Evidence map›Paper›PMID 35462605›Full record

ReviewCancer metastasis reviews2022

The paradoxical role of inositol in cancer: a consequence of the metabolic state of a tumor.

Kendall C Case, Michael W Schmidtke, Miriam L Greenberg

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer metastasis reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. NMR in biomedicine · 2026
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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

3 authors at 1 institution in 1 country.

Kendall C CaseDepartment of Biological Sciences, Wayne State University, Detroit, MI, USA.ORCID 0000-0001-6694-8409
Michael W SchmidtkeDepartment of Biological Sciences, Wayne State University, Detroit, MI, USA.ORCID 0000-0002-6985-4835
Miriam L GreenbergDepartment of Biological Sciences, Wayne State University, Detroit, MI, USA. mgreenberg@wayne.edu.ORCID 0000-0001-7724-5426
Wayne State University · US

Funding

Novel Mechanisms of Regulation of Inositol BiosynthesisR01GM125082 · NIGMS · WAYNE STATE UNIVERSITY · PI GREENBERG, MIRIAM L · 2017 to 2020
$1.5M
NIGMS NIH HHS R01 GM125082
6 · The paper itself

Abstract

Inositol is an essential nutrient, obtained either by uptake from the environment or by de novo synthesis from glucose. Inositol and its derivatives exhibit tumor-suppressive effects, potentially mediated by inhibition of the ERK-MAPK or PI3K-Akt pathways. Accordingly, many cancers have been documented to silence expression of the ISYNA1 gene, which encodes the rate-limiting enzyme of inositol synthesis. Paradoxically, recent studies have also reported upregulation of ISYNA1 in some cancers. Upregulation may reflect a compensatory response brought about by defective inositol uptake or oncogenic mutations that preclude its tumor-suppressive effects. In these scenarios, de novo synthesis of inositol may be upregulated to promote cell proliferation. The role of inositol in cancer is further complicated by its ability to inhibit the master metabolic regulator AMPK, which upon activation can either decrease cell proliferation and metastasis or promote cell survival. Due to its potential dual role in cancer, inositol homeostasis must be tightly regulated in tumor cells. Thus, whether inositol acts to suppress or promote tumor progression is determined by the metabolic profile and oncogenic background of the cancer.

Indexed as

InositolNeoplasmsCell ProliferationHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktInositolPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAMPKCancerInositolISYNA1MetabolismPI3K-Akt

Identifiers

PMID35462605
OpenAlexW4224313704

What OpenQuestion holds

Textmetadata
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.