Nucleostemin silencing induces differentiation and potentiates all- trans -retinoic acid effects in human acute promyelocytic leukemia NB4 cells via autophagy

Fakhimahmadi, Aila; Nazmi, Farinaz; Rahmati, Mohammad; Bonab, Nazila Moghtaran; Hashemi, Mehrdad; Moosavi, Mohammad Amin

doi:10.1016/j.leukres.2017.10.007

Cited by 10 publications

(13 citation statements)

References 52 publications

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“…Cells were stained using 0.5‐μg/ml AO for 15 min in the dark, washed, and resuspended in PBS. The red (PE‐Cy5) and green (FITC) fluorescence emissions from 10 4 cells illuminated with blue (488 nm) excitation light were measured with through LSRII flow cytometry and analyzed with FlowJo (version 10; Fakhimahmadi et al, ; Kanzawa, Kondo, Ito, Kondo, & Germano, ; Wu et al, ).…”

Section: Methodsmentioning

confidence: 99%

Curcumin and tetrahydrocurcumin induce cell death in Ara‐C‐resistant acute myeloid leukemia

Tseng

Chiou

Weng

et al. 2019

Phytotherapy Research

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Most anticancer agents induce cancer cell death; however, multidrug-resistant cancers often lead to treatment failure. The effective use of curcumin as an anticancer agent has been demonstrated in clinical trials. Tetrahydrocurcumin, a major curcumin metabolite, exhibits pharmacological activities similar to those of curcumin. Curcumin induces cell death mainly through the apoptosis pathway, and tetrahydrocurcumin induces cell death mainly via an autophagy pathway in HL60 cells. Here, we investigated whether curcumin and tetrahydrocurcumin can induce apoptosis-and autophagy-mediated cell deaths in Ara-C-resistant cancer cells, respectively. The results demonstrated that curcumin and tetrahydrocurcumin induced cell death by apoptosis and autophagy, respectively, in Ara-C-resistant HL60 cells. Thus, curcumin and tetrahydrocurcumin have potential applications in the treatment of acute myeloid leukemia with Ara-C resistance.

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Section: Methodsmentioning

confidence: 99%

Curcumin and tetrahydrocurcumin induce cell death in Ara‐C‐resistant acute myeloid leukemia

Tseng

Chiou

Weng

et al. 2019

Phytotherapy Research

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“…The development of acidic vesicular organelles (AVOs) is one of the hallmarks of autophagy, which can be determined by acridine orange (AO) staining of the cells. KG-1 and HL-60 cells staining with AO (100 µg/ml) were accomplished based on the published procedures (32). Cells were resuspended by PBS, and then by adding AO.…”

Section: Detection Of Acidic Vesicular Organelles During Autophagy Fomentioning

confidence: 99%

Effects of different autophagy inhibitors on treatment with ATO/ATRA in KG-1 and HL-60 leukemia cells

Haghi

Salemi

Fakhimahmadi³

et al. 2020

Preprint

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Background : Few current autophagy inhibitors may have beneficial effects for acute myeloid leukemia (AML) patients in clinical phases. However, there is a strong need to figure out which settings should be activated or inhibited in autophagy pathway to prevail drug resistance and improve current treatment options in leukemia. This study aimed to compare the effects of 3 well-known inhibitors of autophagy (3-MA, BafA1 and HCQ) in human leukemia KG1 and HL-60 cells exposed to ATO and/or ATRA. Methods : Cell proliferation and cytotoxicity of KG-1 and HL-60 cells were examined by MTT assay. Autophagy was studied by evaluating the development of acidic vesicular organelles, and the autophagosomes formation was investigated by acridine orange staining and transmission electron microscopy. Gene and protein expression levels of autophagy markers ( ATGs , p62/SQSTM1 and LC-3B) were also performed by qPCR and western blotting, respectively. The rate of apoptosis (annexin-V/PI staining) and cell cycle were evaluated using flow cytometry. Result: We compared the cytotoxic and apoptotic effects of arsenic trioxide (ATO) and/or all-trans retinoic acid (ATRA) in KG1 and HL-60 cells, and demonstrated that some autophagy markers can be upregulated in this context. Also, autophagy blockers HCQ and/or BafA1 could potentiate the cytotoxic effects of ATO/ATRA, which were more pronounced in KG-1 cells compared with HL-60 cell line. Conclusion: This study showed the involvement of autophagy during treatment of KG1 and HL-60 cells with ATO/ATRA.also, this study propose was to propose that combination therapy of ATO/ATRA with the autophagy inhibitor HCQ can be considered as a more effective strategy for targeting leukemic KG-1 cells. Key words: Autophagy, AML, ATO, ATRA

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“…Hence, NS is thought to perform an important function in the control of cell proliferation (Tsai and McKay 2002). Indeed, NS silencing reduces proliferation, induces differentiation, and eventually drives acute promyelocytic leukemia cells to autophagy (Fakhimahmadi et al 2017). Similarly, the crucial role of NS in functioning of cancer cells is witnessed by the fact that the NS-deficient ovarian cancer cells are led to cell cycle arrest and to an increase in apoptosis.…”

Section: A Nucleolus As a Support Of Cancer Cellsmentioning

confidence: 99%

The nucleolus, an ally, and an enemy of cancer cells

Stępiński

2018

Histochem Cell Biol

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The rates of ribosome production by a nucleolus and of protein biosynthesis by ribosomes are tightly correlated with the rate of cell growth and proliferation. All these processes must be matched and appropriately regulated to provide optimal cell functioning. Deregulation of certain factors, including oncogenes, controlling these processes, especially ribosome biosynthesis, can lead to cell transformation. Cancer cells are characterized by intense ribosome biosynthesis which is advantageous for their growth and proliferation. On the other hand, this feature can be engaged as an anticancer strategy. Numerous nucleolar factors such as nucleolar and ribosomal proteins as well as different RNAs, in addition to their role in ribosome biosynthesis, have other functions, including those associated with cancer biology. Some of them can contribute to cell transformation and cancer development. Others, under stress evoked by different factors which often hamper function of nucleoli and thus induce nucleolar/ribosomal stress, can participate in combating cancer cells. In this sense, intentional application of therapeutic agents affecting ribosome biosynthesis can cause either release of these molecules from nucleoli or their de novo biosynthesis to mediate the activation of pathways leading to elimination of harmful cells. This review underlines the role of a nucleolus not only as a ribosome constituting apparatus but also as a hub of both positive and negative control of cancer development. The article is mainly based on original papers concerning mechanisms in which the nucleolus is implicated directly or indirectly in processes associated with neoplasia.

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Nucleostemin silencing induces differentiation and potentiates all- trans -retinoic acid effects in human acute promyelocytic leukemia NB4 cells via autophagy

Cited by 10 publications

References 52 publications

Curcumin and tetrahydrocurcumin induce cell death in Ara‐C‐resistant acute myeloid leukemia

Curcumin and tetrahydrocurcumin induce cell death in Ara‐C‐resistant acute myeloid leukemia

Effects of different autophagy inhibitors on treatment with ATO/ATRA in KG-1 and HL-60 leukemia cells

The nucleolus, an ally, and an enemy of cancer cells

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