Mometasone furoate inhibits growth of acute leukemia cells in childhood by regulating PI3K signaling pathway

Wang, Xiaojing; Shi, Jing; Gong, De

doi:10.1080/10245332.2018.1436395

Cited by 5 publications

(12 citation statements)

References 48 publications

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“…Since glucocorticoids could promote cell apoptosis via binging with glucocorticoid receptors in lymphoid cells, most extensive application of glucocorticoids in cancer is to treat lymphoid malignancies [23,34]. Consistent with that, it was reported MF could inhibit the growth of acute leukemia cells through promoting cell apoptosis [10]. While there was still no exploration of the pharmacological effect of MF on solid tumor.…”

Section: Discussionmentioning

confidence: 80%

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Mometasone furoate inhibits the progression of head and neck squamous cell carcinoma via regulating PTPN11

Qiu

Gao

Tao

et al. 2023

Preprint

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Background: Mometasone Furoate (MF) is a kind of glucocorticoid with extensive pharmacological action including inhibiting tumor progression, however, the role of MF in head and neck squamous cell carcinoma (HNSCC) was still unclear. This study was aim to evaluate the inhibitory effect of MF against HNSCC and investigate the underlying mechanism. Methods: Cell viability, colony formation, cell cycle and cell apoptosis were detected to explore the effect of MF on HNSCC cells. Xenograft study model was conducted to investigate the effect of MF on HNSCC in vivo. The core target of MF against HNSCC was identified by network pharmacology analysis, TCGA database analysis and real-time PCR. Molecular docking was performed to detect the binding energy. Protein tyrosine phosphatase non-receptor type 11 (PTPN11) overexpressed cells were constructed and then cell viability and the expression levels of proliferation- and apoptosis-related proteins were detected after treated with MF to explore the role of PTPN11 in the inhibitory of MF against HNSCC. Results: After cells treated with MF, cell viability and the number of colonies were decreased, cell cycle was arrested and cell apoptosis was increased. Xenograft study results showed that MF could inhibit cell proliferation via promoting cell apoptosis in vivo. PTPN11 was the core target of MF against HNSCC via network pharmacology analysis, TCGA database analysis and real-time PCR. Molecular docking results revealed PTPN11 exhibited the strongest binding ability to MF. Finally, MF could attenuate the effect of increased cell viability and decreased cell apoptosis caused by PTPN11 overexpression, suggesting that MF could inhibit the progression of HNSCC by regulating PTPN11. Conclusion: MF targeted PTPN11 to promote cycle arrest and cell apoptosis subsequently performed an effective anti-tumor activity.

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Section: Discussionmentioning

confidence: 80%

“…Previous studies regarding MF mostly focused on its treatment for in ammation. In a recent study, MF inhibited the growth and induced the apoptosis of acute leukemia cells by regulating PI3K signaling pathway [10]. For the above-mentioned reasons, MF could be identi ed as a promising anti-cancer drug for HNSCC.…”

Section: Introductionmentioning

confidence: 99%

Mometasone furoate inhibits the progression of head and neck squamous cell carcinoma via regulating PTPN11

Qiu

Gao

Tao

et al. 2023

Preprint

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“…In the pathogenesis of ALL, several members of the PI3K/AKT pathway, including AKT1, AKT2, PTEN, and BCL-2, have been implicated. [8][9][10] This study focuses on the impact of SNPs in miRNAs that are known to target these genes. Genetic variants occurring in miRNA sequences can alter binding ability or processing of mature miRNAs, which can subsequently affect the expression of their target coding genes at an epigenetic level.…”

Section: Discussionmentioning

confidence: 99%

“…7 For example, Wang et al have shown that the expression of p-AKT decreased in ALL cell lines treated with mometasone furoate. 8 Paganin et al found that PTEN genomic aberrations and PTEN inactivation contributed to adverse therapy response in T-ALL patients. 9 Khaw et al have reported that venetoclax, a selective inhibitor of BCL-2, exhibited effective antileukemic activity in the majority of ALL xenografts.…”

Section: Introductionmentioning

confidence: 99%

PI3K/AKT pathway‐related microRNA variants in childhood acute lymphoblastic leukemia

Xue

Sun

et al. 2023

Pediatric Blood & Cancer

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BackgroundDysregulation of microRNAs (miRNAs) targeting genes in the PI3K/Akt pathway has been implicated in the pathogenesis of childhood acute lymphoblastic leukemia (ALL). However, the impact of genetic variants in these miRNAs on ALL susceptibility has not been extensively explored in the Chinese population.MethodsTo address this gap, we conducted a case–control study to evaluate the association between genetic variants in five PI3K/AKT pathway‐related miRNAs (miR‐149, miR‐126, miR‐492, miR‐612, and miR‐423) and childhood ALL susceptibility in the Chinese population. Additionally, we investigated the effects of the rs2292832 mutation on ALL cell proliferation and apoptosis.ResultsOur analyses revealed that the miR‐149 rs2292832 mutant heterozygous CT genotype was more frequent in the control group than in the ALL cases, indicating a protective effect against ALL (adjusted odds ratio [OR] = 0.78, 95% confidence interval [CI] = 0.63–0.97, p = .024). Stratification analyses further revealed that the miR‐149 rs2292832 CC genotype was associated with an increased risk of childhood ALL in subgroups of older children, females, those with parents who never smoked or drank alcohol, those living in painted houses, those with B‐ALL, and those with high‐risk ALL. Finally, we observed that the rs2292832 mutation inhibited ALL cell proliferation and induced apoptosis (p = .001), providing a potential mechanism by which this genetic variant may influence ALL susceptibility.ConclusionOur study highlights the significant association between the miR‐149 rs2292832 genetic variant and childhood ALL susceptibility in the Chinese population. These findings expand our understanding of the complex genetic landscape underlying ALL and have implications for the development of personalized therapeutic strategies.

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“…Hulkko et al (56,57) reports that DAP3 interacted with GR mainly via the N-terminal region of DAP3, modulating the cytoplasmic GR-hsp90 complex, finally induced apoptosis. Wang et al (58) found that mometasone furoate could inhibit proliferation and migration of acute leukemia cells via regulating PI3K signaling pathway.…”

Section: Glucocorticoids As Therapeutic Agentsmentioning

confidence: 99%

A narrative review of the role of glucocorticoid receptors in prostate cancer: developments in last 5 years

Zhou¹,

Shi²,

Zhao³

et al. 2022

Transl Androl Urol

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Background and Objective: Glucocorticoids, secreted from the adrenal gland, are commonly used in the treatment of castration-resistant prostate cancer (CRPC) because of their anti-inflammatory and antitoxic effects. However, glucocorticoids have been reported to have the opposite effects within the course of treatment. Many studies have shown that glucocorticoid receptors (GRs) are involved in the establishment of a dominant population of androgen-independent malignant cells, which may result in CRPC. In this review, we summarized the mechanisms of GRs in CRPC and the clinical application of glucocorticoids based on the present evidence. Methods:We summarized the isoforms of GRs and the mechanisms involved in CRPC. An updated literature search was performed from the ClinicalTrials database, the National Center for Biotechnology Information database and European Union Drug Regulating Authorities Clinical Trials database. The focus was on the timeframe from 2017 to 2022. At least one primary or secondary outcome [prostate-specific antigen (PSA) response rate, progression-free survival (PFS) or overall survival (OS) and median time to PSA progression] according to studies should be included.

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Mometasone furoate inhibits growth of acute leukemia cells in childhood by regulating PI3K signaling pathway

Abstract: This study reveals that MF can inhibit proliferation and invasion/migration and induce apoptosis in Childhood ALL cells, which may be regulated by Phosphatidylinositol 3-kinase signaling pathway. These results suggest MF may be a potential new drug target for clinical ALL treatment.

Cited by 5 publications

References 48 publications

Mometasone furoate inhibits the progression of head and neck squamous cell carcinoma via regulating PTPN11

Mometasone furoate inhibits the progression of head and neck squamous cell carcinoma via regulating PTPN11

PI3K/AKT pathway‐related microRNA variants in childhood acute lymphoblastic leukemia

A narrative review of the role of glucocorticoid receptors in prostate cancer: developments in last 5 years

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