Evidence map›Paper›PMID 36927528›Full record

ArticleJournal for immunotherapy of cancer2023

Inactivation of interleukin-30 in colon cancer stem cells via CRISPR/Cas9 genome editing inhibits their oncogenicity and improves host survival.

Luigi D'Antonio, Cristiano Fieni, Stefania Livia Ciummo, Simone Vespa, Lavinia Lotti, Carlo Sorrentino, Emma Di Carlo

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
9.4field-weighted citation impact, top 2% 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

15 citing papers in PubMed, 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

7 authors at 2 institutions in 1 country.

Luigi D'AntonioDipartimento di Medicina e Scienze dell'Invecchiamento, Università degli Studi "G. d'Annunzio" di Chieti-Pescara, Chieti, Italy.
Cristiano FieniDipartimento di Medicina e Scienze dell'Invecchiamento, Università degli Studi "G. d'Annunzio" di Chieti-Pescara, Chieti, Italy.ORCID 0000-0001-7203-6545
Stefania Livia CiummoDipartimento di Medicina e Scienze dell'Invecchiamento, Università degli Studi "G. d'Annunzio" di Chieti-Pescara, Chieti, Italy.
Simone VespaDipartimento di Medicina e Scienze dell'Invecchiamento, Università degli Studi "G. d'Annunzio" di Chieti-Pescara, Chieti, Italy.
Lavinia LottiDepartment of Experimental Medicine, University of Rome La Sapienza, Rome, Italy.
Carlo SorrentinoDipartimento di Medicina e Scienze dell'Invecchiamento, Università degli Studi "G. d'Annunzio" di Chieti-Pescara, Chieti, Italy.
Emma Di CarloDipartimento di Medicina e Scienze dell'Invecchiamento, Università degli Studi "G. d'Annunzio" di Chieti-Pescara, Chieti, Italy edicarlo@unich.it.ORCID 0000-0001-7778-1042
University of Chieti-Pescara · ITSapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProgression of colorectal cancer (CRC), a leading cause of cancer-related death worldwide, is driven by colorectal cancer stem cells (CR-CSCs), which are regulated by endogenous and microenvironmental signals. Interleukin (IL)-30 has proven to be crucial for CSC viability and tumor progression. Whether it is involved in CRC tumorigenesis and impacts clinical behavior is unknown.

methodsIL30 production and functions, in stem and non-stem CRC cells, were determined by western blot, immunoelectron microscopy, flow cytometry, cell viability and sphere formation assays. CRISPR/Cas9-mediated deletion of the

resultsWe demonstrated that both CR-CSCs and CRC cells express membrane-anchored IL30 that regulates their self-renewal, via WNT5A and RAB33A, and/or proliferation and migration, primarily by upregulating CXCR4

conclusionsIL30 is a new CRC driver, since its inactivation, which disables oncogenic pathways and multiple autocrine loops, inhibits CR-CSC tumorigenicity and metastatic ability. The development of CRISPR/Cas9-mediated targeting of IL30 could improve the current therapeutic landscape of CRC.

Indexed as

Colonic NeoplasmsColorectal NeoplasmsAnimalsCarcinogenesisCell Line, TumorCell ProliferationCell Transformation, NeoplasticCRISPR-Cas SystemsGene EditingInterleukinsMiceNeoplastic Stem CellsInterleukinscytokinesgastrointestinal neoplasms

Identifiers

PMID36927528
PMCPMC10030651
OpenAlexW4327560993

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.