Evidence map›Paper›PMID 35440095›Full record

ArticleCell death & disease2022

Leukemia inhibitory factor drives glucose metabolic reprogramming to promote breast tumorigenesis.

Xuetian Yue, Jianming Wang, Chun-Yuan Chang, Juan Liu, Xue Yang, Fan Zhou, Xia Qiu, Vrushank Bhatt, Jessie Yanxiang Guo, Xiaoyang Su and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  12. Leukemia inhibitory factor, a double-edged sword with therapeutic implications in human diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  13. O-GlcNAcylation in Renal (Patho)Physiology.International journal of molecular sciences · 2022
    Review
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

13 authors at 1 institution in 1 country.

Xuetian Yue *Department of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Jianming Wang *Department of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.ORCID 0000-0002-7265-1764
Chun-Yuan ChangDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.ORCID 0000-0002-4562-9393
Juan LiuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Xue YangDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Fan ZhouDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Xia QiuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Vrushank BhattRutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Jessie Yanxiang GuoRutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.ORCID 0000-0001-9212-7954
Xiaoyang SuDepartment of Medicine, Rutgers Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ, USA.ORCID 0000-0001-8081-1396
Lanjing ZhangDepartment of Pathology, Princeton Medical Center, Plainsboro, NJ, USA.
Zhaohui FengDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA. fengzh@cinj.rutgers.edu.ORCID 0000-0002-8912-6456
Wenwei HuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA. wh221@cinj.rutgers.edu.ORCID 0000-0003-3971-4257
Rutgers, The State University of New Jersey · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Tracie Saunders · 1997 to 2026
$94.5M
Gain-of-function mutant p53 and metabolic reprogramming in colorectal cancerR01CA260837 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI FENG, ZHAOHUI, HU, WENWEI · 2021 to 2025
$2.2M
The regulation of mutant p53 protein accumulation in cancer: molecular basis and therapeutic potentialR01CA229257 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI FENG, ZHAOHUI · 2021 to 2025
$2.0M
The role of leukemia inhibitory factor in colorectal cancerR01CA260838 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI Wenwei Hu · 2022 to 2026
$1.9M
The role of chronic stress in regulation of mutant p53 and tumorigenesisR01CA203965 · NCI · RBHS -CANCER INSTITUTE OF NEW JERSEY · PI HU, WENWEI · 2017 to 2021
$1.8M
Metabolic reprogramming in breast cancerR01CA227912 · NCI · RBHS -CANCER INSTITUTE OF NEW JERSEY · PI FENG, ZHAOHUI, HU, WENWEI · 2018 to 2022
$1.8M
SENP6, a novel p53 negative regulator, is an important new player in cancerR01CA214746 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI FENG, ZHAOHUI · 2018 to 2022
$1.8M
NCI NIH HHS P30 CA072720NCI NIH HHS R01 CA203965NCI NIH HHS R01 CA214746NCI NIH HHS R01 CA227912NCI NIH HHS R01 CA229257NCI NIH HHS R01 CA260837NCI NIH HHS R01 CA260838
6 · The paper itself

Abstract

LIF, a multifunctional cytokine, is frequently overexpressed in many types of solid tumors, including breast cancer, and plays an important role in promoting tumorigenesis. Currently, how LIF promotes tumorigenesis is not well-understood. Metabolic reprogramming is a hallmark of cancer cells and a key contributor to cancer progression. However, the role of LIF in cancer metabolic reprogramming is unclear. In this study, we found that LIF increases glucose uptake and drives glycolysis, contributing to breast tumorigenesis. Blocking glucose uptake largely abolishes the promoting effect of LIF on breast tumorigenesis. Mechanistically, LIF overexpression enhances glucose uptake via activating the AKT/GLUT1 axis to promote glycolysis. Blocking the AKT signaling by shRNA or its inhibitors greatly inhibits glycolysis driven by LIF and largely abolishes the promoting effect of LIF on breast tumorigenesis. These results demonstrate an important role of LIF overexpression in glucose metabolism reprogramming in breast cancers, which contributes to breast tumorigenesis. This study also reveals an important mechanism underlying metabolic reprogramming of breast cancers, and identifies LIF and its downstream signaling as potential therapeutic targets for breast cancers, especially those with LIF overexpression.

Indexed as

Breast NeoplasmsGlucoseCarcinogenesisCell Line, TumorCell Transformation, NeoplasticFemaleGlycolysisHumansLeukemia Inhibitory FactorProto-Oncogene Proteins c-aktGlucoseLeukemia Inhibitory FactorProto-Oncogene Proteins c-akt

Identifiers

PMID35440095
PMCPMC9018736
OpenAlexW4224271380

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.