, Fuzhou, 350025, Fujian, China.
Kaixiang ZhangDepartment of Oncology, 900 Hospital of the Joint Logistics Supports Force, No.156 West Second Ring North Road, Gulou District, Fuzhou, 350025, Fujian, China. zhangkaixiang49@163.com.ORCID http://orcid.org/0000-0001-7067-4041
Fuzhou General Hospital of Nanjing Military Command · CNFuzhou Second Hospital · CN

Funding

Launching Fundation of Fujian Medical University 2020QH1250Scientific research plan Fundation of 900 Hospital of the Joint Logistics Support Force 2021JQ08
6 · The paper itself

Abstract

purposeThis study was designed to explore the role of COPZ1 in breast cancer as well as discuss its specific reaction mechanism.

methodsWith the help of RT-qPCR and western blot, the expression of BMI1 and COPZ1 were measured. Then, the proliferation, colony formation and apoptosis were evaluated by CCK-8, colony formation and TUNEL assays, separately. Luciferase reporter assay and ChIP were applied to assess the relative activity of COPZ1 promoter as well as its binding with BMI1. Moreover, western blot was utilized to measure the expression of proliferation-, apoptosis- and autophagy-related proteins.

resultsAccording to GEPIA2 database, COPZ1 was upregulated in breast cancer tissues and was associated with the poor prognosis (P = 0.03). Results obtained from RT-qPCR and western blot verified that COPZ1 expression was greatly increased at both mRNA and protein levels in breast cancer cells as compared to control cells (P < 0.05 or P < 0.001). COPZ1 knockdown inhibited the proliferation, induced the autophagy and promoted the apoptosis of breast cancer cells. HumanTFDB predicted the binding sites of BMI1 and COPZ1. The increased relative luciferase activity of COPZ1 promoter following BMI1 overexpression (P < 0.001) and the binding of BMI1 with COPZ1 promoter indicated that BMI1 could activate COPZ1. Further experiments suggested that the effects of COPZ1 knockdown on the proliferation, apoptosis and autophagy of breast cancer cells were reversed by BMI1 overexpression, implying that BMI1 promoted the proliferation and repressed the autophagy of breast cancer cells via activating COPZ1.

conclusionsTo sum up, BMI1 exhibited promotive effects on the malignant progression of breast cancer through the activation of COPZ1. These findings might offer a preliminary theoretical basis for COPZ1 participation in autophagy in breast cancer cells.

Indexed as

Breast NeoplasmsMicroRNAsApoptosisAutophagyAutophagy-Related ProteinsCell Line, TumorCell ProliferationCoatomer ProteinFemaleGene Expression Regulation, NeoplasticHumansPolycomb Repressive Complex 1RNA, MessengerSincalideAutophagy-Related ProteinsBMI1 protein, humanCoatomer ProteinCOPZ1 protein, humanMicroRNAsPolycomb Repressive Complex 1RNA, MessengerSincalideAutophagyBMI1Breast cancerCOPZ1Proliferation

Identifiers

PMID35789980
OpenAlexW4283819803

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.