Evidence map›Paper›PMID 29844404›Full record

ArticleCell death & disease2018

DSGOST regulates resistance via activation of autophagy in gastric cancer.

Tae Woo Kim, Seon Young Lee, Mia Kim, Chunhoo Cheon, Bo-Hyoung Jang, Yong Cheol Shin, Seong-Gyu Ko

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Facing Cell Autophagy in Gastric Cancer - What Do We Know so Far?International journal of general medicine · 2021
    Review
  9. Review
  10. Review
  11. Article
  12. The Role of Autophagy in Gastric Cancer Chemoresistance: Friend or Foe?Frontiers in cell and developmental biology · 2020
    Review
  13. Article
  14. Article
  15. 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

7 authors at 1 institution in 1 country.

Tae Woo KimDepartment of Preventive Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Korea.
Seon Young LeeDepartment of Preventive Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Korea.
Mia KimDepartment of Cardiovascular and Neurologic Disease (Stroke center), College of Korean Medicine, Kyung Hee University, Seoul, Korea.
Chunhoo CheonDepartment of Preventive Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Korea.
Bo-Hyoung JangDepartment of Preventive Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Korea.
Yong Cheol ShinDepartment of Preventive Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Korea.
Seong-Gyu KoDepartment of Preventive Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Korea. epiko@khu.ac.kr.
Kyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Danggui-Sayuk-Ga-Osuyu-Saenggang-Tang (DSGOST in Korean, Danggui-Sini-Jia-Wuzhuyu-Shengian-Tang in Chinese, and Tokishigyakukagoshuyushokyoto (TJ-38) in Japanese), a well-known traditional Korean/Chinese/Japanese medicine, has long been used to treat vascular diseases such as Raynaud's phenomenon (RP). However, anticancer effect of DSGOST remains elusive. In this study, we checked if DSGOST has an anticancer effect against gastric cancer cells, and investigated the mechanisms underlying DSGOST resistance. Moreover, DSGOST regulates chemoresistance in cisplatin-treated gastric cancer cells. Interestingly, DSGOST treatment induced the accumulation of GFP-LC3 puncta and increased the level of autophagy markers, such as LC3-II, ATG5, and Beclin-1, indicating activated autophagy. Furthermore, DSGOST could activate epithelial-to-mesenchymal transition (EMT) and exosomes via induction of autophagy. DSGOST in combination with TGFβ also induced autophagy and EMT. However, autophagy inhibition induces DSGOST-mediated cell death in gastric cancer cells. In addition, autophagy inhibition blocks the activation of DSGOST-mediated EMT markers including N-cadherin, Snail, Slug, vimentin, β-catenin, p-Smad2, and p-Smad3. Taken together, these findings indicated that prosurvival autophagy was one of the mechanisms involved in the resistance of gastric cancer to DSGOST. Targeting the inhibition of autophagy could be an effective therapeutic approach to overcome resistance to DSGOST in gastric cancer.

Indexed as

AutophagyBeclin-1Cell Line, TumorCisplatinDrug Resistance, NeoplasmDrugs, Chinese HerbalEpithelial-Mesenchymal TransitionHumansProto-Oncogene Proteins c-bcl-2Signal TransductionStomach NeoplasmsBeclin-1CisplatinDrugs, Chinese HerbalDSGOSTProto-Oncogene Proteins c-bcl-2

Identifiers

PMID29844404
PMCPMC5974125
OpenAlexW2807448148

What OpenQuestion holds

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Registered trials

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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.