Leukemia Stem Cells in Chronic Myeloid Leukemia

Shan, Yi; DeSouza, Ngoc; Qiu, Qiang; Li, Shaoguang

doi:10.1007/978-981-13-7342-8_9

Cited by 7 publications

(6 citation statements)

References 95 publications

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“…Clinically, the targeting and elimination of LSCs are essential for CML elimination. 4 , 5 Strikingly, we found that high Tspan32 expression also suppressed LSC proliferation and impaired their function (Fig. 4 ), which suggested that targeting Tspan32 network might offer a potential strategy for LSC elimination.…”

Section: Discussionmentioning

confidence: 79%

“… 2 BCR-ABL activates multiple signaling pathways upon activation of its kinase activity, including PI3K-AKT, JAK/STAT, RAS/RAF/MEK/ERK, MYC and WNT/CTNNB1. 3 Some genes, such as Alox5 , Alox15 , Scd1 , and Blk , 4 , 5 are essential for CML stem cells (LSC) survival and are activated by BCR-ABL independent of its kinase activity. Clinically, BCR-ABL tyrosine kinase inhibitors (TKIs) have achieved great treatment outcomes for Ph + leukemias.…”

Section: Introductionmentioning

confidence: 99%

“… 4 Therefore, the complete elimination of LSCs could provide a more optimal curative therapy for CML. 4 , 5 There is still a need to develop new therapeutic strategies (and identify potential targets) to effectively restrain LSCs or overcome TKIs resistance.…”

Section: Introductionmentioning

confidence: 99%

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TSPAN32 suppresses chronic myeloid leukemia pathogenesis and progression by stabilizing PTEN

Qiu

Sun

Yang

et al. 2023

Sig Transduct Target Ther

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We report herein that TSPAN32 is a key node factor for Philadelphia (Ph+) leukemia pathogenesis. We found that TSPAN32 expression was repressed by BCR-ABL and ectopic TSPAN32 expression upon Imatinib treatment inhibited the proliferation of Ph+ cell lines. Tspan32 overexpression significantly prevented BCR-ABL induced leukemia progression in a murine model and impaired leukemia stem cell (LSC) proliferation. LSCs represent an obstacle for chronic myeloid leukemia (CML) elimination, which continually replenish leukemia cells and are associated with disease relapse. Therefore, the identification of essential targets that contribute to the survival and self-renewal of LSCs is important for novel curative CML. Mechanistically, TSPAN32 was shown to interact with PTEN, increased its protein level and caused a reduction in PI3K-AKT signaling activity. We also found that TSPAN32 was repressed by BCR-ABL via the suppression of an important transcription factor, TAL1. Ectopic expression of TAL1 significantly increased TSPAN32 mRNA and protein level, which indicated that BCR-ABL repressed TSPAN32 transcription by decreasing TAL1 expression. Overall, we identified a new signaling axis composed of “BCR-ABL-TAL1-TSPAN32-PTEN-PI3K-AKT”. Our findings further complement the known mechanisms underlying the transformation potential of BCR-ABL in CML pathogenesis. This new signaling axis also provides a potential means to target PI3K-AKT for CML treatment.

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Section: Discussionmentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

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TSPAN32 suppresses chronic myeloid leukemia pathogenesis and progression by stabilizing PTEN

Qiu

Sun

Yang

et al. 2023

Sig Transduct Target Ther

Self Cite

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“…Disorders of differentiation and maturation are considered to be common features of leukemia cells [ 24 ]. Inhibiting abnormal proliferation and promoting normal differentiation of leukemia cells may be novel therapeutic strategies for various hematological malignancies [ 25 ]. ASP, as a common secondary metabolite of iridoid glycosides, has a wide range of pharmacological effects [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

Asperuloside regulates the proliferation, apoptosis, and differentiation of chronic myeloid leukemia cell line K562 through the RAS/MEK/ERK pathway

Zhao,

Che,

et al. 2024

Heliyon

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“…This has been considered the molecular basis for the development of CML. 2 , 3 The natural course of CML consists of three phases: chronic phase (CP), accelerated phase (AP), and blast crisis (BC). Patients with CML which has progressed to BP have an extremely poor prognosis.…”

Section: Introductionmentioning

confidence: 99%

The m6A regulator KIAA1429 stabilizes RAB27B mRNA and promotes the progression of chronic myeloid leukemia and resistance to targeted therapy

Yao¹,

Zhong²,

Jiang³

et al. 2024

Genes & Diseases

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Leukemia Stem Cells in Chronic Myeloid Leukemia

Cited by 7 publications

References 95 publications

TSPAN32 suppresses chronic myeloid leukemia pathogenesis and progression by stabilizing PTEN

TSPAN32 suppresses chronic myeloid leukemia pathogenesis and progression by stabilizing PTEN

Asperuloside regulates the proliferation, apoptosis, and differentiation of chronic myeloid leukemia cell line K562 through the RAS/MEK/ERK pathway

The m6A regulator KIAA1429 stabilizes RAB27B mRNA and promotes the progression of chronic myeloid leukemia and resistance to targeted therapy

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