Evidence map›Paper›PMID 31215145›Full record

ArticleCancer medicine2019

DACH1 suppresses epithelial to mesenchymal transition (EMT) through Notch1 pathway and reverses progestin resistance in endometrial carcinoma.

Qing Zhou, Wenzhi Li, Deshui Kong, Zhiming Liu, Zhengzheng Shi, Xiaohong Ma, Yongmei Li, Jie Jiang

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 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.

Qing ZhouDepartment of Obstetrics and Gynecology, Qi Lu Hospital, Shandong University, Jinan, Shandong, China.ORCID 0000-0001-8977-3429
Wenzhi LiDepartment of Obstetrics and Gynecology, Qi Lu Hospital, Shandong University, Jinan, Shandong, China.ORCID 0000-0002-3272-245X
Deshui KongDepartment of Obstetrics and Gynecology, Qi Lu Hospital, Shandong University, Jinan, Shandong, China.ORCID 0000-0002-7933-3494
Zhiming LiuDepartment of Obstetrics and Gynecology, Qi Lu Hospital, Shandong University, Jinan, Shandong, China.ORCID 0000-0003-0291-0430
Zhengzheng ShiDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Xiaohong MaDepartment of Obstetrics and Gynecology, Qi Lu Hospital, Shandong University, Jinan, Shandong, China.ORCID 0000-0001-8625-237X
Yongmei LiDepartment of Obstetrics and Gynecology, Qi Lu Hospital, Shandong University, Jinan, Shandong, China.
Jie JiangDepartment of Obstetrics and Gynecology, Qi Lu Hospital, Shandong University, Jinan, Shandong, China.ORCID 0000-0002-9634-4152
Qilu Hospital of Shandong University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progestin resistance limits the effectiveness of progestin therapy in endometrial carcinoma for patients who desire to preserve fertility. To investigate the molecular mechanism of progestin resistance in endometrial carcinoma, we performed microarray analysis among Ishikawa and progestin resistant cell IshikawaPR cells. We found that epithelial to mesenchymal transition (EMT) was involved in progestin resistance and dachshund family transcription factor 1 (DACH1) is positively correlated with progesterone receptor (PGR). Knockdown of DACH1 in Ishikawa cell promoted proliferation, metastasis ability, and resistance to progestin. Conversely, overexpression of DACH1 in IshikawaPR cell rendered more sensitive to progestin treatment. Xenograft model assay also had similar results. In addition, our data showed that DACH1 overexpression inhibited EMT and decreased c-Jun, Notch1 and Hes1expression. Our study demonstrated for the first time that EMT is involved in progestin resistance of EC. The response to progestin could be reserved by DACH1 suppressed EMT through Notch1 pathway via c-Jun.

Indexed as

AnimalsCell Line, TumorCell ProliferationCell SurvivalDrug Resistance, NeoplasmEndometrial NeoplasmsEpithelial-Mesenchymal TransitionEye ProteinsFemaleGene Knockdown TechniquesHumansMiceProgestinsProto-Oncogene Proteins c-junReceptor, Notch1Receptors, ProgesteroneDACH1 protein, humanEye ProteinsJUN protein, humanNOTCH1 protein, humanProgestinsProto-Oncogene Proteins c-junReceptor, Notch1Receptors, ProgesteroneTranscription FactorsbioinformaticsDACH1EMTendometrial carcinomaprogestin resistance

Identifiers

PMID31215145
PMCPMC6675747
OpenAlexW2951106431

What OpenQuestion holds

Textmetadata
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.