Evidence map›Paper›PMID 33280236›Full record

ArticleCancer medicine2021

HELLS, a chromatin remodeler is highly expressed in pancreatic cancer and downregulation of it impairs tumor growth and sensitizes to cisplatin by reexpressing the tumor suppressor TGFBR3.

Xuyang Hou, Leping Yang, Kunpeng Wang, Yan Zhou, Qinglong Li, Fanhua Kong, Xi Liu, Jun He

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 34 citations in OpenAlex.

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  13. SFPQ and Its Isoform as Potential Biomarker for Non-Small-Cell Lung Cancer.International journal of molecular sciences · 2023
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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.

Xuyang HouDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Leping YangDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Kunpeng WangDepartment of General Surgery, Taizhou Central Hospital, Taizhou University Hospital, Taizhou, Zhejiang, China.
Yan ZhouDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Qinglong LiDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Fanhua KongDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xi LiuDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jun HeDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID 0000-0001-5309-0765
Central South University · CNTaizhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer (PC) is the most malignant cancer type in the digestive system with a poor prognosis. Chemotherapy such as cisplatin is the last chance for PC patients diagnosed with advanced or metastatic disease. Obtaining a deep understanding of the molecular mechanism underlying PC tumorigenesis and identifying optimal biomarkers to estimate chemotherapy sensitivity are essential for PC treatment. The chromatin remodeler HELLS was found to regulate various tumor suppressors through an epigenetic pathway in several cancers. We analyzed HELLS expression in clinical samples by Western blotting and immunohistochemical staining. Next, we identified the variation in tumor growth and cisplatin sensitivity after knockdown of HELLS and explored the downstream mediators of HELLS in PC via RNA-seq, chromatin immunoprecipitation, and gain- and loss-of-function assays. We found that HELLS is upregulated in PC tissues and correlates with advanced clinical stage and a poor prognosis, and the knockdown of HELLS leads to tumor growth arrest and increased sensitivity to cisplatin. Mechanistically, the tumor suppressor TGFBR3 is markedly reexpressed after HELLS knockdown; conversely, compromising TGFBR3 rescues HELLS knockdown-mediated effects in PC cells. Thus, our data provide evidence that HELLS can serve as a potential oncogene and suitable biomarker to evaluate chemotherapy sensitivity via epigenetically silencing the tumor suppressor TGFBR3 in PC.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell Line, TumorCell ProliferationCisplatinDNA HelicasesEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudePancreatic NeoplasmsProteoglycansReceptors, Transforming Growth Factor betaAntineoplastic AgentsbetaglycanCisplatinDNA HelicasesHELLS protein, humanProteoglycansReceptors, Transforming Growth Factor betachromatin remodelercisplatinepigeneticHELLSpancreatic cancer

Identifiers

PMID33280236
PMCPMC7826454
OpenAlexW3112658011

What OpenQuestion holds

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LicenceCC BY
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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.