The Clinicopathological Significance of BiP/GRP-78 in Breast Cancer: A Meta-Analysis of Public Datasets and Immunohistochemical Detection

Direito, Inês; Gomes, Daniela; Monteiro, Fátima Liliana; Carneiro, Isa; Lobo, João; Henrique, Rui; Jerónimo, Carmen; Helguero, Luísa A.

doi:10.3390/curroncol29120710

Cited by 4 publications

(3 citation statements)

References 61 publications

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“…It is upregulated in bone marrow-derived disseminated breast tumor cells displaying cancer stem cell character (Bartkowiak et al, 2010). A meta-analysis of BiP and its clinicopathological potential in breast cancer found a correlation between high BiP expression and HER2 and basallike subtypes as well as metastatic tumors (Direito et al, 2022). XBP1 is critical for the tumorigenicity, progression, and relapse of TNBC, where it forms a complex with HIF1α (Hypoxia Inducible Factor 1 subunit α) to maintain CSCs (Chen et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Transcription Factor EB (TFEB) activity increases resistance of TNBC stem cells to metabolic stress

Berg

Goyal

Somma

et al. 2023

Preprint

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Breast Cancer Stem Cells (CSCs) are difficult to therapeutically target, but continued efforts are critical given their contribution to tumor heterogeneity and treatment resistance in Triple-Negative Breast Cancer (TNBC). CSC properties are influenced by metabolic stress, but specific mechanisms are lacking for effective drug intervention. Our previous work on TFEB suggested a key function in CSC metabolism. Indeed, TFEB knockdown (KD) inhibited mammosphere formation in vitro and tumor initiation/growth in vivo. These phenotypic effects were accompanied by a decline in CD44high/CD24low cells. Glycolysis inhibitor 2-deoxy-D-glucose (2-DG) induced TFEB nuclear translocation, indicative of TFEB transcriptional activity. TFEB KD blunted, whereas TFEB (S142A) augmented 2-DG-driven UPR mediators, notably BiP/HSPA5 and CHOP. Like TFEB KD, silencing BiP/HSPA5 inhibited CSC self-renewal, suggesting that TFEB augments UPR-related survival. Further studies showed that TFEB KD attenuated 2-DG-directed autophagy, suggesting a mechanism whereby TFEB protects CSCs against 2-DG-induced stress. Our data indicate that TFEB modulates CSC metabolic stress response via autophagy and UPR. These findings reveal the novel role of TFEB in regulating CSCs during metabolic stress in TNBC.

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Section: Discussionmentioning

confidence: 99%

Transcription Factor EB (TFEB) activity increases resistance of TNBC stem cells to metabolic stress

Berg

Goyal

Somma

et al. 2023

Preprint

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“…1. Binding immunoglobulin protein (BiP, also known as GRP-78): BiP is an ER chaperone that assists in protein folding and prevents protein aggregation (184). It is upregulated during ER stress and helps properly fold unfolded proteins (185).…”

Section: Neuroprotective Effects Of Resveratrol On Rgcs In Glaucomamentioning

confidence: 99%

Neuroprotective effects of resveratrol on retinal ganglion cells in glaucoma: Focusing on oxidative stress, cellular, and molecular mechanisms

Zamanian,

Golmohammadi,

Meibodi

et al. 2024

Preprint

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Retinal ganglion cells (RGCs) are the major cells that are damaged in glaucoma leading to vision loss and blindness. The damage to RGCs in glaucoma is caused by various mechanisms such as elevated intraocular pressure, oxidative stress, inflammation, and other neurodegenerative processes. As the disease progresses, more and more RGCs are lost, leading to a gradual loss of vision. Therefore, protecting RGCs from damage and promoting their survival is an important goal in the treatment of glaucoma. Resveratrol (RES) exerts anti-oxidant effects and slows down the evolution and progression of glaucoma. This review was prepared using databases such as Google Scholar, PubMed, Scopus, and ScienceDirect. Based on the findings of this review, RES has a protective role on RGCs in cases of ischemic injury and hypoxia as well as ErbB2 protein expression in the retina. Additionally, RES has protective effects on RGCs by promoting cell growth, reducing apoptosis, and decreasing oxidative stress in H2O2-exposed RGCs. RES was also found to inhibit oxidative stress damage in RGCs and suppress the activation of MAPK signaling pathways. Moreover, RES could alleviate retinal function impairment by suppressing the HIF-1a/VEGF and p38/p53 axis while stimulating the PI3K/Akt pathway. Hence, RES might exert potential therapeutic effects in the treatment of glaucoma by protecting RGCs from damage and promoting their survival.

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“…Binding immunoglobulin protein (BiP, also known as GRP‐78) is an ER chaperone that assists in protein folding and prevents protein aggregation. 177 It is upregulated during ER stress and helps to properly fold unfolded proteins. 178 …”

Section: Neuroprotective Effects Of Res On Rgcs In...mentioning

confidence: 99%

Neuroprotective effects of resveratrol on retinal ganglion cells in glaucoma in rodents: A narrative review

Golmohammadi,

Meibodi,

Al‐Hawary

et al. 2024

Anim Models and Exp Med

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Glaucoma, an irreversible optic neuropathy, primarily affects retinal ganglion cells (RGC) and causes vision loss and blindness. The damage to RGCs in glaucoma occurs by various mechanisms, including elevated intraocular pressure, oxidative stress, inflammation, and other neurodegenerative processes. As the disease progresses, the loss of RGCs leads to vision loss. Therefore, protecting RGCs from damage and promoting their survival are important goals in managing glaucoma. In this regard, resveratrol (RES), a polyphenolic phytoalexin, exerts antioxidant effects and slows down the evolution and progression of glaucoma. The present review shows that RES plays a protective role in RGCs in cases of ischemic injury and hypoxia as well as in ErbB2 protein expression in the retina. Additionally, RES plays protective roles in RGCs by promoting cell growth, reducing apoptosis, and decreasing oxidative stress in H2O2‐exposed RGCs. RES was also found to inhibit oxidative stress damage in RGCs and suppress the activation of mitogen‐activated protein kinase signaling pathways. RES could alleviate retinal function impairment by suppressing the hypoxia‐inducible factor‐1 alpha/vascular endothelial growth factor and p38/p53 axes while stimulating the PI3K/Akt pathway. Therefore, RES might exert potential therapeutic effects for managing glaucoma by protecting RGCs from damage and promoting their survival.

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The Clinicopathological Significance of BiP/GRP-78 in Breast Cancer: A Meta-Analysis of Public Datasets and Immunohistochemical Detection

Cited by 4 publications

References 61 publications

Transcription Factor EB (TFEB) activity increases resistance of TNBC stem cells to metabolic stress

Transcription Factor EB (TFEB) activity increases resistance of TNBC stem cells to metabolic stress

Neuroprotective effects of resveratrol on retinal ganglion cells in glaucoma: Focusing on oxidative stress, cellular, and molecular mechanisms

Neuroprotective effects of resveratrol on retinal ganglion cells in glaucoma in rodents: A narrative review

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