Evidence map›Paper›PMID 30131854›Full record

ArticleOncotarget2018

Follistatin-like protein 1 sustains colon cancer cell growth and survival.

Gerolamo Bevivino, Silvia Sedda, Eleonora Franzè, Carmine Stolfi, Antonio Di Grazia, Vincenzo Dinallo, Flavio Caprioli, Federica Facciotti, Alfredo Colantoni, Angela Ortenzi and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 44% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
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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 3 institutions in 1 country.

Gerolamo BevivinoDepartment of Systems Medicine, University of Tor Vergata, Rome, Italy.
Silvia SeddaDepartment of Systems Medicine, University of Tor Vergata, Rome, Italy.
Eleonora FranzèDepartment of Systems Medicine, University of Tor Vergata, Rome, Italy.
Carmine StolfiDepartment of Systems Medicine, University of Tor Vergata, Rome, Italy.
Antonio Di GraziaDepartment of Systems Medicine, University of Tor Vergata, Rome, Italy.
Vincenzo DinalloDepartment of Systems Medicine, University of Tor Vergata, Rome, Italy.
Flavio CaprioliDepartment of Pathophysiology and Transplantation, Università degli Studi di Milano, Milan, Italy.
Federica FacciottiDepartment of Experimental Oncology, European Institute of Oncology, Milan, Italy.
Alfredo ColantoniDepartment of Systems Medicine, University of Tor Vergata, Rome, Italy.
Angela OrtenziDepartment of Systems Medicine, University of Tor Vergata, Rome, Italy.
Piero RossiDepartment of Surgery, University of Tor Vergata, Rome, Italy.
Giovanni MonteleoneDepartment of Systems Medicine, University of Tor Vergata, Rome, Italy.
University of Rome Tor Vergata · ITEuropean Institute of Oncology · ITUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Follistatin-like protein 1 (FSTL1) is a secreted glycoprotein, which controls several physiological and pathological events. FSTL1 expression is deregulated in many tumors, but its contribution to colon carcinogenesis is not fully understood. Here, we investigated the expression and functional role of FSTL1 in colorectal cancer (CRC). A significant increase of FSTL1 was seen in human CRC as compared to the surrounding non-tumor tissues and this occurred at both RNA and protein level. Knockdown of FSTL1 in CRC cells with a specific antisense oligonucleotide (AS) reduced expression of regulators of the late G1 phase, such as phosphorylated retinoblastoma protein, E2F-1, cyclin E and phospho-cyclin-dependent kinase-2, and promoted accumulation of cells in the G1 phase of the cell cycle thus resulting in diminished cell proliferation. Consistently, recombinant FSTL1 induced proliferation of normal intestinal epithelial cells through an ERK1/2-dependent mechanism. Cell cycle arrest driven by FSTL1 AS in CRC cells was accompanied by activation of caspases and subsequent induction of apoptosis. Moreover, FSTL1 knockdown made CRC cells more susceptible to oxaliplatin and irinotecan-induced death. Data indicate that FSTL1 is over-expressed in human CRC and suggest a role for this protein in favouring intestinal tumorigenesis.

Indexed as

cell deathcellular cyclecolon tumorigenesisERK1/2FSTL1

Identifiers

PMID30131854
PMCPMC6101290
OpenAlexW2883950003

What OpenQuestion holds

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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.