Autophagy-deficient mice are more susceptible to engrafted leukemogenesis

Ge, Chaorong; An, Ni; Li, Lei; Wen, Wei; Li, Ji; Yuan, Na; Fang, Yixuan; Xu, Li; Lin, Shiu‐Ru; Zhang, Jingyi; Song, Chenglin; Wang, Jianrong; Zhang, Suping

doi:10.1016/j.bcmd.2019.04.013

Cited by 3 publications

(2 citation statements)

References 38 publications

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“… 31 Deletion of Atg7, by conditional knockout in B-ALL xenograft mouse model, produces Atg7 deficient mice which are more susceptible to the occurrence of engrafted human leukemia cells. 32 Bone marrow cells of pediatric B-ALL patients display lower levels of expressing autophagy genes, like Beclin-1, Atg5, Atg7, LC3 and p62. When autophagy is activated by rapamycin, leukemia bone marrow cell cycle arrest is inhibited, and thereby improving the survival of ALL xenograft mice.…”

Section: Autophagy and B-cell Acute Lymphoblastic Leukemia (B-all)mentioning

confidence: 99%

Role of Autophagy and Apoptosis in Acute Lymphoblastic Leukemia

Huang

2021

Cancer Control

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Background: Acute lymphoblastic leukemia (ALL) is a malignant disease characterized by an excessive number of immature lymphocytes, including immature precursors of both B- and T cells. ALL affects children more often than adults. Immature lymphocytes lead to arrested differentiation and proliferation of cells. Its conventional treatments involve medication with dexamethasone, vincristine, and other anticancer drugs. Although the current first-line drugs can achieve effective treatment, they still cannot prevent the recurrence of some patients with ALL. Treatments have high risk of recurrence especially after the first remission. Currently, novel therapies to treat ALL are in need. Autophagy and apoptosis play important roles in regulating cancer development. Autophagy involves degradation of proteins and organelles, and apoptosis leads to cell death. These phenomena are crucial in cancer progression. Past studies reported that many potential anticancer agents regulate intracellular signaling pathways. Methods: The authors discuss the recent research findings on the role of autophagy and apoptosis in ALL. Results: The autophagy and apoptosis are widely used in the treatment of ALL. Most studies showed that many agents regulate autophagy and apoptosis in ALL cell models, clinical trials, and ALL animal models. Conclusions: In summary, activating autophagy and apoptosis pathways are the main strategies for ALL treatments. For ALL, combining new drugs with traditional chemotherapy and glucocorticoids treatments can achieve the greatest therapeutic effect by activating autophagy and apoptosis.

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Section: Autophagy and B-cell Acute Lymphoblastic Leukemia (B-all)mentioning

confidence: 99%

Role of Autophagy and Apoptosis in Acute Lymphoblastic Leukemia

Huang

2021

Cancer Control

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“…Moreover, Ge et al . [54] reported that autophagy regulation is an important step in engrafted leukemogenesis. In particular, CCND1 destabilization by lacking the binding capacity of hnRNP A1 to CCND1 mRNA might act as a central cause of our result that ΔRRM1‐expressing cell inoculation did not exhibit any tumour mass.…”

Section: Discussionmentioning

confidence: 99%

Serum/glucose starvation strikingly reduces heterogeneous nuclear ribonucleoprotein A1 protein and its target, cyclin D1

et al. 2023

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Our investigation to explore cellular alterations related to undernutrition in cancer cells revealed that the protein level of heterogenous nuclear ribonucleoprotein A1 (hnRNP A1) is drastically decreased by serum/glucose starvation. Its loss was reversible, serum/glucose starvation‐specific and universal throughout cell types and species. The hnRNP A1 mRNA level and hnRNP A1 mRNA/protein stability were not altered under this condition. CCND1 mRNA, which we newly identified as the binding target of hnRNP A1, was decreased by serum/glucose starvation. Under similar conditions, CCND1 protein was reduced in vitro and in vivo, whereas hnRNP A1 mRNA level and CCND1 mRNA level revealed no correlation in most clinical samples. Functional analyses revealed that CCND1 mRNA stability is certainly dependent on hnRNP A1 protein level and that RNA recognition motif‐1 (RRM1) in hnRNP A1 plays a central role in maintaining CCND1 mRNA stability and subsequent protein expression. The injection of RRM1‐deleted hnRNP A1‐expressing cancer cells in the mouse xenograft model did not form any tumours, and that of hnRNP A1‐expressing cancer cells retained CCND1 expression at the lesion adjacent to necrosis with a slight increase in tumour volume. Furthermore, RRM1 deletion caused growth suppression with the induction of apoptosis and autophagy, whereas CCND1 restoration completely recovered it. Our results indicate that serum/glucose starvation triggers entire hnRNP A1 protein loss, and its loss may play a role in CCND1 mRNA destabilization and CCND1‐mediated cellular event inhibition, i.e. growth promotion, apoptosis induction and autophagosome formation.

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Insights on E1-like enzyme ATG7: functional regulation and relationships with aging-related diseases

Liu,

Xiao,

Cao

et al. 2024

Commun Biol

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Autophagy is a dynamic self-renovation biological process that maintains cell homeostasis and is responsible for the quality control of proteins, organelles, and energy metabolism. The E1-like ubiquitin-activating enzyme autophagy-related gene 7 (ATG7) is a critical factor that initiates classic autophagy reactions by promoting the formation and extension of autophagosome membranes. Recent studies have identified the key functions of ATG7 in regulating the cell cycle, apoptosis, and metabolism associated with the occurrence and development of multiple diseases. This review summarizes how ATG7 is precisely programmed by genetic, transcriptional, and epigenetic modifications in cells and the relationship between ATG7 and aging-related diseases.

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Autophagy-deficient mice are more susceptible to engrafted leukemogenesis

Cited by 3 publications

References 38 publications

Role of Autophagy and Apoptosis in Acute Lymphoblastic Leukemia

Role of Autophagy and Apoptosis in Acute Lymphoblastic Leukemia

Serum/glucose starvation strikingly reduces heterogeneous nuclear ribonucleoprotein A1 protein and its target, cyclin D1

Insights on E1-like enzyme ATG7: functional regulation and relationships with aging-related diseases

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