Evidence map›Paper›PMID 25431258›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015

Glucose-regulated protein 78 (GRP78) regulates colon cancer metastasis through EMT biomarkers and the NRF-2/HO-1 pathway.

Yu-Jia Chang, Wei-Yu Chen, Chien-Yu Huang, Hui-Hsiung Liu, Po-Li Wei

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. 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
2.0field-weighted citation impact, top 16% 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, 44 citations in OpenAlex.

  1. The role of endoplasmic reticulum stress in the pathogenesis of oral diseases.Journal of the Korean Association of Oral and Maxillofacial Surgeons · 2024
    Review
  2. Review
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  4. Heme Oxygenase-1 and Its Role in Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. GRP78 in lung cancer.Journal of translational medicine · 2021
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
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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

5 authors at 3 institutions in 1 country.

Yu-Jia ChangGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Wei-Yu Chen
Chien-Yu Huang
Hui-Hsiung Liu
Po-Li Wei
Taipei Medical University · TWTaipei Medical University-Shuang Ho Hospital · TWWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose-regulated protein 78 (GRP78) is a key chaperone and stress response protein. Previous studies have demonstrated that high GRP78 expression may be correlated with cancer progression and therapeutic response. However, the role of GRP78 in the metastasis of colon cancer is unclear. In this study, we used small interfering RNA (siRNA) to knock down GRP78 expression in colon cancer cells (HT-29 and DLD-1 cells). In wound-healing migration assays, we found that GRP78-knockdown (GRP78KD) cells showed better wound-healing ability than control cells. We also found that GRP78KD cells displayed a better migratory ability than control cells in migration and invasion assays. As we further dissected the underlying molecular mechanism, we found that silencing GRP78 may cause an increase in vimentin expression and a decrease in the E-cadherin level, which was correlated with the increase in migratory ability. In addition, we found that GRP78KD may activate the NRF-2/HO-1 pathway, and this activation was also correlated with the increase in cell invasiveness. Furthermore, we examined GRP78 expression in a tissue array and found that the GRP78 expression in metastatic adenocarcinoma in lymph nodes tended to be weaker than that in primary colonic adenocarcinoma. In conclusion, a low level of GRP78 may cause an increase in metastasis ability in colon cancer cells by altering E-cadherin and vimentin expression and activating the NRF-2/HO-1 signaling pathway. Our study demonstrates that low expression of GRP78 may correlate with a high risk of metastasis in colon cancer.

Indexed as

AdenocarcinomaBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationColonic NeoplasmsEndoplasmic Reticulum Chaperone BiPEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHeat-Shock ProteinsHeme Oxygenase-1HT29 CellsHumansNeoplasm MetastasisNF-E2-Related Factor 2Signal TransductionBiomarkers, TumorEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHeme Oxygenase-1HMOX1 protein, humanHSPA5 protein, humanNFE2L2 protein, humanNF-E2-Related Factor 2

Identifiers

PMID25431258
OpenAlexW2011556115

What OpenQuestion holds

Textmetadata
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.