Reversal of glucocorticoid resistance in Acute Lymphoblastic Leukemia cells by miR-145

Long, Sili; Ren, Dan-Wei; Zhong, Fangfang; Niu, Ya-Na; Qin, Xiang; Mu, Dan; Chen, Li

doi:10.7717/peerj.9337

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…The induction of apoptosis and autophagy is an effective antitumor therapy strategy (42,43). Long et al (44) demonstrated that by promoting the induction of autophagy and apoptosis, this process could increase the sensitivity to GC treatment in human acute lymphoblastic leukemia cells.…”

Section: Discussionmentioning

confidence: 99%

Salidroside overcomes dexamethasone resistance in T‑acute lymphoblastic leukemia cells

et al. 2021

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The aim of the present study was to analyze whether the use of salidroside (SAL) could overcome dexamethasone (DEX) resistance in T-acute lymphocytic leukemia cells. The human T-ALL DEX-resistant cell line, CEM-C1 and the DEX-sensitive cell line, CEM-C7 were used in the current study. The proliferation inhibition rates in these cells, treated with SAL and DEX alone, and in combination were detected using a Cell Counting Kit-8 assay, while the morphological changes of the cells were observed using an inverted microscope. Reverse transcription-quantitative PCR was used to detect the mRNA expression levels of the c-Myc and LC3 genes, while flow cytometry was used to detect the cell cycle distribution and the rate of apoptosis. In addition, western blot analysis was used to detect the protein expression levels of c-Myc, BCL-2, Bax, cleaved PARP and LC3. and acridine orange staining was used to detect the changes in acidic autophagy vesicles. It was found that SAL could effectively inhibit cell proliferation and induce apoptosis in the CEM-C1 and CEM-C7 cells. In addition, SAL promoted the induction of autophagy. The protein expression levels of c-Myc in the CEM-C1 cells were significantly higher compared with that in the CEM-C7 cells. SAL downregulated the mRNA expression levels of the c-Myc gene and protein in a dose-dependent manner. This suggested that SAL could inhibit the proliferation of the CEM-C1 and CEM-C7 cells, induce apoptosis and autophagy and overcome DEX resistance in the CEM-C1 cells. The mechanism may be associated with the downregulation of c-Myc.

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Section: Discussionmentioning

confidence: 99%

Salidroside overcomes dexamethasone resistance in T‑acute lymphoblastic leukemia cells

et al. 2021

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“…It has been reported that roughly 20% of children with ALL are resistant to glucocorticoids, and even up to 70% of children with recurrent ALL are resistant to glucocorticoids ( Inaba and Pui, 2010 ). miRNAs have a wide range of roles in leukemia, among which, miR-145 enhances the sensitivity of ALL cell lines to glucocorticoids, which is achieved by promoting the expression of Beclin-1 and Bax genes and inhibiting the expression of Bcl-2 genes to induce autophagy and apoptosis production ( Long et al, 2020 ). The first-generation tyrosine kinase inhibitor (TKI) imatinib (IM) can be used not only for the treatment of CML, but has also been widely used in patients with Ph(+) ALL.…”

Section: Autophagy Initiation and Phagophore Formationmentioning

confidence: 99%

Progress in the study of autophagy-related proteins affecting resistance to chemotherapeutic drugs in leukemia

Li,

Zhang

et al. 2024

Front. Cell Dev. Biol.

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Leukemia is a life-threatening malignant tumor of the hematopoietic system. Currently, the main treatment modalities are chemotherapy and hematopoietic stem cell transplantation. However, increased drug resistance due to decreased sensitivity of leukemia cells to chemotherapeutic drugs presents a major challenge in current treatments. Autophagy-associated proteins involved in autophagy initiation have now been shown to be involved in the development of various types of leukemia cells and are associated with drug resistance. Therefore, this review will explore the roles of autophagy-related proteins involved in four key autophagic processes: induction of autophagy and phagophore formation, phagophore extension, and autophagosome formation, on the development of various types of leukemias as well as drug resistance. Autophagy may become a promising therapeutic target for treating leukemia.

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“…Impaired apoptotic processes are indication of cancer and are instigated by an overexpression of antiapoptotic proteins. [ 6 ] Therefore, an innovative approach to treat leukemia by targeting the antiapoptotic proteins is necessary to augment the leukemia patient's prognosis.…”

Section: Introductionmentioning

confidence: 99%

Tomentosin inhibits cell proliferation and induces apoptosis in MOLT‐4 leukemia cancer cells through the inhibition of mTOR/PI3K/Akt signaling pathway

Yang

Xie

Almoallim

et al. 2021

J Biochem & Molecular Tox

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Leukemia is amongst the cancers accountable for substantial mortality around the world. Tomentosin is a bioactive compound with a pharmacological significance, and its anticancer property against human leukemia MOLT‐4 cell line has never been reported. Hence, the objective of this study was to explore the anticancer activity of tomentosin in MOLT‐4 human leukemia cells. In the current investigation, the cytotoxic effects of tomentosin ensuing potent toxicity (IC50: 10 µM) in MOLT‐4 cells after incubation at 24 h have been presented. Furthermore, tomentosin triggered intracellular reactive oxygen species production and showed the induction of intrinsic/mitochondrial pathways in treated MOLT‐4 cells, revealing a significant cytotoxicity activity. Also, fluorescent microscopic studies using acridine orange/ethidium bromide and propidium iodide staining confirmed the occurrence of apoptosis in tomentosin‐treated MOLT‐4 cells. Quantitative reverse transcription polymerase chain reaction presented a negative regulation of cyclin D1 and BcL‐2 expression and a positive regulated BAX and caspase‐3 messenger RNA expression in tomentosin‐treated MOLT‐4 cells. Tomentosin further inhibited the inflammatory transcription factors such as nuclear factor κB (NF‐κB), tumor necrosis factor α, interleukin 1β (IL‐1β), and IL‐6. Additionally, inhibition of the m‐TOR/PI3K/AKT protein expression by tomentosin in MOLT‐4 cells was confirmed. Overall, these findings lead to a conclusion that tomentosin induces apoptosis in MOLT‐4 cells through caspase‐facilitated proapoptotic pathway, and inhibition of the NF‐κB‐stimulated Bcl‐2 facilitated the antiapoptotic pathway.

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Reversal of glucocorticoid resistance in Acute Lymphoblastic Leukemia cells by miR-145

Cited by 7 publications

References 23 publications

Salidroside overcomes dexamethasone resistance in T‑acute lymphoblastic leukemia cells

Salidroside overcomes dexamethasone resistance in T‑acute lymphoblastic leukemia cells

Progress in the study of autophagy-related proteins affecting resistance to chemotherapeutic drugs in leukemia

Tomentosin inhibits cell proliferation and induces apoptosis in MOLT‐4 leukemia cancer cells through the inhibition of mTOR/PI3K/Akt signaling pathway

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