scholarly journals Lack of GAGA protein in Trl mutants causes massive cell death in Drosophila spermatogenesis and oogenesis

2021 ◽  
Vol 25 (3) ◽  
pp. 292-300
Author(s):  
N. V. Dorogova ◽  
A. E. Zubkova ◽  
E. V. Fedorova ◽  
E. U. Bolobolova ◽  
E. M. Baricheva
Keyword(s):  
Cell Death ◽  
Germ Cell ◽  
Target Genes ◽  
Germ Line ◽  
Gaga Factor ◽  
Cellular Functions ◽  
Massive Cell Death ◽  
Egg Chambers ◽  
Drosophila Protein ◽  
Massive Cell

Drosophila protein GAGA (GAF) is a factor of epigenetic transcription regulation of a large group of genes with a wide variety of cellular functions. GAF is encoded by the Trithorax-like (Trl) gene, which is important for the formation of various organs and tissues at all stages of ontogenesis. In our previous works, we showed that this protein is necessary for the development of the reproductive system, both in males and females of Drosophila. Decreased expression of the Trl gene led to multiple disorders of spermatogenesis and oogenesis. One of the significant disorders was associated with massive degradation and loss of cells in the germline. In this work, we carried out a more detailed cytological study to determine what type of germ cell death is characteristic of Trl mutants, and whether there are disturbances or changes in this process compared to the norm. The results obtained showed that the lack of GAF protein causes massive germ cell death in both females and males of Drosophila, but this death manifests itself in different ways, depending on the sex. In Trl females, this process does not differ phenotypically from the norm. In the dying egg chambers, signs of apoptosis and autophagy were revealed, as well as morphological features that are characteristic of the wild type. In males, Trl mutations induce mass germ cell death through autophagy, which is not typical of Drosophila spermatogenesis, and has not been previously described, neither in the norm nor in other genes’ mutations. Thus, GAF lack in Trl mutants leads to increased germ cell death through apoptosis and autophagy. Ectopic cell death and germ line atrophy are probably associated with impaired expression of the GAGA factor target genes, among which there are genes that regulate both apoptosis and autophagy.

scholarly journals Loss of Drosophila E3 Ubiquitin Ligase Hyd Promotes Extra Mitosis in Germline Cysts and Massive Cell Death During Oogenesis

2020 ◽  
Vol 8 ◽  
Author(s):  
Natalia V. Dorogova ◽  
Yuliya A. Galimova ◽  
Elena Us. Bolobolova ◽  
Elina M. Baricheva ◽  
Svetlana A. Fedorova
Keyword(s):  
Cell Death ◽  
Ubiquitin Ligase ◽  
E3 Ubiquitin Ligase ◽  
Massive Cell Death ◽  
Massive Cell

55Reintroduction of bladder cancer-downregulated miR-145 results in massive cell death of bladder cancer cell lines

Apmis ◽  
2008 ◽  
Vol 116 (5) ◽  
pp. 417-417
Author(s):  
Marie S. Ostenfeld ◽  
Jesper B. Bramsen ◽  
Jørgen Kjems ◽  
Torben Ørntoft ◽  
Lars Dyrskjøt
Keyword(s):  
Bladder Cancer ◽  
Cell Death ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Bladder Cancer Cell ◽  
Massive Cell Death ◽  
Massive Cell

scholarly journals Methylene blue photodynamic therapy induces selective and massive cell death in human breast cancer cells

BMC Cancer ◽  
2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Ancély F. dos Santos ◽  
Letícia F. Terra ◽  
Rosangela A. M. Wailemann ◽  
Talita C. Oliveira ◽  
Vinícius de Morais Gomes ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Methylene Blue ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Massive Cell Death ◽  
Massive Cell

Oestrogens as apoptosis regulators in mammalian testis: angels or devils?

2015 ◽  
Vol 17 ◽  
Author(s):  
Sara Correia ◽  
Henrique J. Cardoso ◽  
José E. Cavaco ◽  
Sílvia Socorro
Keyword(s):  
Cell Death ◽  
Germ Cell ◽  
Cell Survival ◽  
Cell Fate ◽  
Germ Line ◽  
Clinical Findings ◽  
Molecular Events ◽  
Mammalian Testis ◽  
Induced Apoptosis ◽  
Available Information

In the mammalian testis, spermatogenesis is a highly coordinated process of germ cell development, which ends with the release of ‘mature’ spermatozoa. The fine regulation of spermatogenesis is strictly dependent on sex steroid hormones, which orchestrate the cellular and molecular events underlying normal development of germ cells. Sex steroids actions also rely on the control of germ cell survival, and the programmed cell death by apoptosis has been indicated as a critical process in regulating the size and quality of the germ line. Recently, oestrogens have emerged as important regulators of germ cell fate. However, the beneficial or detrimental effects of oestrogens in spermatogenesis are controversial, with independent reports arguing for their role as cell survival factors or as apoptosis-inducers. The dual behaviour of oestrogens, shifting from ‘angels to devils’ is supported by the clinical findings of increased oestrogens levels in serum and intratesticular milieu of idiopathic infertile men. This review aims to discuss the available information concerning the role of oestrogens in the control of germ cell death and summarises the signalling mechanisms driven oestrogen-induced apoptosis. The present data represent a valuable basis for the clinical management of hyperoestrogenism-related infertility and provide a rationale for the use of oestrogen-target therapies in male infertility.

55 Reintroduction of bladder cancer-downregulated miR-145 results in massive cell death of bladder cancer cell lines

Apmis ◽  
2008 ◽  
Vol 116 (5) ◽  
pp. 417-417
Author(s):  
Marie S. Ostenfeld ◽  
Jesper B. Bramsen ◽  
Jørgen Kjems ◽  
Torben Ørntoft ◽  
Lars Dyrskjøt
Keyword(s):  
Bladder Cancer ◽  
Cell Death ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Bladder Cancer Cell ◽  
Massive Cell Death ◽  
Massive Cell

scholarly journals Dexamethasone Treatment Limits Efficacy of Radiation, but Does Not Interfere With Glioma Cell Death Induced by Tumor Treating Fields

2021 ◽  
Vol 11 ◽  
Author(s):  
Benedikt Linder ◽  
Abigail Schiesl ◽  
Martin Voss ◽  
Franz Rödel ◽  
Stephanie Hehlgans ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Clinical Analysis ◽  
Concomitant Treatment ◽  
Tumor Treating Fields ◽  
Cell Counts ◽  
Anti Cancer ◽  
Massive Cell Death ◽  
Human Gbm ◽  
Massive Cell

PurposeDexamethasone (Dex) is the most common corticosteroid to treat edema in glioblastoma (GBM) patients. Recent studies identified the addition of Dex to radiation therapy (RT) to be associated with poor survival. Independently, Tumor Treating Fields (TTFields) provides a novel anti-cancer modality for patients with primary and recurrent GBM. Whether Dex influences the efficacy of TTFields, however, remains elusive.MethodsHuman GBM cell lines MZ54 and U251 were treated with RT or TTFields in combination with Dex and the effects on cell counts and cell death were determined via flow cytometry. We further performed a retrospective analysis of GBM patients with TTFields treatment +/- concomitant Dex and analysed its impact on progression-free (PFS) and overall survival (OS).ResultsThe addition of Dex significantly reduced the efficacy of RT in U251, but not in MZ54 cells. TTFields (200 kHz/250 kHz) induced massive cell death in both cell lines. Concomitant treatment of TTFields and Dex did not reduce the overall efficacy of TTFields. Further, in our retrospective clinical analysis, we found that the addition of Dex to TTFields therapy did not influence PFS nor OS.ConclusionOur translational investigation indicates that the efficacy of TTFields therapy in patients with GBM and GBM cell lines is not affected by the addition of Dex.

scholarly journals Theranostic Role of 32P-ATP as Radiopharmaceutical for the Induction of Massive Cell Death within Avascular Tumor Core

Theranostics ◽  
2017 ◽  
Vol 7 (18) ◽  
pp. 4399-4409 ◽  
Author(s):  
Mirco Galiè ◽  
Federico Boschi ◽  
Ilaria Scambi ◽  
Flavia Merigo ◽  
Pasquina Marzola ◽  
...  
Keyword(s):  
Cell Death ◽  
Massive Cell Death ◽  
Massive Cell ◽  
Avascular Tumor

scholarly journals Regression of apoptosis-resistant colorectal tumors by induction of necroptosis in mice

2017 ◽  
Vol 214 (6) ◽  
pp. 1655-1662 ◽  
Author(s):  
Gui-Wei He ◽  
Claudia Günther ◽  
Veronika Thonn ◽  
Yu-Qiang Yu ◽  
Eva Martini ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Death ◽  
Death Receptor ◽  
Caspase 8 ◽  
Colorectal Tumors ◽  
Interacting Protein ◽  
Massive Cell Death ◽  
Smac Mimetic ◽  
Chemotherapeutic Treatment ◽  
Massive Cell

Cancer cells often acquire capabilities to evade cell death induced by current chemotherapeutic treatment approaches. Caspase-8, a central initiator of death receptor–mediated apoptosis, for example, is frequently inactivated in human cancers via multiple mechanisms such as mutation. Here, we show an approach to overcome cell death resistance in caspase-8–deficient colorectal cancer (CRC) by induction of necroptosis. In both a hereditary and a xenograft mouse model of caspase-8–deficient CRC, second mitochondria-derived activator of caspase (SMAC) mimetic treatment induced massive cell death and led to regression of tumors. We further demonstrate that receptor-interacting protein kinase 3 (RIP3), which is highly expressed in mouse models of CRC and in a subset of human CRC cell lines, is the deciding factor of cancer cell susceptibility to SMAC mimetic–induced necroptosis. Thus, our data implicate that it may be worthwhile to selectively evaluate the efficacy of SMAC mimetic treatment in CRC patients with caspase-8 deficiency in clinical trials for the development of more effective personalized therapy.

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