Evidence map›Paper›PMID 42577702›Full record

ReviewMolecular and clinical oncology2026

Biology and function of the autotaxin/lysophosphatidic acid axis in cancer (Review).

Angelina Boccarelli, Stefano Castellani

Abstract readReview
In one paragraph

Review in Molecular and clinical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Angelina BoccarelliDepartment of Precision and Regenerative Medicine and Ionian Area, University of Bari 'Aldo Moro', I-70124 Bari, Italy.
Stefano CastellaniDepartment of Precision and Regenerative Medicine and Ionian Area, University of Bari 'Aldo Moro', I-70124 Bari, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autotaxin (ATX) lysophospholipase D has been identified as an 'autocrine motility factor' for tumour cells. The tumour microenvironment (TME) serves a critical role in cancer development, with ATX, as a component of the ATX/lysophosphatidic acid (LPA) axis, integrated into a complex network of molecular signalling. This axis is particularly significant because it activates multiple overlapping signal transduction pathways, thereby mediating pleiotropic effects across nearly all cell types within the TME. The ATX/LPA pathway has multiple molecular and cellular drivers, making the signalling mechanisms activated by ATX/LPA an interesting subject for evaluation in cancer development. The present review discusses the multiple effects of ATX/LPA on three macroevents involving several TME components: i) Inflammation and immunity; ii) cellular proliferation and metabolism; and iii) invasion and metastasis. The aim of the present review was to highlight the clinical impact of the ATX/LPA pathways in the pathogenesis of cancer. Clarifying the role of ATX and blocking this pathway in the inflammatory cycle may open novel therapeutic avenues to improve cancer treatment. Although several reviews have addressed the ATX/LPA axis in cancer, most have focused primarily on its roles in tumour growth, migration and metastasis. By contrast, the present review provides an updated, integrative perspective that emphasizes recent advances (2020-2025) regarding the role of the ATX/LPA axis in shaping the immunometabolic landscape of the TME, with particular attention to inflammation-driven immune regulation.

Indexed as

autotaxincancerimmunityinflammationinvasionmetabolismmetastasisproliferationtumour microenvironment

Identifiers

PMID42577702
PMCPMC13454990

What Socratic 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 Socratic graph.