Evidence map›Paper›PMID 30235236›Full record

ArticlePloS one2018

TFDP3 regulates the apoptosis and autophagy in breast cancer cell line MDA-MB-231.

Ling-Yu Ding, Ming Chu, Yun-Shen Jiao, Qi Hao, Peng Xiao, Huan-Huan Li, Qi Guo, Yue-Dan Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. 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
0.5field-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

5 citing papers in PubMed, 12 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

8 authors at 2 institutions in 1 country.

Ling-Yu DingDepartment of Immunology, School of Basic Medical Science, Peking University, Beijing, China.ORCID 0000-0003-1777-2122
Ming ChuDepartment of Immunology, School of Basic Medical Science, Peking University, Beijing, China.ORCID 0000-0002-0507-9569
Yun-Shen JiaoDepartment of Immunology, School of Basic Medical Science, Peking University, Beijing, China.
Qi HaoDepartment of Medical Genetics, School of Basic Medical Science, Peking University, Beijing, China.
Peng XiaoState Key Laboratory of Genetic Engineering, School of Life Science, Collaborative Innovation Center of Genetics and Development, Fudan University, Shanghai, China.
Huan-Huan LiDepartment of Immunology, School of Basic Medical Science, Peking University, Beijing, China.
Qi GuoSchool of Basic Medical Science, Peking University, Beijing, China.
Yue-Dan WangDepartment of Immunology, School of Basic Medical Science, Peking University, Beijing, China.
Peking University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer/testis antigen TFDP3 belongs to the transcription factor DP(TFDP) family. It can bind to E2F family molecules to form a heterodimeric transcription factor E2F/TFDP complex. The complex is an important regulatory activator of cell cycle, involved in the regulation of cell proliferation, differentiation, apoptosis and other important physiological activities. In addition, TFDP3 has also been found to be a tumor-associated antigen that only expresses in malignant tumor tissue and normal testicular tissue; Thus, it is closely related to tumor occurrence and development. In this study, our group investigated the expression of TFDP3 in mononuclear cell samples from a variety of tissue-derived malignant tumors, breast cancer and benign breast lesions. The results show that TFDP3 is expressed in the malignant form of various tissues. Moreover, our recent research had focused on the ability of TFDP3 to influence the drug resistance and apoptosis of tumor cells. To further clarify the mechanisms involved in tumor resistance, this study also examined the expression of TFDP3 and tumor cell autophagy regulation; Autophagy helps cells cope with metabolic stress (such as in cases of malnutrition, growth factor depletion, hypoxia or hypoxia) removes erroneously folded proteins or defective organelles to prevent the accumulation of abnormal proteins; and removes intracellular pathogens. Our results showed that TFDP3 expression can induce autophagy by up-regulating the expression of autophagic key protein LC3(MAP1LC3) and increasing the number of autophagosomes during chemotherapy of malignant tumors. Then, DNA and organelles damage caused by the chemotherapy medicine are repaired. Thus, TFDP3 contributes toward tumor cell resistance. When siRNA inhibits TFDP3 expression, it can reduce cell autophagy, improving the sensitivity of tumor cells to chemotherapy drugs.

Indexed as

ApoptosisAutophagyBreast NeoplasmsCell Line, TumorCell ProliferationE2F1 Transcription FactorFemaleGene Expression Regulation, NeoplasticHumansMicrotubule-Associated ProteinsTranscriptional ActivationTranscription Factor DP1Transcription FactorsTranscriptomeE2F1 Transcription FactorMAP1LC3A protein, humanMicrotubule-Associated ProteinsTFDP3 protein, humanTranscription Factor DP1Transcription Factors

Identifiers

PMID30235236
PMCPMC6147432
OpenAlexW2891055597

What OpenQuestion holds

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LicenceCC BY
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.