Evidence map›Paper›PMID 26913609›Full record

ArticleCell death & disease2016

Proteomic screening identifies calreticulin as a miR-27a direct target repressing MHC class I cell surface exposure in colorectal cancer.

T Colangelo, G Polcaro, P Ziccardi, B Pucci, L Muccillo, M Galgani, A Fucci, M R Milone, A Budillon, M Santopaolo and 12 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

53 citing papers in PubMed, 82 citations in OpenAlex.

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  7. CD8 + T Cells in Gastrointestinal Cancer: a Perspective on Targeting MicroRNA.Journal of molecular medicine (Berlin, Germany) · 2025
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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

22 authors at 8 institutions in 1 country.

T ColangeloDepartment of Sciences and Technologies, University of Sannio, Benevento, Italy.
G PolcaroDepartment of Sciences and Technologies, University of Sannio, Benevento, Italy.
P ZiccardiDepartment of Sciences and Technologies, University of Sannio, Benevento, Italy.
B PucciCentro Ricerche Oncologiche Mercogliano, Istituto Nazionale Tumori Fondazione G. Pascale-IRCCS, Mercogliano (AV), Italy.
L MuccilloDepartment of Sciences and Technologies, University of Sannio, Benevento, Italy.
M GalganiIstituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), Napoli, Italy.ORCID http://orcid.org/0000-0001-8414-1676
A FucciDepartment of Sciences and Technologies, University of Sannio, Benevento, Italy.
M R MiloneCentro Ricerche Oncologiche Mercogliano, Istituto Nazionale Tumori Fondazione G. Pascale-IRCCS, Mercogliano (AV), Italy.
A BudillonCentro Ricerche Oncologiche Mercogliano, Istituto Nazionale Tumori Fondazione G. Pascale-IRCCS, Mercogliano (AV), Italy.
M SantopaoloDipartimento di Medicina Molecolare e Biotecnologie Mediche, Università di Napoli 'Federico II', Napoli, Italy.
C VotinoDepartment of Sciences and Technologies, University of Sannio, Benevento, Italy.
M PancioneDepartment of Sciences and Technologies, University of Sannio, Benevento, Italy.
A PiepoliDivision of Epidemiology and Health Statistics, IRCCS-'Casa Sollievo della Sofferenza' Hospital, San Giovanni Rotondo (FG), Italy.
G MazzoccoliDivision of Internal Medicine and Chronobiology Unit, IRCCS-'Casa Sollievo della Sofferenza' Hospital, San Giovanni Rotondo (FG), Italy.
M BinaschiDepartment of Pharmacology, Menarini Ricerche, Pomezia (RM), Italy.
M BigioniDepartment of Pharmacology, Menarini Ricerche, Pomezia (RM), Italy.
C A MaggiMenarini Ricerche, Florence, Italy.
M FassanDepartment of Pathology and Diagnostic, ARC-NET Research Centre, University of Verona, Verona, Italy.ORCID http://orcid.org/0000-0001-6515-5482
C LaudannaDepartment of Experimental and Clinical Medicine, Laboratory of Molecular Oncology, Magna Græcia University of Catanzaro, Catanzaro, Italy.
G MatareseIstituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), Napoli, Italy.ORCID http://orcid.org/0000-0001-9429-0616
L SabatinoDepartment of Sciences and Technologies, University of Sannio, Benevento, Italy.
V ColantuoniDepartment of Sciences and Technologies, University of Sannio, Benevento, Italy.
University of Sannio · ITIstituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · ITMenarini Group (Italy) · ITCasa Sollievo della Sofferenza · ITInstitute for Experimental Endocrinology and Oncology · ITMagna Graecia University · ITUniversity of Naples Federico II · ITUniversity of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impairment of the immune response and aberrant expression of microRNAs are emerging hallmarks of tumour initiation/progression, in addition to driver gene mutations and epigenetic modifications. We performed a preliminary survey of independent adenoma and colorectal cancer (CRC) miRnoma data sets and, among the most dysregulated miRNAs, we selected miR-27a and disclosed that it is already upregulated in adenoma and further increases during the evolution to adenocarcinoma. To identify novel genes and pathways regulated by this miRNA, we employed a differential 2DE-DIGE proteome analysis. We showed that miR-27a modulates a group of proteins involved in MHC class I cell surface exposure and, mechanistically, demonstrated that calreticulin is a miR-27a direct target responsible for most downstream effects in epistasis experiments. In vitro miR-27a affected cell proliferation and angiogenesis; mouse xenografts of human CRC cell lines expressing different miR-27a levels confirmed the protein variations and recapitulated the cell growth and apoptosis effects. In vivo miR-27a inversely correlated with MHC class I molecules and calreticulin expression, CD8(+) T cells infiltration and cytotoxic activity (LAMP-1 exposure and perforin release). Tumours with high miR-27a, low calreticulin and CD8(+) T cells' infiltration were associated with distant metastasis and poor prognosis. Our data demonstrate that miR-27a acts as an oncomiRNA, represses MHC class I expression through calreticulin downregulation and affects tumour progression. These results may pave the way for better diagnosis, patient stratification and novel therapeutic approaches.

Indexed as

AdenocarcinomaAnimalsApoptosisBase SequenceCalreticulinCD8-Positive T-LymphocytesCell Line, TumorCell ProliferationColorectal NeoplasmsDown-RegulationFemaleHCT116 CellsHistocompatibility Antigens Class IHumansMiceMice, Inbred BALB CCalreticulinHistocompatibility Antigens Class IMicroRNAs

Identifiers

PMID26913609
PMCPMC4849154
OpenAlexW2288178311

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.