Evidence map›Paper›PMID 28260082›Full record

ArticleOncology reports2017

Cancer-associated fibroblasts enhance pancreatic cancer cell invasion by remodeling the metabolic conversion mechanism.

Tao Shan, Shuo Chen, Xi Chen, Wan Run Lin, Wei Li, Jiancang Ma, Tao Wu, Xijuan Cui, Hong Ji, Yiming Li and 1 more

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

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
3.8field-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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

14 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

11 authors at 5 institutions in 2 countries.

Tao ShanDepartment of General Surgery, The Second Affiliated Hospital of the Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
Shuo ChenDepartment of General Surgery, The Second Affiliated Hospital of the Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
Xi ChenDepartment of General Surgery, The Second Affiliated Hospital of the Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
Wan Run LinDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Wei LiGraduate School, Fourth Military Medical University, Xi'an, Shaanxi 710033, P.R. China.
Jiancang MaDepartment of General Surgery, The Second Affiliated Hospital of the Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
Tao WuDepartment of General Surgery, The Second Affiliated Hospital of the Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
Xijuan CuiDepartment of General Surgery, First Affiliated Hospital of the Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Hong JiDepartment of General Surgery, The Second Affiliated Hospital of the Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
Yiming LiDepartment of General Surgery, The Second Affiliated Hospital of the Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
Ya'an KangDepartment of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Second Affiliated Hospital of Xi'an Jiaotong University · CNAir Force Medical University · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNFudan University Shanghai Cancer Center · CNThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the mechanism of cancer-associated fibroblasts (CAFs) in promoting the invasion and metastasis of pancreatic cancer cells in a non-vascular manner. We verified the original generation of isolated cultured CAFs and normal fibroblasts (NFs) based on the expression of α-SMA and vimentin, and we examined the cell glycolysis level through glucose consumption and lactate production experiments. The mRNA and protein expression of CAF glycolytic enzymes, lactate dehydrogenase and pyruvate kinase m2, were examined by RT-PCR and western blotting, respectively. In vitro culture first-generation pancreatic CAFs were collected and cultured together with pancreas cancer BxPc-3 and Panc-1 cells. Cell invasion and migration were assessed using a Transwell assay and scratch test, respectively. Mitochondrial activity was assessed by experimentally determining oxidative phosphorylation (OP) activity. The aerobic oxidation index of cancer cells was also examined. Succinate dehydrogenase, fumarate hydratase (FH), and monocarboxylate transporter 1 (MCT1) expression were examined using an MCT1-specific inhibitor to remove 'tumor-stromal' metabolic coupling to observe the influence of cell interstices on pancreas cancer progression. First-generation isolated cultured CAFs and NFs both grew well, and showed active proliferation. Glucose absorption and lactate production were significantly enhanced in CAFs compared with that in NFs. PCR and western blotting showed that the lactate dehydrogenase and pyruvate kinase m2 mRNA and protein expression levels were increased in the CAFs. After indirect co-culture, OP was increased in the BxPc-3 and Panc-1 cells; correspondingly, succinate dehydrogenase, FH and MCT expression were increased. After the MCT1-specific inhibitor removed 'tumor-stromal' metabolic coupling, the migration and invasion abilities of the pancreatic cancer cells were decreased. Pancreatic CAFs can alter metabolism as well as communicate with and respond to cancer cell migration and invasion. This may be an important mechanism for promoting tumor progression in a non-vascular manner in the tumor microenvironment. The mechanism by which CAFs reshape metabolic transition requires further analysis.

Indexed as

ActinsCancer-Associated FibroblastsCell AdhesionCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationFumarate HydrataseGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessOncogene ProteinsOxidative PhosphorylationPancreatic NeoplasmsSuccinate DehydrogenaseTumor MicroenvironmentACTA2 protein, humanActinsCell Cycle ProteinsFumarate HydrataseMCTS1 protein, humanOncogene ProteinsSuccinate DehydrogenaseVimentin

Identifiers

PMID28260082
PMCPMC5367364
OpenAlexW2594360359

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.