Phosphorylation of BECLIN-1 by BCR-ABL suppresses autophagy in chronic myeloid leukemia

Yu, Chunxia; Gorantla, Sivahari Prasad; Müller-Rudorf, Alina; Müller, Tony Andreas; Kreutmair, Stefanie; Albers, Corinna; Jakob, Lena; Lippert, Lena J; Yue, Zhenyu; Engelhardt, Monika; Follo, Marie; Zeiser, Robert; Huber, Tobias B.; Duyster, Justus; Illert, Anna Lena

doi:10.3324/haematol.2018.212027

Cited by 24 publications

(21 citation statements)

References 62 publications

(44 reference statements)

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“…The BCR-ABL fusion protein activity is deregulated and promotes the activation of oncogenic downstream pathways, leading to cell growth and proliferation and to the inhibition of apoptosis [76]. A recent report showed that BCR-ABL binds to Beclin 1 and phosphorylates it at Y233 and Y352, leading to its inactivation and autophagy inhibition [77]. Mice transplanted with bone marrow derived cells (BMDCs) depleted of Beclin 1 through a miR sequence showed an increased survival compared to the mice transplanted with the BMDCs expressing a miR control.…”

Section: Bcr-ablmentioning

confidence: 99%

The Role of Beclin 1-Dependent Autophagy in Cancer

Vega-Rubín-de-Celis

2019

Biology

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Autophagy (self-eating) is an intracellular degradation process used by cells to keep a "clean house"; as it degrades abnormal or damaged proteins and organelles, it helps to fight infections and also provides energy in times of fasting or exercising. Autophagy also plays a role in cancer, although its precise function in each cancer type is still obscure, and whether autophagy plays a protecting (through the clearing of damaged organelles and protein aggregates and preventing DNA damage) or a promoting (by fueling the already stablished tumor) role in cancer remains to be fully characterized. Beclin 1, the mammalian ortholog of yeast Atg6/Vps30, is an essential autophagy protein and has been shown to play a role in tumor suppression. Here, an update of the tumorigenesis regulation by Beclin 1-dependent autophagy is provided.

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Section: Bcr-ablmentioning

confidence: 99%

The Role of Beclin 1-Dependent Autophagy in Cancer

Vega-Rubín-de-Celis

2019

Biology

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“…Phoenix E helper virus-free ecotropic packaging cells (G. Nolan, Stanford University, Stanford, California, USA) and HeLa cells (ATCC) were maintained in DMEM supplemented with 10% FCS. The mouse pro-B cell line Ba/F3 (DSMZ) and the BMderived cell line 32D were cultured in RPMI 1640 (Life Technologies) supplemented with 10% FCS, 2 ng/mL IL-3, and penicillin/streptomycin (65). HPC7 cells (RRID:CVCL_RB19) were cultured in IMDM (Gibco) supplemented with 10% FCS, 200 mM l-glutamine, 1-thyioglycerol, stem cell factor, and penicillin/streptomycin.…”

Section: Methodsmentioning

confidence: 99%

Loss of the Fanconi anemia–associated protein NIPA causes bone marrow failure

Kreutmair

Erlacher

Andrieux

et al. 2020

Journal of Clinical Investigation

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“…Some reports implicated autophagy as a potential target in Ph+ leukemias [81][82][83][84][85][86][87], and a recent paper highlighted the role of Beclin 1 phosphorylation in autophagy regulation by BCR-ABL [88]. In vitro experiments of Beclin 1 depletion through miRNA in Ba/F3 cells indicated a role of Beclin 1 in cell proliferation and apoptosis, and in vivo transplantation analysis showed a prolonged survival on Beclin 1 knock-down BCR-ABL+ BMDC compared to control samples [88]. Interestingly, these effects might be autophagy-independent, since similar experiments depleting another autophagy essential gene, Atg5, had no effect on survival.…”

Section: Bcr-ablmentioning

confidence: 99%

Regulation of Beclin 1-Mediated Autophagy by Oncogenic Tyrosine Kinases

Vega-Rubín-de-Celis

Kinch

Peña-Llopis

2020

IJMS

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Beclin 1 is a major regulator of autophagy, and it is a core component of the class III PI3K complexes. Beclin 1 is a highly conserved protein and its function is regulated in a number of ways, including post-translational modifications. Several studies indicate that receptor and non-receptor tyrosine kinases regulate autophagy activity in cancer, and some suggest the importance of Beclin 1 tyrosine phosphorylation in this process. Here we summarize the current knowledge of the mechanism whereby some oncogenic tyrosine kinases regulate autophagy through Beclin 1.

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Phosphorylation of BECLIN-1 by BCR-ABL suppresses autophagy in chronic myeloid leukemia

Cited by 24 publications

References 62 publications

The Role of Beclin 1-Dependent Autophagy in Cancer

The Role of Beclin 1-Dependent Autophagy in Cancer

Loss of the Fanconi anemia–associated protein NIPA causes bone marrow failure

Regulation of Beclin 1-Mediated Autophagy by Oncogenic Tyrosine Kinases

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