ALBERT — All Library Books, journals and Electronic Records Telegrafenberg

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Gastric organoids—an in vitro model system for the study of gastric development and road to personalized medicine (2020)

Seidlitz, Therese ; Koo, Bon-Kyoung ; Stange, Daniel E.

Springer Nature

In: Cell Death and Differentiation. 2020; 28(1): 68-83. Published 2020 Nov 22. doi: 10.1038/s41418-020-00662-2.

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Publication Date: 2020-11-22

Description: Gastric cancer ranks as the fifth most common human malignancy and the third leading cause of cancer related deaths. Depending on tumor stage, endoscopic or surgical resection supported by perioperative chemotherapy is the only curative option for patients. Due to late clinical manifestation and missing reliable biomarkers, early detection is challenging and overall survival remains poor. Organoids are cell aggregates cultured in three-dimensions that grow with similar characteristics as their tissue-of-origin. Due to their self-renewal and proliferative capacity, organoids can be maintained long term in culture and expanded in many cases in an unlimited fashion. Patient-derived organoid (PDO) libraries function as living biobanks, allowing the in depth analysis of tissue specific function, development and disease. The recent successful establishment of gastric cancer PDOs opens up new perspectives for multiple translational clinical applications. Here, we review different adult stem cell derived gastric organoid model systems and focus on their establishment, phenotypic and genotypic characterizations as well as their use in predicting therapy response.

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Electronic ISSN: 1476-5403

Topics: Biology , Medicine

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Neuronal cell life, death, and axonal degeneration as regulated by the BCL-2 family proteins (2020)

Pemberton, James M. ; Pogmore, Justin P. ; Andrews, David W.

Springer Nature

In: Cell Death and Differentiation. 2020; 28(1): 108-122. Published 2020 Nov 08. doi: 10.1038/s41418-020-00654-2.

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Publication Date: 2020-11-08

Description: Axonal degeneration and neuronal cell death are fundamental processes in development and contribute to the pathology of neurological disease in adults. Both processes are regulated by BCL-2 family proteins which orchestrate the permeabilization of the mitochondrial outer membrane (MOM). MOM permeabilization (MOMP) results in the activation of pro-apoptotic molecules that commit neurons to either die or degenerate. With the success of small-molecule inhibitors targeting anti-apoptotic BCL-2 proteins for the treatment of lymphoma, we can now envision the use of inhibitors of apoptosis with exquisite selectivity for BCL-2 family protein regulation of neuronal apoptosis in the treatment of nervous system disease. Critical to this development is deciphering which subset of proteins is required for neuronal apoptosis and axon degeneration, and how these two different outcomes are separately regulated. Moreover, noncanonical BCL-2 family protein functions unrelated to the regulation of MOMP, including impacting necroptosis and other modes of cell death may reveal additional potential targets and/or confounders. This review highlights our current understanding of BCL-2 family mediated neuronal cell death and axon degeneration, while identifying future research questions to be resolved to enable regulating neuronal survival pharmacologically.

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CircRNA-vgll3 promotes osteogenic differentiation of adipose-derived mesenchymal stem cells via modulating miRNA-dependent integrin α5 expression (2020)

Zhang, Dandan ; Ni, Ni ; Wang, Yuyao ; [et al.]

Springer Nature

In: Cell Death and Differentiation. 2020; 28(1): 283-302. Published 2020 Aug 19. doi: 10.1038/s41418-020-0600-6.

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Publication Date: 2020-08-19

Description: Adipose-derived mesenchymal stem cells (ADSCs) are promising candidate for regenerative medicine to repair non-healing bone defects due to their high and easy availability. However, the limited osteogenic differentiation potential greatly hinders the clinical application of ADSCs in bone repair. Accumulating evidences demonstrate that circular RNAs (circRNAs) are involved in stem/progenitor cell fate determination, but their specific role in stem/progenitor cell osteogenesis, remains mostly undescribed. Here, we show that circRNA-vgll3 originating from the vgll3 locus markedly enhances osteogenic differentiation of ADSCs; nevertheless, silencing of circRNA-vgll3 dramatically attenuates ADSC osteogenesis. Furthermore, we validate that circRNA-vgll3 functions in ADSC osteogenesis through a circRNA-vgll3/miR-326-5p/integrin α5 (Itga5) pathway. Itga5 promotes ADSC osteogenic differentiation and miR-326-5p suppresses Itga5 translation. CircRNA-vgll3 directly sequesters miR-326-5p in the cytoplasm and inhibits its activity to promote osteogenic differentiation. Moreover, the therapeutic potential of circRNA-vgll3-modified ADSCs with calcium phosphate cement (CPC) scaffolds was systematically evaluated in a critical-sized defect model in rats. Our results demonstrate that circRNA-vgll3 markedly enhances new bone formation with upregulated bone mineral density, bone volume/tissue volume, trabeculae number, and increased new bone generation. This study reveals the important role of circRNA-vgll3 during new bone biogenesis. Thus, circRNA-vgll3 engineered ADSCs may be effective potential therapeutic targets for bone regenerative medicine.

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Topics: Biology , Medicine

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Urolithin A suppresses high glucose-induced neuronal amyloidogenesis by modulating TGM2-dependent ER-mitochondria contacts and calcium homeostasis (2020)

Lee, Hyun Jik ; Jung, Young Hyun ; Choi, Gee Euhn ; [et al.]

Springer Nature

In: Cell Death and Differentiation. 2020; 28(1): 184-202. Published 2020 Jul 23. doi: 10.1038/s41418-020-0593-1.

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Publication Date: 2020-07-23

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Nuclear miR-30b-5p suppresses TFEB-mediated lysosomal biogenesis and autophagy (2020)

Guo, Huijie ; Pu, Mei ; Tai, Yusi ; [et al.]

Springer Nature

In: Cell Death and Differentiation. 2020; 28(1): 320-336. Published 2020 Aug 06. doi: 10.1038/s41418-020-0602-4.

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Publication Date: 2020-08-06

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Deubiquitinase USP35 restrains STING-mediated interferon signaling in ovarian cancer (2020)

Zhang, Jiawen ; Chen, Yunfei ; Chen, Xianfei ; [et al.]

Springer Nature

In: Cell Death and Differentiation. 2020; 28(1): 139-155. Published 2020 Jul 16. doi: 10.1038/s41418-020-0588-y.

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Publication Date: 2020-07-16

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Brain organoids: an ensemble of bioassays to investigate human neurodevelopment and disease (2020)

Sidhaye, Jaydeep ; Knoblich, Jürgen A.

Springer Nature

In: Cell Death and Differentiation. 2020; 28(1): 52-67. Published 2020 Jun 01. doi: 10.1038/s41418-020-0566-4.

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Publication Date: 2020-06-01

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Trends and challenges in modeling glioma using 3D human brain organoids (2020)

Mariappan, Aruljothi ; Goranci-Buzhala, Gladiola ; Ricci-Vitiani, Lucia ; [et al.]

Springer Nature

In: Cell Death and Differentiation. 2020; 28(1): 15-23. Published 2020 Dec 01. doi: 10.1038/s41418-020-00679-7.

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Publication Date: 2020-12-01

Description: The human brain organoids derived from pluripotent cells are a new class of three-dimensional tissue systems that recapitulates several neural epithelial aspects. Brain organoids have already helped efficient modeling of crucial elements of brain development and disorders. Brain organoids’ suitability in modeling glioma has started to emerge, offering another usefulness of brain organoids in disease modeling. Although the current state-of-the organoids mostly reflect the immature state of the brain, with their vast cell diversity, human brain-like cytoarchitecture, feasibility in culturing, handling, imaging, and tractability can offer enormous potential in reflecting the glioma invasion, integration, and interaction with different neuronal cell types. Here, we summarize the current trend of employing brain organoids in glioma modeling and discuss the immediate challenges. Solving them might lay a foundation for using brain organoids as a pre-clinical 3D substrate to dissect the glioma invasion mechanisms in detail.

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RPS23RG1 modulates tau phosphorylation and axon outgrowth through regulating p35 proteasomal degradation (2020)

Zhao, Dongdong ; Zhou, Yunqiang ; Huo, Yuanhui ; [et al.]

Springer Nature

In: Cell Death and Differentiation. 2020; 28(1): 337-348. Published 2020 Sep 09. doi: 10.1038/s41418-020-00620-y.

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Publication Date: 2020-09-09

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Phosphorylation by Aurora B kinase regulates caspase-2 activity and function (2020)

Lim, Yoon ; De Bellis, Dylan ; Sandow, Jarrod J. ; [et al.]

Springer Nature

In: Cell Death and Differentiation. 2020; 28(1): 349-366. Published 2020 Aug 18. doi: 10.1038/s41418-020-00604-y.

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Publication Date: 2020-08-18

Description: Mitotic catastrophe (MC) is an important oncosuppressive mechanism that serves to eliminate cells that become polyploid or aneuploid due to aberrant mitosis. Previous studies have demonstrated that the activation and catalytic function of caspase-2 are key steps in MC to trigger apoptosis and/or cell cycle arrest of mitotically defective cells. However, the molecular mechanisms that regulate caspase-2 activation and its function are unclear. Here, we identify six new phosphorylation sites in caspase-2 and show that a key mitotic kinase, Aurora B kinase (AURKB), phosphorylates caspase-2 at the highly conserved residue S384. We demonstrate that phosphorylation at S384 blocks caspase-2 catalytic activity and apoptosis function in response to mitotic insults, without affecting caspase-2 dimerisation. Moreover, molecular modelling suggests that phosphorylation at S384 may affect substrate binding by caspase-2. We propose that caspase-2 S384 phosphorylation by AURKB is a key mechanism that controls caspase-2 activation during mitosis.

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