BMI1 promotes the proliferation and inhibits autophagy of breast cancer cells by activating COPZ1

Chen, Shuming; Li, He; Chen, Siyu; Wang, Bing; Zhang, Kaixiang

doi:10.1007/s12094-022-02869-w

Cited by 8 publications

(3 citation statements)

References 23 publications

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“…Herein, the data from CRISPR Achilles’ project in CCLE confirmed that knockout of COPZ1 could suppress tumor cell viability in most cancer cell lines. Additionally, BMI1 can promote breast cancer cell proliferation and inhibit autophagy by activating COPZ1 transcription [ 20 ]. Recent research has discovered an antibody conjugated polymer nanogel system called Nano-ERASER, which could degrade COPZ1 in cancer cells and finally cause cancer cell death [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

A Comprehensive Pan-Cancer Analysis of the Regulation and Prognostic Effect of Coat Complex Subunit Zeta 1

Hong

Xia

Sun

et al. 2023

Genes

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The Coatomer protein complex Zeta 1 (COPZ1) has been reported to play an essential role in maintaining the survival of some types of tumors. In this study, we sought to explore the molecular characteristics of COPZ1 and its clinical prognostic value through a pan-cancers bioinformatic analysis. We found that COPZ1 was extremely prevalent in a variety of cancer types, and high expression of COPZ1 was linked to poor overall survival in many cancers, while low expression in LAML and PADC was correlated with tumorigenesis. Besides, the CRISPR Achilles’ knockout analysis revealed that COPZ1 was vital for many tumor cells’ survival. We further demonstrated that the high expression level of COPZ1 in tumors was regulated in multi-aspects, including abnormal CNV, DNA-methylation, transcription factor and microRNAs. As for the functional exploration of COPZ1, we found a positive relationship between COPZ1’s expression and stemness and hypoxia signature, especially the contribution of COPZ1 on EMT ability in SARC. GSEA analysis revealed that COPZ1 was associated with many immune response pathways. Further investigation demonstrated that COPZ expression was negatively correlated with immune score and stromal score, and low expression of COPZ1 has been associated to more antitumor immune cell infiltration and pro-inflammatory cytokines. The further analysis of COPZ1 expression and anti-inflammatory M2 cells showed a consistent result. Finally, we verified the expression of COPZ1 in HCC cells, and proved its ability of sustaining tumor growth and invasion with biological experiments. Our study provides a multi-dimensional pan-cancer analysis of COPZ and demonstrates that COPZ1 can serve as both a prospective target for the treatment of cancer and a prognostic marker for a variety of cancer types.

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Section: Discussionmentioning

confidence: 99%

A Comprehensive Pan-Cancer Analysis of the Regulation and Prognostic Effect of Coat Complex Subunit Zeta 1

Hong

Xia

Sun

et al. 2023

Genes

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“…These diseases caused by mutations or expression alterations to subunits of coated transport vesicles are collectively named 'coatopathies'. In some cases, high expression of coat subunits is associated with a poorer outcome, such as for α-COP in cervical cancer [72], and β′-COP (COPB2) and ζ1-COP (COPZ1) in breast cancer [73,74]. In contrast, for some subunits, low expression is associated with a poor outcome, such as ε-COP (COPE) in pancreatic adenocarcinoma [75] and ζ2-COP (COPZ2) in breast cancer [76].…”

Section: Dysregulation Of Key Rt Machinery and Their Function In Diseasementioning

confidence: 99%

Exploring Retrograde Trafficking: Mechanisms and Consequences in Cancer and Disease

Bingham,

McCarthy,

Buckley

2024

Traffic

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Retrograde trafficking (RT) orchestrates the intracellular movement of cargo from the plasma membrane, endosomes, Golgi or endoplasmic reticulum (ER)–Golgi intermediate compartment (ERGIC) in an inward/ER‐directed manner. RT works as the opposing movement to anterograde trafficking (outward secretion), and the two work together to maintain cellular homeostasis. This is achieved through maintaining cell polarity, retrieving proteins responsible for anterograde trafficking and redirecting proteins that become mis‐localised. However, aberrant RT can alter the correct location of key proteins, and thus inhibit or indeed change their canonical function, potentially causing disease. This review highlights the recent advances in the understanding of how upregulation, downregulation or hijacking of RT impacts the localisation of key proteins in cancer and disease to drive progression. Cargoes impacted by aberrant RT are varied amongst maladies including neurodegenerative diseases, autoimmune diseases, bacterial and viral infections (including SARS‐CoV‐2), and cancer. As we explore the intricacies of RT, it becomes increasingly apparent that it holds significant potential as a target for future therapies to offer more effective interventions in a wide range of pathological conditions.

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“…Sodium butyrate induced AMPK/mTOR pathway-dependent autophagy via the miR-139-5p/Bmi-1 axis in human bladder cancer cells [ 13 ]. Knockdown of Bmi-1 in breast cancer cells also induced autophagy [ 102 , 103 ]. Additionally, betulinic acid induced autophagy and apoptosis in bladder cancer cells through the Bmi-1/ROS/AMPK/mTOR/ULK1 axis [ 86 ].…”

Section: Bmi-1-targeted Processes In Cancermentioning

confidence: 99%

The Crucial Roles of Bmi-1 in Cancer: Implications in Pathogenesis, Metastasis, Drug Resistance, and Targeted Therapies

Shi

et al. 2022

IJMS

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B-cell-specific Moloney murine leukemia virus integration region 1 (Bmi-1, also known as RNF51 or PCGF4) is one of the important members of the PcG gene family, and is involved in regulating cell proliferation, differentiation and senescence, and maintaining the self-renewal of stem cells. Many studies in recent years have emphasized the role of Bmi-1 in the occurrence and development of tumors. In fact, Bmi-1 has multiple functions in cancer biology and is closely related to many classical molecules, including Akt, c-MYC, Pten, etc. This review summarizes the regulatory mechanisms of Bmi-1 in multiple pathways, and the interaction of Bmi-1 with noncoding RNAs. In particular, we focus on the pathological processes of Bmi-1 in cancer, and explore the clinical relevance of Bmi-1 in cancer biomarkers and prognosis, as well as its implications for chemoresistance and radioresistance. In conclusion, we summarize the role of Bmi-1 in tumor progression, reveal the pathophysiological process and molecular mechanism of Bmi-1 in tumors, and provide useful information for tumor diagnosis, treatment, and prognosis.

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BMI1 promotes the proliferation and inhibits autophagy of breast cancer cells by activating COPZ1

Cited by 8 publications

References 23 publications

A Comprehensive Pan-Cancer Analysis of the Regulation and Prognostic Effect of Coat Complex Subunit Zeta 1

A Comprehensive Pan-Cancer Analysis of the Regulation and Prognostic Effect of Coat Complex Subunit Zeta 1

Exploring Retrograde Trafficking: Mechanisms and Consequences in Cancer and Disease

The Crucial Roles of Bmi-1 in Cancer: Implications in Pathogenesis, Metastasis, Drug Resistance, and Targeted Therapies

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