Evidence map›Paper›PMID 27224918›Full record

ArticleOncotarget2016

MCT4 as a potential therapeutic target for metastatic gastric cancer with peritoneal carcinomatosis.

Ji Yun Lee, InKyoung Lee, Won Jin Chang, Su Min Ahn, Sung Hee Lim, Hae Su Kim, Kwai Han Yoo, Ki Sun Jung, Haa-Na Song, Jin Hyun Cho and 10 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Role of histone modifications in gastric cancer (Review).International journal of oncology · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Lactate and lactylation in cancer.Signal transduction and targeted therapy · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Curcumin-Based β-Diketo Ligands for GaPharmaceuticals (Basel, Switzerland) · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

20 authors at 3 institutions in 1 country.

Ji Yun LeeDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
InKyoung LeeBiological Research Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Won Jin ChangDivision of Hematology-Oncology, Department of Medicine, Korea University College of Medicine, Seoul, Korea.
Su Min AhnInnovative Cancer Medicine Institute, Samsung Cancer Center, Samsung Medical Center, Seoul, Korea.
Sung Hee LimDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Hae Su KimDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Kwai Han YooDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Ki Sun JungDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Haa-Na SongDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Jin Hyun ChoDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Sun Young KimDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Kyoung-Mee KimInnovative Cancer Medicine Institute, Samsung Cancer Center, Samsung Medical Center, Seoul, Korea.
Soojin LeeDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Seung Tae KimDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Se Hoon ParkDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Jeeyun LeeDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Joon Oh ParkDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Young Suk ParkDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Ho Yeong LimDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Won Ki KangDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Sungkyunkwan University · KRSamsung Medical Center · KRKorea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocarboxylate transporters (MCTs) play a major role in up-regulation of glycolysis and adaptation to acidosis. However, the role of MCTs in gastric cancer (GC) is not fully understood. We investigated the potential utilization of a new cancer therapy for GC. We characterized the expression patterns of the MCT isoforms 1, 2, and 4 and investigated the role of MCT in GC through in vitro and in vivo tests using siRNA targeting MCTs. In GC cell lines, MCT1, 2, and 4 were up-regulated with different expression levels; MCT1 and MCT4 were more widely expressed in GC cell lines compared with MCT2. Inhibition of MCTs by siRNA or AR-C155858 reduced cell viability and lactate uptake in GC cell lines. The effect of inhibition of MCTs on tumor growth was also confirmed in xenograft models. Furthermore, MCT inhibition in GC cells increased the sensitivity of cells to radiotherapy or chemotherapy. Compared with normal gastric tissue, no significant alterations of expression levels in tumors were identified for MCT1 and MCT2, whereas a significant increase in MCT4 expression was observed. Most importantly, MCT4 was highly overexpressed in malignant cells of acsites and its silencing resulted in reduced tumor cell proliferation and lactate uptake in malignant ascites. Our study suggests that MCT4 is a clinically relevant target in GC with peritoneal carcinomatosis.

Indexed as

AdultAgedAged, 80 and overAnimalsAntineoplastic AgentsCell ProliferationCell SurvivalFemaleHumansLactic AcidMaleMice, Inbred BALB CMice, NudeMiddle AgedMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersAntineoplastic AgentsAR C155858Lactic AcidMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersMuscle ProteinsRNA, Small InterferingSLC16A4 protein, humanSLC16A7 protein, humanSymportersThiophenesUracilgastric cancerglycolysismonocarboxylate transporterprognosis

Identifiers

PMID27224918
PMCPMC5190039
OpenAlexW2394961775

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.