MicroRNA 30a Mediated Autophagy and Imatinib Response in Egyptian Chronic Myeloid Leukemia Patients

Khalil, Nehal A; Desouky, Mohammed N; Diab, Iman; Hamed, Nahla A M; Mannaa, Hazem Farag

doi:10.1007/s12288-019-01241-3

Cited by 8 publications

(6 citation statements)

References 14 publications

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“…It is reported that miR-30 or its homology miR-30a, miR-30a-5p binds to Beclin-1 mRNA to block autophagy-induced chemoresistance in chronic myeloid leukemia (118,128), gastric cancer (129), osteosarcoma (130), small cell lung cancer (SCLC) (131) and other variety of cancers (132). A clinical study on Egyptian patients with chronic myeloid leukemia also confirmed this result (133). It was found that a single miRNA in different cancer types may share a common mechanism in mediating chemoresistance/chemosensitivity.…”

Section: Overexpression Of Mirna Reverses Chemoresistance By Inhibiti...mentioning

confidence: 76%

The MicroRNA-Based Strategies to Combat Cancer Chemoresistance via Regulating Autophagy

et al. 2022

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Chemoresistance frequently occurs in cancer treatment, which results in chemotherapy failure and is one of the most leading causes of cancer-related death worldwide. Understanding the mechanism of chemoresistance and exploring strategies to overcome chemoresistance have become an urgent need. Autophagy is a highly conserved self-degraded process in cells. The dual roles of autophagy (pro-death or pro-survival) have been implicated in cancers and chemotherapy. MicroRNA (miRNA) is a class of small non-coding molecules that regulate autophagy at the post-transcriptional level in cancer cells. The association between miRNAs and autophagy in cancer chemoresistance has been emphasized. In this review, we focus on the dual roles of miRNA-mediated autophagy in facilitating or combating chemoresistance, aiming to shed lights on the potential role of miRNAs as targets to overcome chemoresistance.

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Section: Overexpression Of Mirna Reverses Chemoresistance By Inhibiti...mentioning

confidence: 76%

The MicroRNA-Based Strategies to Combat Cancer Chemoresistance via Regulating Autophagy

et al. 2022

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“…Recently, Khalil and co-workers reported that miRNA-30a is upregulated in imatinib-responders compared to imatinibresistant patients, which confirms that decreasing autophagy benefits imatinib-induced cytotoxicity [155]. Additionally, the authors were able to negatively correlate miRNA-30a level with Sokal score and BCR-ABL1 following treatment [155].…”

Section: Mirna-21mentioning

confidence: 80%

“…Yu and collaborators demonstrated that upregulation of miRNA-30a leads to downregulation of the pro-autophagic proteins Beclin 1 and autophagy protein 5 (ATG5) and, consequently, autophagy downregulation, thus increasing imatinib-induced cytotoxicity and promoting mitochondria-dependent intrinsic apoptosis [154]. Recently, Khalil and co-workers reported that miRNA-30a is upregulated in imatinib-responders compared to imatinibresistant patients, which confirms that decreasing autophagy benefits imatinib-induced cytotoxicity [155]. Additionally, the authors were able to negatively correlate miRNA-30a level with Sokal score and BCR-ABL1 following treatment [155].…”

Section: Mirna-21mentioning

confidence: 94%

“…Expression levels are negatively correlated with Sokal score and BCR-ABL1 following treatment. [154,155] miRNA-138 Downregulated Associated with downregulation of BCR-ABL1, inhibition of proliferation, and IM-induced apoptosis.…”

Section: Mirna-29b Downregulatedmentioning

confidence: 99%

“…Other studies have addressed the autophagy role in CML and demonstrated that this catabolic pathway allows imatinib-treated CML cells to evade cell death [154,155]. Yu and collaborators demonstrated that upregulation of miRNA-30a leads to downregulation of the pro-autophagic proteins Beclin 1 and autophagy protein 5 (ATG5) and, consequently, autophagy downregulation, thus increasing imatinib-induced cytotoxicity and promoting mitochondria-dependent intrinsic apoptosis [154].…”

Section: Mirna-21mentioning

confidence: 99%

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Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?

Abdulmawjood

Costa

Roma‐Rodrigues

et al. 2021

IJMS

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Chronic Myeloid Leukemia (CML) is a rare malignant proliferative disease of the hematopoietic system, whose molecular hallmark is the Philadelphia chromosome (Ph). The Ph chromosome originates an aberrant fusion gene with abnormal kinase activity, leading to the buildup of reactive oxygen species and genetic instability of relevance in disease progression. Several genetic abnormalities have been correlated with CML in the blast phase, including chromosomal aberrations and common altered genes. Some of these genes are involved in the regulation of cell apoptosis and proliferation, such as the epidermal growth factor receptor (EGFR), tumor protein p53 (TP53), or Schmidt-Ruppin A-2 proto-oncogene (SRC); cell adhesion, e.g., catenin beta 1 (CTNNB1); or genes associated to TGF-β, such as SKI like proto-oncogene (SKIL), transforming growth factor beta 1 (TGFB1) or transforming growth factor beta 2 (TGFB2); and TNF-α pathways, such as Tumor necrosis factor (TNFA) or Nuclear factor kappa B subunit 1 (NFKB1). The involvement of miRNAs in CML is also gaining momentum, where dysregulation of some critical miRNAs, such as miRNA-451 and miRNA-21, which have been associated to the molecular modulation of pathogenesis, progression of disease states, and response to therapeutics. In this review, the most relevant genomic alterations found in CML will be addressed.

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Unveiling autophagy complexity in leukemia: The molecular landscape and possible interactions with apoptosis and ferroptosis

Jung,

Ahn,

Shen

2024

Cancer Letters

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MicroRNA 30a Mediated Autophagy and Imatinib Response in Egyptian Chronic Myeloid Leukemia Patients

Cited by 8 publications

References 14 publications

The MicroRNA-Based Strategies to Combat Cancer Chemoresistance via Regulating Autophagy

The MicroRNA-Based Strategies to Combat Cancer Chemoresistance via Regulating Autophagy

Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?

Unveiling autophagy complexity in leukemia: The molecular landscape and possible interactions with apoptosis and ferroptosis

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