Evidence map›Paper›PMID 28052027›Full record

ArticleOncotarget2017

Estrogen receptor β ligation inhibits Hodgkin lymphoma growth by inducing autophagy.

Marina Pierdominici, Angela Maselli, Silvia L Locatelli, Laura Ciarlo, Giuseppa Careddu, Mario Patrizio, Barbara Ascione, Antonella Tinari, Carmelo Carlo-Stella, Walter Malorni and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 43 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

12 authors at 2 institutions in 1 country.

Marina PierdominiciDepartment of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy.
Angela MaselliDepartment of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, Italy.
Silvia L LocatelliDepartment of Oncology and Hematology, Humanitas Cancer Center - Humanitas Clinical and Research Center, Milano, Italy.
Laura CiarloDepartment of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, Italy.
Giuseppa CaredduDepartment of Oncology and Hematology, Humanitas Cancer Center - Humanitas Clinical and Research Center, Milano, Italy.
Mario PatrizioDepartment of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, Italy.
Barbara AscioneDepartment of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, Italy.
Antonella TinariDepartment of Technology and Health, Istituto Superiore di Sanità, Rome, Italy.
Carmelo Carlo-StellaDepartment of Oncology and Hematology, Humanitas Cancer Center - Humanitas Clinical and Research Center, Milano, Italy.
Walter MalorniDepartment of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, Italy.
Paola MatarreseDepartment of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, Italy.
Elena OrtonaDepartment of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy.
Istituto Superiore di Sanità · ITHumanitas University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although Hodgkin lymphoma (HL) is curable with current therapy, at least 20% of patients relapse or fail to make complete remission. In addition, patients who achieve long-term disease-free survival frequently undergo infertility, secondary malignancies, and cardiac failure, which are related to chemotherapeutic agents and radiation therapies. Hence, new therapeutic strategies able to counteract the HL disease in this important patient population are still a matter of study. Estrogens, in particular 17β-estradiol (E2), have been suggested to play a role in lymphoma cell homeostasis by estrogen receptors (ER) β activation. On these bases, we investigated whether the ligation of ERβ by a selective agonist, the 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN), could impact HL tumor growth. We found that DPN-mediated ERβ activation led to a reduction of in vitro cell proliferation and cell cycle progression by inducing autophagy. In nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice engrafted with HL cells, ERβ activation by DPN was able to reduce lymphoma growth up to 60% and this associated with the induction of tumor cell autophagy. Molecular characterization of ERβ-induced autophagy revealed an overexpression of damage-regulated autophagy modulator 2 (DRAM2) molecule, whose role in autophagy modulation is still debated. After ERβ activation, both DRAM2 and protein 1 light chain 3 (LC3), a key actor in the autophagosome formation, strictly interacted each other and localized at mitochondrial level.Altogether these results suggest that targeting ERβ with selective agonists might affect HL cell proliferation and tumor growth via a mechanism that brings into play DRAM2-dependent autophagic cascade.

Indexed as

AnimalsAutophagyCell CycleCell Line, TumorCell ProliferationDose-Response Relationship, DrugEstrogen Receptor betaGene Expression Regulation, NeoplasticHodgkin DiseaseHumansLigandsMembrane ProteinsMice, Inbred NODMice, SCIDMicrotubule-Associated ProteinsNitriles2,3-bis(4-hydroxyphenyl)-propionitrileDRAM2 protein, humanESR2 protein, humanEstrogen Receptor betaLigandsMAP1LC3A protein, humanMembrane ProteinsMicrotubule-Associated ProteinsNitrilesPropionatesSelective Estrogen Receptor ModulatorsautophagyDRAM2estrogen receptor βHodgkin lymphomatumor growth

Identifiers

PMID28052027
PMCPMC5352419
OpenAlexW2561794149

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.