Evidence map›Paper›PMID 37481516›Full record

ArticleBMC cancer2023

KRAS activation in gastric cancer stem-like cells promotes tumor angiogenesis and metastasis.

Changhwan Yoon, Jun Lu, Yukyung Jun, Yun-Suhk Suh, Bang-Jin Kim, Jacob E Till, Jong Hyun Kim, Sara H Keshavjee, Sandra Ryeom, Sam S Yoon

RetractedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 23% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 6 institutions in 3 countries.

Changhwan Yoon *Department of Surgery, Columbia University Irving Medical Center, Milstein Hospital Building 7-002, 177 Fort Washington Avenue, New York, NY, 10032, USA.
Jun Lu *Department of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
Yukyung Jun *Center for Supercomputing Applications, Korea Institute of Science and Technology Information, Division of National, SupercomputingDaejeon, Korea.
Yun-Suhk SuhDepartment of Surgery, Seoul National University, Bundang Hospital, Seongnam, Korea.
Bang-Jin KimDepartment of Surgery, Columbia University Irving Medical Center, Milstein Hospital Building 7-002, 177 Fort Washington Avenue, New York, NY, 10032, USA.
Jacob E TillDepartment of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Jong Hyun KimDepartment of Biological Science, Hyupsung University, Hwasung-Si, Republic of Korea.
Sara H KeshavjeeDepartment of Surgery, Columbia University Irving Medical Center, Milstein Hospital Building 7-002, 177 Fort Washington Avenue, New York, NY, 10032, USA.
Sandra RyeomDepartment of Surgery, Columbia University Irving Medical Center, Milstein Hospital Building 7-002, 177 Fort Washington Avenue, New York, NY, 10032, USA.
Sam S YoonDepartment of Surgery, Columbia University Irving Medical Center, Milstein Hospital Building 7-002, 177 Fort Washington Avenue, New York, NY, 10032, USA. ssy2129@cumc.columbia.edu.
Columbia University · USHyupsung University · KRKorea Institute of Science & Technology Information · KRSeoul National University Bundang Hospital · KRUnion Hospital · CNUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous work showed that KRAS activation in gastric cancer cells leads to activation of an epithelial-to-mesenchymal transition (EMT) program and generation of cancer stem-like cells (CSCs). Here we analyze how this KRAS activation in gastric CSCs promotes tumor angiogenesis and metastasis. Gastric cancer CSCs were found to secrete pro-angiogenic factors such as vascular endothelial growth factor A (VEGF-A), and inhibition of KRAS markedly reduced secretion of these factors. In a genetically engineered mouse model, gastric tumorigenesis was markedly attenuated when both KRAS and VEGF-A signaling were blocked. In orthotropic implant and experimental metastasis models, silencing of KRAS and VEGF-A using shRNA in gastric CSCs abrogated primary tumor formation, lymph node metastasis, and lung metastasis far greater than individual silencing of KRAS or VEGF-A. Analysis of gastric cancer patient samples using RNA sequencing revealed a clear association between high expression of the gastric CSC marker CD44 and expression of both KRAS and VEGF-A, and high CD44 and VEGF-A expression predicted worse overall survival. In conclusion, KRAS activation in gastric CSCs enhances secretion of pro-angiogenic factors and promotes tumor progression and metastasis.

Indexed as

Stomach NeoplasmsAnimalsLymphatic MetastasisMiceProto-Oncogene Proteins p21(ras)Vascular Endothelial Growth Factor AProto-Oncogene Proteins p21(ras)Vascular Endothelial Growth Factor ACancer stem cellsEpithelial-to-mesenchymal transitionGastric adenocarcinomaKRAS

Identifiers

PMID37481516
PMCPMC10362758
OpenAlexW4385074688

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.