Evidence map›Paper›PMID 29137367›Full record

ArticleOncotarget2017

Glycolytic reprogramming through PCK2 regulates tumor initiation of prostate cancer cells.

Jiangsha Zhao, Jieran Li, Teresa W M Fan, Steven X Hou

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Interplay Between Glucose Metabolism and Chromatin Modifications in Cancer.Frontiers in cell and developmental biology · 2021
    Pooled it
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  4. Cancer biology & therapy · 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

4 authors at 4 institutions in 1 country.

Jiangsha ZhaoThe Basic Research Laboratory, National Cancer Institute, National Institutes of Health Frederick, Frederick, MD 21702, USA.
Jieran LiGraduate Center of Toxicology and Cancer Biology, Center for Environmental and Systems Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.
Teresa W M FanGraduate Center of Toxicology and Cancer Biology, Center for Environmental and Systems Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.
Steven X HouThe Basic Research Laboratory, National Cancer Institute, National Institutes of Health Frederick, Frederick, MD 21702, USA.
Frederick National Laboratory for Cancer Research · USMarkey Cancer Center · USNational Cancer Institute · USUniversity of Kentucky · US

Funding

SAMPLE COREU24DK097215 · NIDDK · UNIVERSITY OF KENTUCKY · PI FAN, TERESA WHEI-MEI, HIGASHI, RICHARD M · 2013 to 2017
$8.7M
Systems Biochemistry in Lung Cancer: Toward a Mechanistic Understanding of NSCLCP01CA163223 · NCI · UNIVERSITY OF LOUISVILLE · PI FAN, TERESA WHEI-MEI, FAN, TERESA WHEI-MEI · 2013 to 2017
$6.5M
Integrated Chemoselective and Informatic Platform for Large-Scale MetabolomicsR01ES022191 · NIEHS · UNIVERSITY OF LOUISVILLE · PI FAN, TERESA WHEI-MEI, HIGASHI, RICHARD M · 2012 to 2016
$3.4M
NCI NIH HHS P01 CA163223NIDDK NIH HHS U24 DK097215NIEHS NIH HHS R01 ES022191
6 · The paper itself

Abstract

Tumor-initiating cells (TICs) play important roles in tumor progression and metastasis. Identifying the factors regulating TICs may open new avenues in cancer therapy. Here, we show that TIC-enriched prostate cancer cell clones use more glucose and secrete more lactate than TIC-low clones. We determined that elevated levels of phosphoenolpyruvate carboxykinase isoform 2 (PCK2) are critical for the metabolic switch and the maintenance of TICs in prostate cancer. Information from prostate cancer patient databases revealed that higher PCK2 levels correlated with more aggressive tumors and lower survival rates. PCK2 knockdown resulted in low TIC numbers, increased cytosolic acetyl-CoA and cellular protein acetylation. Our data suggest PCK2 promotes tumor initiation by lowering acetyl-CoA level through reducing the mitochondrial tricarboxylic acid (TCA) cycle. Thus, PCK2 is a potential therapeutic target for aggressive prostate tumors.

Indexed as

cancerglucose metabolismphosphoenolpyruvate carboxykinase isoform 2prostatetumorigenicity

Identifiers

PMID29137367
PMCPMC5663539
OpenAlexW2729141866

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.