Evidence map›Paper›PMID 30671168›Full record

ReviewOxidative medicine and cellular longevity2018

Oncogenic Metabolism Acts as a Prerequisite Step for Induction of Cancer Metastasis and Cancer Stem Cell Phenotype.

Su Yeon Lee, Min Kyung Ju, Hyun Min Jeon, Yig Ji Lee, Cho Hee Kim, Hye Gyeong Park, Song Iy Han, Ho Sung Kang

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

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  14. Role of c-Myc in lung cancer: Progress, challenges, and prospects.Chinese medical journal pulmonary and critical care medicine · 2023
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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

8 authors at 4 institutions in 1 country.

Su Yeon LeeDepartment of Molecular Biology, College of Natural Sciences, Pusan National University, Pusan 609-735, Republic of Korea.ORCID 0000-0002-9401-2306
Min Kyung JuDepartment of Molecular Biology, College of Natural Sciences, Pusan National University, Pusan 609-735, Republic of Korea.ORCID 0000-0001-9574-7294
Hyun Min JeonDepartment of Molecular Biology, College of Natural Sciences, Pusan National University, Pusan 609-735, Republic of Korea.
Yig Ji LeeDepartment of Molecular Biology, College of Natural Sciences, Pusan National University, Pusan 609-735, Republic of Korea.
Cho Hee KimDepartment of Molecular Biology, College of Natural Sciences, Pusan National University, Pusan 609-735, Republic of Korea.
Hye Gyeong ParkNanobiotechnology Center, Pusan National University, Pusan 609-735, Republic of Korea.
Song Iy HanThe Division of Natural Medical Sciences, College of Health Science, Chosun University, Gwangju 501-759, Republic of Korea.ORCID 0000-0003-4975-480X
Ho Sung KangDepartment of Molecular Biology, College of Natural Sciences, Pusan National University, Pusan 609-735, Republic of Korea.ORCID 0000-0002-8449-9907
Pusan National University · KRChosun University · KRGyeongsang National University Hospital · KRNational Forensic Institute · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is a major obstacle to the efficient and successful treatment of cancer. Initiation of metastasis requires epithelial-mesenchymal transition (EMT) that is regulated by several transcription factors, including Snail and ZEB1/2. EMT is closely linked to the acquisition of cancer stem cell (CSC) properties and chemoresistance, which contribute to tumor malignancy. Tumor suppressor p53 inhibits EMT and metastasis by negatively regulating several EMT-inducing transcription factors and regulatory molecules; thus, its inhibition is crucial in EMT, invasion, metastasis, and stemness. Metabolic alterations are another hallmark of cancer. Most cancer cells are more dependent on glycolysis than on mitochondrial oxidative phosphorylation for their energy production, even in the presence of oxygen. Cancer cells enhance other oncogenic metabolic pathways, such as glutamine metabolism, pentose phosphate pathway, and the synthesis of fatty acids and cholesterol. Metabolic reprogramming in cancer is regulated by the activation of oncogenes or loss of tumor suppressors that contribute to tumor progression. Oncogenic metabolism has been recently linked closely with the induction of EMT or CSC phenotypes by the induction of several metabolic enzyme genes. In addition, several transcription factors and molecules involved in EMT or CSCs, including Snail, Dlx-2, HIF-1

Indexed as

Epithelial-Mesenchymal TransitionAnimalsHumansNeoplasm MetastasisNeoplasm ProteinsNeoplasmsNeoplastic Stem CellsTranscription FactorsNeoplasm ProteinsTranscription Factors

Identifiers

PMID30671168
PMCPMC6323533
OpenAlexW2905852219

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.