TNFRSF19 promotes endoplasmic reticulum stress-induced paraptosis via the activation of the MAPK pathway in triple-negative breast cancer cells

Liu, Shiyang; Tian, Yao; Liu, Chenguang; Gui, Zhengwei; Yu, Tianyao; Zhang, Lin

doi:10.1038/s41417-023-00696-x

Cited by 3 publications

(1 citation statement)

References 36 publications

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“…Indeed, the MAPK activator elaiophylin induces paraptosis in ovarian cancer cells, and gene expression analysis showed that elaiophylin activates the ER-stress pathway, suggesting that ER-stress pathway activation is crucial for the execution of paraptosis (105). A member of TNF receptor superfamily, TNFRSF19, promotes ERstress via MAPK pathway activation and induces paraptosis in triple negative breast cancer cells (106). A recent study demonstrated that the deletion of the pancreatic ER kinase (PKR)-like ER kinase (PERK) in cancer cells induces paraptosis (107).…”

Section: Paraptosismentioning

confidence: 99%

Emerging role of immunogenic cell death in cancer immunotherapy

Arimoto,

Miyauchi,

Liu

et al. 2024

Front. Immunol.

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Cancer immunotherapy, such as immune checkpoint blockade (ICB), has emerged as a groundbreaking approach for effective cancer treatment. Despite its considerable potential, clinical studies have indicated that the current response rate to cancer immunotherapy is suboptimal, primarily attributed to low immunogenicity in certain types of malignant tumors. Immunogenic cell death (ICD) represents a form of regulated cell death (RCD) capable of enhancing tumor immunogenicity and activating tumor-specific innate and adaptive immune responses in immunocompetent hosts. Therefore, gaining a deeper understanding of ICD and its evolution is crucial for developing more effective cancer therapeutic strategies. This review focuses exclusively on both historical and recent discoveries related to ICD modes and their mechanistic insights, particularly within the context of cancer immunotherapy. Our recent findings are also highlighted, revealing a mode of ICD induction facilitated by atypical interferon (IFN)-stimulated genes (ISGs), including polo-like kinase 2 (PLK2), during hyperactive type I IFN signaling. The review concludes by discussing the therapeutic potential of ICD, with special attention to its relevance in both preclinical and clinical settings within the field of cancer immunotherapy.

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Section: Paraptosismentioning

confidence: 99%

Emerging role of immunogenic cell death in cancer immunotherapy

Arimoto,

Miyauchi,

Liu

et al. 2024

Front. Immunol.

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Paraptosome: A Novel Pathological Feature in Paraptotic Cell Death

Cui,

Zheng,

et al. 2024

Preprint

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Paraptosis is a novel form of programmed cell death characterized by distinct morphological features such as swelling of the endoplasmic reticulum and mitochondria, and cytoplasmic vacuolation. Unlike apoptosis, paraptosis does not involve the activation of caspases or DNA fragmentation. These unique features make paraptosis an intriguing target for cancer therapy, particularly against apoptosis-resistant cells. Here, we report a novel morphological feature of paraptosis: the formation of high-density spherical structure, which we tentatively term “paraptosome.” We found that these putative paraptosomes originate from the Golgi apparatus, appearing as high-density formations under light microscopy and colocalizing with the trans-Golgi marker β4GALT1-RFP. Time-lapse confocal microscopy and immunostaining demonstrated that putative paraptosomes form due to Golgi stress or disintegration, leading to severe disruption of Golgi function. Furthermore, we show that paraptosis inducers such as glabridin, morusin, and honokiol can cause significant alterations in the endoplasmic reticulum, mitochondria, autophagosomes, and lysosomes in U251MG glioblastoma cells; however, the formation of putative paraptosomes is not induced by isolated stress inducers. Collectively, these findings suggest that the putative paraptosome may be a novel characteristic structure of paraptosis. The discovery of paraptosomes provides a unique marker for defining paraptotic cell death and offers new insights into the characteristic pathological phenomena associated with multiple organelle dysfunction. This finding broadens the scope of cell biology research by introducing a new structural paradigm linked to paraptosis and may have implications for developing targeted therapies against apoptosis-resistant cancers.

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Paraptosis and Other Types of Non-Apoptotic Regulated Cell Death

Solovieva,

Shatalin,

Akatov

2024

Biofizika

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The review is devoted to modern ideas about paraptosis, as one of the types of regulated cell death, in comparison with other types of cell death. Paraptosis is a form of cell death caused by endoplasmic reticulum stress, accompanied by an accumulation of damaged or misfolded proteins, extensive non-autophagic vacuolation of cisterns of endoplasmic reticulum and, in some cases, mitochondria, with subsequent damage to mitochondria, the cytoskeleton, and cell death. The knowledge regarding the molecular mechanisms of paraptosis is of interest for the treatment of cancers resistant to apoptosis-inducing agents.

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TNFRSF19 promotes endoplasmic reticulum stress-induced paraptosis via the activation of the MAPK pathway in triple-negative breast cancer cells

Cited by 3 publications

References 36 publications

Emerging role of immunogenic cell death in cancer immunotherapy

Emerging role of immunogenic cell death in cancer immunotherapy

Paraptosome: A Novel Pathological Feature in Paraptotic Cell Death

Paraptosis and Other Types of Non-Apoptotic Regulated Cell Death

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