ArticleCancer biology & therapy2009
The Par-4-GRP78 TRAIL, more twists and turns.
Article in Cancer biology & therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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.
Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
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- Article
- Cancer-associated fibroblasts promote cancer cell growth through a miR-7-RASSF2-PAR-4 axis in the tumor microenvironment.Oncotarget · 2017Article
- A journey beyond apoptosis: new enigma of controlling metastasis by pro-apoptotic Par-4.Clinical & experimental metastasis · 2016Review
- The Role of Prostate Apoptosis Response-4 (Par-4) in Mycobacterium tuberculosis Infected Macrophages.Scientific reports · 2016Article
- The role of c-Src in the invasion and metastasis of hepatocellular carcinoma cells induced by association of cell surface GRP78 with activated α2M.BMC cancer · 2015Article
- Generation of human ER chaperone BiP in yeast Saccharomyces cerevisiae.Microbial cell factories · 2014Article
- The endoplasmic reticulum stress marker, glucose-regulated protein-78 (GRP78) in visceral adipocytes predicts endometrial cancer progression and patient survival.Gynecologic oncology · 2013Article
- Involvement of membrane GRP78 in trophoblastic cell fusion.PloS one · 2012Article
- GRP78 Protein Expression in Ovarian Cancer Patients and Perspectives for a Drug-Targeting Approach.Journal of oncology · 2012Article
- Beyond the endoplasmic reticulum: atypical GRP78 in cell viability, signalling and therapeutic targeting.The Biochemical journal · 2011Review
- Cell surface relocalization of the endoplasmic reticulum chaperone and unfolded protein response regulator GRP78/BiP.The Journal of biological chemistry · 2010Article
- AnBioTechniquesArticle
- Curcumin Sensitizes 4T1 Murine Breast Cancer Cells to Cisplatin Through PAR4 Secretion.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
GRP78, also referred to as BiP, is an essential molecular chaperone and a master regulator of the unfolded protein response. Traditionally, GRP78 is regarded as localized in the lumen of the endoplasmic reticulum (ER). However, recent findings revealed that a subfraction of GRP78 can localize to the surface of specific cell types. Furthermore, preferential expression of GRP78 on the surface of tumor cells but not in normal organs suggests that surface GRP78 can serve both as a target as well as mediator for cancer-specific therapy. Recent reports further established that GRP78 forms complexes with specific proteins on the cell surface and plays an important role in signaling, impacting cell survival and proliferation. Burikhanov et al. (Cell 2009, 138:377) reported that Par-4, generally regarded as a cytosolic and nuclear protein that promotes cell death via the mitochondrial cell death pathway, is spontaneously secreted by normal and cancer cells and this process is enhanced by ER stress or with addition of TRAIL. It is proposed that ER stress, induced by extracellular insults such as TRAIL, causes translocation of the Par-4-GRP78 complex from the ER to the plasma membrane, and through a positive feedback loop, extracellular Par-4 binds to cell surface GRP78 and activates the extrinsic apoptotic pathway. In this journal club, we discuss some open questions and how these new findings integrate with current understanding of GRP78 function in vivo.
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What OpenQuestion holds
Registered trials
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.