Evidence map›Paper›PMID 39827214›Full record

ReviewMedical oncology (Northwood, London, England)2025

GRP78 as a potential therapeutic target in cancer treatment: an updated review of its role in chemoradiotherapy resistance of cancer cells.

Min Lin, Yan Mo, Cheng-Min Li, Ying-Zhe Liu, Xue-Ping Feng

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. High-Penetrance Rare Variants Underlying Familial Lung Cancer Risk: Insights From Genetic Epidemiology of Lung Cancer Consortium.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2026
    Article
  6. Article
  7. Enhancing Cytosolic Internalization of [International journal of molecular sciences · 2025
    Article
  8. Targeted Degradation of sGRP78 Alleviates the Immunosuppressive Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  9. Review
  10. Review
  11. Review
  12. Review
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.

Min LinDepartment of Oncology and Institute of Medical Sciences, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410013, China.ORCID http://orcid.org/0000-0002-8427-1777
Yan MoDepartment of Oncology and Institute of Medical Sciences, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410013, China.
Cheng-Min LiDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, 410013, China.
Ying-Zhe LiuXiangya International Medical Center, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410013, China. liuyingzhe365@126.com.
Xue-Ping FengDepartment of Oncology and Institute of Medical Sciences, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410013, China. Xuepfeng@CSU.edu.cn.ORCID http://orcid.org/0000-0003-0481-3853

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GRP78 (Glucose-related protein 78, BiP/HSPA5) is commonly overexpressed in cancer cells. Acting as an activator of endoplasmic reticulum stress, GRP78 is involved in the resistance of cancer cells to injury. Current evidence suggests that GRP78 plays a significant role in the radiotherapy resistance and chemotherapy resistance of cancers, which is accomplished through a variety of complex pathways. These include the promotion of tumor stemness, inhibition of apoptosis, regulation of autophagy, maintenance of tumor microenvironment homeostasis, protection of dormant cells, evasion of senescence, counteraction of autoantibodies against GRP78, facilitation of DNA damage repair, suppression of ferroptosis, and modulation of metabolic reprogramming in tumor cells. Importantly, chemoradiotherapy resistance in cancers are the main reasons for treatment failure in patients, severely affecting their survival. Investigating the mechanisms of GRP78 in tumor therapeutic resistance is essential. In this article, we review the mechanisms by which GRP78 mediates cell survival and chemoradiotherapy resistance in cancers and provide an overview of clinical trials targeting GRP78 therapy.

Indexed as

ChemoradiotherapyDrug Resistance, NeoplasmHeat-Shock ProteinsNeoplasmsRadiation ToleranceAnimalsEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressHumansEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHSPA5 protein, humanCancerGRP78ResistanceTargetTherapy

Identifiers

PMID39827214

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.