Evidence map›Paper›PMID 34163033›Full record

ArticleOncogene2021

A novel homeostatic loop of sorcin drives paclitaxel-resistance and malignant progression via Smad4/ZEB1/miR-142-5p in human ovarian cancer.

Jinguo Zhang, Wencai Guan, Xiaolin Xu, Fanchen Wang, Xin Li, Guoxiong Xu

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

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  16. RBM15‑mediating MDR1 mRNA mInternational journal of oncology · 2023
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  18. Linc-ROR Promotes EMT by Targeting miR-204-5p/SMAD4 in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2023
    Article
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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

6 authors at 2 institutions in 1 country.

Jinguo ZhangResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai, 201508, China.ORCID http://orcid.org/0000-0001-9952-9307
Wencai GuanResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai, 201508, China.ORCID http://orcid.org/0000-0001-8168-0711
Xiaolin XuResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai, 201508, China.ORCID http://orcid.org/0000-0001-7462-3508
Fanchen WangResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai, 201508, China.ORCID http://orcid.org/0000-0001-5001-1013
Xin LiResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai, 201508, China.ORCID http://orcid.org/0000-0002-1761-4127
Guoxiong XuResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai, 201508, China. guoxiong.xu@fudan.edu.cn.ORCID http://orcid.org/0000-0002-9074-8754
Shanghai Medical College of Fudan University · CNJinshan Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The primary chemotherapy of ovarian cancer (OC) often acquires chemoresistance. Sorcin (SRI), a soluble resistance-related calcium-binding protein, has been reported to be an oncogenic protein in cancer. However, the molecular mechanisms of SRI regulation and the role and aberrant expression of SRI in chemoresistant OC remain unclear. Here, we identified SRI as a key driver of paclitaxel (PTX)-resistance and explored its regulatory mechanism. Using transcriptome profiles, qRT-PCR, proteomics, Western blot, immunohistochemistry, and bioinformatics analyses, we found that SRI was overexpressed in PTX-resistant OC cells and the overexpression of SRI was related to the poor prognosis of patients. SRI was a key molecule required for growth, migration, and PTX-resistance in vitro and in vivo and was involved in epithelial-mesenchymal transition (EMT) and stemness. Mechanistic studies showed that miR-142-5p directly bound to the 3'-UTR of SRI to suppress its expression, whereas a transcription factor zinc-finger E-box binding homeobox 1 (ZEB1) inhibited the transcription of miR-142-5p by directly binding to the E-box fragment in the miR-142 promoter region. Furthermore, ZEB1 was negatively regulated by SRI which physically interacted with Smad4 to block its translocation from the cytosol to the nucleus. Taken together, our findings unveil a novel homeostatic loop of SRI that drives the PTX-resistance and malignant progression via Smad4/ZEB1/miR-142-5p in human OC. Targeting this SRI/Smad4/ZEB1/miR-142-5p loop may reverse the PTX-resistance.

Indexed as

Biomarkers, TumorCalcium-Binding ProteinsCell Line, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGene ExpressionHumansMicroRNAsModels, BiologicalNeoplastic Stem CellsOvarian NeoplasmsPaclitaxelPrognosisBiomarkers, TumorCalcium-Binding ProteinsMicroRNAsMIRN142 microRNA, humanPaclitaxelSmad4 ProteinSMAD4 protein, humanSRI protein, humanZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID34163033
PMCPMC8321900
OpenAlexW3174075679

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.