Evidence map›Paper›PMID 26342198›Full record

ArticleOncotarget2015

Twist promotes reprogramming of glucose metabolism in breast cancer cells through PI3K/AKT and p53 signaling pathways.

Li Yang, Yixuan Hou, Jie Yuan, Shifu Tang, Hailong Zhang, Qing Zhu, Yan-e Du, Mingli Zhou, Siyang Wen, Liyun Xu and 3 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

65 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. The Multifaced Role of Collagen in Cancer Development and Progression.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Roles of Twist1 in lipid and glucose metabolism.Cell communication and signaling : CCS · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

5 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Li YangKey Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, China.
Yixuan HouExperimental Teaching Center of Basic Medicine Science, Chongqing Medical University, Chongqing 400016, China.
Jie YuanDepartment of Endocrine and Breast Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Shifu TangKey Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, China.
Hailong ZhangKey Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, China.
Qing ZhuDepartment of Endocrine and Breast Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Yan-e DuKey Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, China.
Mingli ZhouKey Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, China.
Siyang WenKey Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, China.
Liyun XuKey Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, China.
Xi TangKey Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, China.
Xiaojiang CuiDepartment of Surgery, Department of Obstetrics and Gynecology, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Manran LiuKey Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing 400016, China.
Chongqing Medical University · CNChildren's Hospital of Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNCedars-Sinai Medical Center · US

Funding

The Role of FOXCI in Basal-like Breast CancerR01CA151610 · NCI · SAINT JOHN'S CANCER INSTITUTE · PI CUI, XIAOJIANG · 2011 to 2022
$3.8M
NCI NIH HHS CA151610NCI NIH HHS R01 CA151610
6 · The paper itself

Abstract

Twist, a key regulator of epithelial-mesenchymal transition (EMT), plays an important role in the development of a tumorigenic phenotype. Energy metabolism reprogramming (EMR), a newly discovered hallmark of cancer cells, potentiates cancer cell proliferation, survival, and invasion. Currently little is known about the effects of Twist on tumor EMR. In this study, we found that glucose consumption and lactate production were increased and mitochondrial mass was decreased in Twist-overexpressing MCF10A mammary epithelial cells compared with vector-expressing MCF10A cells. Moreover, these Twist-induced phenotypic changes were augmented by hypoxia. The expression of some glucose metabolism-related genes such as PKM2, LDHA, and G6PD was also found to be upregulated. Mechanistically, activated β1-integrin/FAK/PI3K/AKT/mTOR and suppressed P53 signaling were responsible for the observed EMR. Knockdown of Twist reversed the effects of Twist on EMR in Twist-overexpressing MCF10A cells and Twist-positive breast cancer cells. Furthermore, blockage of the β1-integrin/FAK/PI3K/AKT/mTOR pathway by siRNA or specific chemical inhibitors, or rescue of p53 activation can partially reverse the switch of glucose metabolism and inhibit the migration of Twist-overexpressing MCF10A cells and Twist-positive breast cancer cells. Thus, our data suggest that Twist promotes reprogramming of glucose metabolism in MCF10A-Twist cells and Twist-positive breast cancer cells via activation of the β1-integrin/FAK/PI3K/AKT/mTOR pathway and inhibition of the p53 pathway. Our study provides new insight into EMR.

Indexed as

Energy MetabolismSignal TransductionAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFemaleFocal Adhesion Kinase 1Gene Expression Regulation, NeoplasticGlucoseHumansIntegrin beta1Lactic AcidMitochondriaNuclear ProteinsAntineoplastic AgentsFocal Adhesion Kinase 1GlucoseIntegrin beta1Lactic AcidMTOR protein, humanNuclear ProteinsPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktPTK2 protein, humanTOR Serine-Threonine KinasesTP53 protein, humanTumor Suppressor Protein p53TWIST1 protein, humanTwist-Related Protein 1glucose metabolismp53PI3K/AKTTwist

Identifiers

PMID26342198
PMCPMC4694864
OpenAlexW1896288382

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.