The effect of decitabine on the expression and methylation of the PPP1CA, BTG2, and PTEN in association with changes in miR‐125b, miR‐17, and miR‐181b in NALM6 cell line

Vafadar, Asma; Mokaram, Pooneh; Erfani, Mehran; Yousefi, Zahra; Farhadi, Ali; Shirazi, Tehrani Elham; Tamaddon, Gholamhossein

doi:10.1002/jcb.28590

Cited by 11 publications

(13 citation statements)

References 39 publications

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“…And the miR-17 family plays a crucial role in cell cycle, apoptosis, tumorigenesis and angiogenesis. 86 - 88 Table 2 summarizes previous studies showing the use of apoptosis-inducing agents in ALL treatments.…”

Section: Apoptosis and Glucocorticoid (Gc)-resistant Allmentioning

confidence: 99%

Role of Autophagy and Apoptosis in Acute Lymphoblastic Leukemia

Huang

2021

Cancer Control

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Background: Acute lymphoblastic leukemia (ALL) is a malignant disease characterized by an excessive number of immature lymphocytes, including immature precursors of both B- and T cells. ALL affects children more often than adults. Immature lymphocytes lead to arrested differentiation and proliferation of cells. Its conventional treatments involve medication with dexamethasone, vincristine, and other anticancer drugs. Although the current first-line drugs can achieve effective treatment, they still cannot prevent the recurrence of some patients with ALL. Treatments have high risk of recurrence especially after the first remission. Currently, novel therapies to treat ALL are in need. Autophagy and apoptosis play important roles in regulating cancer development. Autophagy involves degradation of proteins and organelles, and apoptosis leads to cell death. These phenomena are crucial in cancer progression. Past studies reported that many potential anticancer agents regulate intracellular signaling pathways. Methods: The authors discuss the recent research findings on the role of autophagy and apoptosis in ALL. Results: The autophagy and apoptosis are widely used in the treatment of ALL. Most studies showed that many agents regulate autophagy and apoptosis in ALL cell models, clinical trials, and ALL animal models. Conclusions: In summary, activating autophagy and apoptosis pathways are the main strategies for ALL treatments. For ALL, combining new drugs with traditional chemotherapy and glucocorticoids treatments can achieve the greatest therapeutic effect by activating autophagy and apoptosis.

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Section: Apoptosis and Glucocorticoid (Gc)-resistant Allmentioning

confidence: 99%

Role of Autophagy and Apoptosis in Acute Lymphoblastic Leukemia

Huang

2021

Cancer Control

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“…It has been applied in therapy for numerous cancers. 9 , 20 , 21 , 22 Herein, we demonstrate that replenishment with decitabine could restore the expression of Syk in SW480 and HCT116 cell lines. Similarly, recent studies have also found that decitabine could reactivate the expression of Syk in breast cancer and nasopharyngeal cancer cells.…”

Section: Discussionmentioning

confidence: 73%

“…Decitabine is an effective inhibitor of DNA methylation, which may restore the expression of hypermethylated genes. It has been applied in therapy for numerous cancers 9,20–22 . Herein, we demonstrate that replenishment with decitabine could restore the expression of Syk in SW480 and HCT116 cell lines.…”

Section: Discussionmentioning

confidence: 82%

Comprehensive analysis of Syk gene methylation in colorectal cancer

Zhu

Liu

et al. 2021

Immunity Inflam & Disease

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Background: Metastasis of colorectal cancer (CRC) extremely affects the prognosis of CRC patients. Recently, the genetic methylation has been shown to associate with tumor metastasis. This research aimed to explore the Syk gene, which is frequently hypermethylated in different cancers, and its impact on the metastasis of CRC cells. Methods: We employed the UALCAN database for the detection of the methylation levels of Syk in different cancers. CIBERSORT, TIMER and TISIDB tools were employed to analyze the association of Syk expression with immune features of CRC. Treatment with decitabine has been noted to restore the expression of Syk in CRC cells. The invasion and migration abilities of CRC cell lines were determined using transwell and wound healing assays. The correlation between Syk and c‐Myc was established using the GEPIA2 database and Western blot assays. Results: Our results, based on UALCAN, revealed that the methylation level of Syk was altered in diverse cancers including colon adenocarcinoma. We found that expression profile and methylation level of Syk was correlated with immune features of colon adenocarcinoma. Decitabine can restore the expression of Syk in HCT116 and SW480 cells, hence affecting their migration and invasion. Results from GEPIA2 showed that Syk expression was correlated with c‐Myc, while Western blotting analysis revealed a negative association between the expression level of Syk and c‐Myc. Conclusions: This study demonstrates that the expression of Syk could be restored by decitabine in colorectal cancer, thus affecting the migration and invasion abilities of CRC cells.

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“…B-ALL is the most widespread type of hematologic malignancy in children and is responsible for most fatalities in pediatric patients [1]. Many reports have suggested that various factors are involved in the expansion of B-ALL, including genetic disorders and epigenetic changes, specifically alterations in the expression of various miRs [23,24].…”

Section: Discussionmentioning

confidence: 99%

“…However, investigations focusing on the association between alterations in miR expression in relation to vincristine are limited [18]. A previous study characterized miR profile to identify their potential roles involved in B-ALL [24]. Previous investigations showed that miR-34, 17 and 181 play critical roles in B-ALL and miR-17 and miR-181/b act as oncomiRs in the Nalm6 cells [24,30,31].…”

Section: Discussionmentioning

confidence: 99%

Anticancer properties of vincristine is modulated by microRNAs in acute lymphoblastic leukemia Nalm6 cell line

Shirazi-Tehrani¹,

Vafadar

Keshavarzi³

et al. 2021

Anti-Cancer Drugs

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Precursor B-cell acute lymphoblastic leukemia (B-ALL), a highly diverse disease, is the most widespread pediatric malignancy characterized by cytogenetic and molecular abnormalities such as altered microRNA (miR) expression signatures. MiRs are a class of short noncoding RNAs. Dysregulation in the expression of miRs plays a crucial role in different types of cancers. Vincristine is an antineoplastic drug with a broad spectrum of activity against different hematologic malignancies and is the firstline treatment for B-ALL. Previous studies have proposed miR-17 and miR-181/b as oncomirs and miR-34/a as a tumor suppressor in Nalm6 cells, thus in the current study, we investigated the effects of vincristine treatment on the expression of miR-17, miR-34/a and miR-181/b expression levels. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was conducted to estimate the optimal concentration of vincristine in the Nalm-6 cell line. Expression of miRs was calculated using real-time PCR. Our results showed significant downregulation of miR-17 (FC = 0.226; P < 0.0004) in Nalm6 cells after vincristine treatment. Conversely, miR-34/a (FC = 4.823; P < 0.0001) was significantly upregulated. Also, the expression of miR-181/b (FC = 0.156; P < 0.3465) was not significantly different between the vincristine treated group and the control group. In conclusion, it is proposed that one of the mechanisms by which vincristine improves B-ALL is by modulating the expression of specific miRs. These specific miRs will serve as good diagnostic and prognostic biomarkers. Anti-Cancer Drugs 33: e680-e685 Copyright

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The effect of decitabine on the expression and methylation of the PPP1CA, BTG2, and PTEN in association with changes in miR‐125b, miR‐17, and miR‐181b in NALM6 cell line

Cited by 11 publications

References 39 publications

Role of Autophagy and Apoptosis in Acute Lymphoblastic Leukemia

Role of Autophagy and Apoptosis in Acute Lymphoblastic Leukemia

Comprehensive analysis of Syk gene methylation in colorectal cancer

Anticancer properties of vincristine is modulated by microRNAs in acute lymphoblastic leukemia Nalm6 cell line

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