Small molecule inhibitor of c-Myc 10058-F4 inhibits proliferation and induces apoptosis in acute leukemia cells, irrespective of PTEN status

Bashash, Davood; Sayyadi, Mohammad; Safaroghli‐Azar, Ava; Sheikh-Zeineddini, Negar; Riyahi, Niknam; Momeny, Majid

doi:10.1016/j.biocel.2019.01.005

Cited by 33 publications

(26 citation statements)

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“…Zirath et al (18) demonstrated that the compound 10058-F4, which is thought to disrupt the interaction between c-MYCN-Myc and MAX, impairs respiratory chain and FAO, resulting in apoptosis. A recent study showed in vitro that 10058-F4 is effective against acute promyelocytic leukemia and acute lymphoblastic leukemia with c-Myc overexpression (19).…”

Section: The Functional Inactivation Of the Mrn Complex Mediated By Mmentioning

confidence: 99%

Beyond the Warburg Effect: N-Myc Contributes to Metabolic Reprogramming in Cancer Cells

Yoshida

2020

Front. Oncol.

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Cancer cells generate large amounts of lactate derived from glucose regardless of the available oxygen level. Cancer cells finely control ATP synthesis by modulating the uptake of substrates and the activity of enzymes involved in aerobic glycolysis (Warburg effect), which enables them to adapt to the tumor microenvironment. However, increasing evidence suggests that mitochondrial metabolism, including the tricarboxylic acid (TCA) cycle, oxidative phosphorylation (OXPHOS), and glutaminolysis, is paradoxically activated in MYCN-amplified malignancies. Unlike non-amplified cells, MYCN-amplified cancer cells significantly promote OXPHOS-dependent ATP synthesis. Furthermore, tumor cells are differentially dependent on fatty acid β-oxidation (FAO) according to N-Myc status. Therefore, upregulation of FAO-associated enzymes is positively correlated with both N-Myc expression level and poor clinical outcome. This review explores therapeutic strategies targeting cancer stem-like cells for the treatment of tumors associated with MYCN amplification.

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Section: The Functional Inactivation Of the Mrn Complex Mediated By Mmentioning

confidence: 99%

Beyond the Warburg Effect: N-Myc Contributes to Metabolic Reprogramming in Cancer Cells

Yoshida

2020

Front. Oncol.

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“…In agreement, accumulating evidence also indicated that the high expression level of c-Myc in the neoplastic myeloid cells could be an important criterion for the development of the disease and the induction of drugresistance in AML patients (23,24). Notably, the results of other investigations showed that by inhibition of c-Myc in acute leukemia cells, not only the survival of the cells were significantly reduced (25,26), but also this suppres- sion resulted in the enhancement of the therapeutic value of chemotherapeutic drugs (26,27), which demonstrates the contributory role of c-Myc in the pathogenesis of AML.…”

Section: Discussionmentioning

confidence: 63%

Contribution Value of Akt, c-Myc, CIP2A, and PP2A Genes Expression in Leukemogenesis: A Bright Perspective on the Molecular Pattern of Patients with Acute Myeloid Leukemia (AML)

et al. 2020

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Background: The heterogeneous nature of acute myeloid leukemia (AML) and the hurdle to find a suitable treatment strategy for this malignancy put this type of leukemia at the top of the list of the priorities for finding a valuable biomarker to improve its treatment and predict the outcome of the patients. Objectives: Given the involvement of the variety of signaling pathways, foremost the PI3K axis in the pathogenesis of human cancers, we aimed to investigate the expression of the most important downstream targets of this pathway to propose a plausible mechanism underlying AML pathogenesis. Methods: In this case-control study, the blood samples from 30 patients diagnosed with AML were collected and after extracting their RNAs, the expression levels of Akt, c-Myc, CIP2A, and PP2A were evaluated using qRT-PCR analysis. For the control group, we also collected blood samples from 10 healthy volunteers. Afterward, by applying statistical analysis, we determined the probable correlation between the expressions of the aforementioned genes. Results: There was a significant elevation in the expression levels of Akt, c-Myc, and CIP2A coupled with the meaningful reduction in the expression level of PP2A in AML samples. However, we failed to find any significant association between the expression level of the indicated genes and age, sex, and the percentage of the blasts. Conclusions: As the most straightforward interpretation of our results, we propose that probably the association between PI3K and c-Myc which is built through the interaction between CIP2A and PP2A may play a pivotal role in the pathogenies of AML and any component of this axis could serve as a potential new target for more profound treatment strategy. However, further detailed investigations in this field are required to clarify the exact role of this interesting testis-specific pathway in the context of hematological malignancies, in particular AML.

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“…Apart from regulation of cell cycle progression, some reports showed that the expression of SIRT1 in cancer cells may lead to the induction of autophagy [31]. Playing as a double edged sword, induction of autophagy could either trigger cell death or induce a resistance phenotype, according to the cancer cell type [21,32,33]. In a study conducted by Helgason et al, it was reported that the activation of autophagy attenuate the efficacy of imatinib in K562 cells [34].…”

Section: Discussionmentioning

confidence: 99%

ZnO/CNT@Fe ₃ O ₄ induces ROS-mediated apoptosis in chronic myeloid leukemia (CML) cells: an emerging prospective for nanoparticles in leukemia treatment

Yousefi

Safaroghli‐Azar

Fakhroueian

et al. 2020

Artificial Cells, Nanomedicine, and Biotechnology

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Small molecule inhibitor of c-Myc 10058-F4 inhibits proliferation and induces apoptosis in acute leukemia cells, irrespective of PTEN status

Cited by 33 publications

References 35 publications

Beyond the Warburg Effect: N-Myc Contributes to Metabolic Reprogramming in Cancer Cells

Beyond the Warburg Effect: N-Myc Contributes to Metabolic Reprogramming in Cancer Cells

Contribution Value of Akt, c-Myc, CIP2A, and PP2A Genes Expression in Leukemogenesis: A Bright Perspective on the Molecular Pattern of Patients with Acute Myeloid Leukemia (AML)

ZnO/CNT@Fe ₃ O ₄ induces ROS-mediated apoptosis in chronic myeloid leukemia (CML) cells: an emerging prospective for nanoparticles in leukemia treatment

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Small molecule inhibitor of c-Myc 10058-F4 inhibits proliferation and induces apoptosis in acute leukemia cells, irrespective of PTEN status

Cited by 33 publications

References 35 publications

Beyond the Warburg Effect: N-Myc Contributes to Metabolic Reprogramming in Cancer Cells

Beyond the Warburg Effect: N-Myc Contributes to Metabolic Reprogramming in Cancer Cells

Contribution Value of Akt, c-Myc, CIP2A, and PP2A Genes Expression in Leukemogenesis: A Bright Perspective on the Molecular Pattern of Patients with Acute Myeloid Leukemia (AML)

ZnO/CNT@Fe 3 O 4 induces ROS-mediated apoptosis in chronic myeloid leukemia (CML) cells: an emerging prospective for nanoparticles in leukemia treatment

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ZnO/CNT@Fe ₃ O ₄ induces ROS-mediated apoptosis in chronic myeloid leukemia (CML) cells: an emerging prospective for nanoparticles in leukemia treatment