ZFX Facilitates Cell Proliferation and Imatinib Resistance in Chronic Myeloid Leukemia Cells

Wu, Jingjing; Wei, Bin; Wang, Qian; Ding, Yihan; Deng, Zhong‐Liang; Lü, Xueying; Li, Yufeng

doi:10.1007/s12013-016-0725-x

Cited by 9 publications

(9 citation statements)

References 28 publications

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“… 19 ZFX promoted the proliferation and elevated the drug resistance of chronic myeloid leukemia cells to imatinib. 33 As for TNBC, CCAT1 contributed to the development of TNBC through upregulating ZFX via acting as a sponge of miR‐218, 20 indicating the oncogenic role of ZFX in TNBC. ZFX was identified as a target of miR‐1296.…”

Section: Discussionmentioning

confidence: 99%

Circ_0000520 contributes to triple‐negative breast cancer progression through mediating the miR‐1296/ZFX axis

et al. 2021

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Background: Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer with a high incidence of local recurrence and metastasis. Circular RNAs (circRNAs) are implicated in the pathomechanism of TNBC. Here, we investigated the function of circ_0000520 in TNBC and its associated mechanism. Methods: Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot assay were used to measure RNA and protein expression. Cell proliferation was analyzed by cell counting kit-8 (CCK8) assay, flow cytometry and colony formation assay. Cell apoptosis was assessed by flow cytometry. Cell migration ability was analyzed by transwell migration and wound healing assays. Transwell invasion assay was conducted to analyze the invasion ability. Dualluciferase reporter assay, RNA immunoprecipitation (RIP) assay, and RNApulldown assay were performed to verify the interaction between microRNA-1296 (miR-1296) and circ_0000520 or zinc finger protein X-linked (ZFX). Xenograft mice model was established to analyze the role of circ_0000520 in xenograft tumor growth in vivo. Results: Circ_0000520 expression was upregulated in TNBC tissues and cell lines. Circ_0000520 knockdown suppressed the proliferation, migration, and invasion whereas induced the apoptosis of TNBC cells. miR-1296 was verified as a target of circ_0000520, and circ_0000520 silencing-mediated suppressive effects on the malignant potential of TNBC cells were partly overturned by miR-1296 knockdown. miR-1296 interacted with the 3 0 untranslated region (3 0 UTR) of ZFX, and ZFX overexpression partly reversed miR-1296 overexpression-mediated effects in TNBC cells. Circ_0000520 absence reduced ZFX expression by upregulating miR-1296 in TNBC cells. Circ_0000520 silencing suppressed xenograft tumor growth in vivo. Conclusions: Circ_0000520 contributed to TNBC development by binding to miR-1296 to induce ZFX expression.

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Section: Discussionmentioning

confidence: 99%

Circ_0000520 contributes to triple‐negative breast cancer progression through mediating the miR‐1296/ZFX axis

et al. 2021

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“…Additionally, ZFX participates in drug resistance in hepatocellular carcinoma (24,25). The results of our previous study also demonstrated that ZFX may be involve in the regulation of cell proliferation and imatinib resistance in CML (26). Thus, the present study investigated the effects and mechanisms of HHT facilitating imatinib sensitivity in K562 human CML cells.…”

Section: Introductionmentioning

confidence: 55%

“…The results of our previous study demonstrated that ZFX silencing may inhibit CML cell growth through the PI3K/AKT pathway (26). To test whether the effect of HHT on CML cells was associated with ZFX expression, RT-qPCR and western blot analyses were performed; the results revealed that the mRNA and protein expression levels of ZFX were dose-dependently decreased by HHT treatment for 24 h in K562 cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

Homoharringtonine enhances the effect of imatinib on chronic myelogenous leukemia cells by downregulating ZFX

Wei

Shi

et al. 2019

Mol Med Report

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Homoharringtonine (HHT) and imatinib have a synergistic effect in the clinical treatment of chronic myeloid leukemia (CML). The purpose of the present study was to explore the underlying mechanisms by which HHT enhanced imatinib sensitivity. K562 CML cells were treated with HHT and imatinib separately or in combination. Cell viability was detected by Cell Counting Kit-8 assay; apoptotic rates and protein expression levels of phosphorylated-tyrosine (p-Tyr) and p-CRK like proto-oncogene, adaptor protein (p-Crkl) were analyzed by flow cytometry; zinc-finger protein, X-linked (ZFX) overexpression plasmid was transfected to cells using electroporation; western blotting was used to detect the protein expression levels of PI3K, AKT, p-AKT and ZFX; and reverse transcription-quantitative PCR was used to measure ZFX mRNA expression levels. The results demonstrated that HHT and imatinib co-treatment had significant effects of proliferation inhibition and apoptosis induction on K562 CML cells compared with imatinib alone. Co-treatment also significantly downregulated the expression levels of p-Tyr, p-Crkl, PI3K and p-Akt compared with imatinib or HHT treatment. In addition, HHT downregulated ZFX mRNA and protein expression. ZFX overexpression reversed cell sensitivity to imatinib and HHT and also reduced the HHT-induced imatinib sensitization by increasing p-Akt expression. In conclusion, HHT may enhance the effect of imatinib on CML cells by downregulating ZFX.

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“…Elsewhere in the hematopoietic system, ZFX has been reported as important for BCRinduced B-cell proliferation and B-cell survival (8). ZFX was also found to be an inhibitor of the differentiation of acute T-lymphoblastic leukemia and myeloid leukemias (9), and important for imatinib resistance and proliferation of chronic myeloid leukemia cells (10).…”

Section: Discussionmentioning

confidence: 99%

Expression of zinc-finger protein X-linked, ZFX, is associated with enhanced survival in patients with breast cancer.

Mamoor¹

2020

Preprint

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We mined published tumor transcriptome data with paired survival data to discover genes associated with survival outcomes in breast cancer (1, 2). We found that the zinc-finger protein X-linked ZFX (3, 4) was among the genes most differentially expressed in both primary and metastatic tumor tissues when comparing tumor transcriptomes based on survival at 24 months. ZFX expression was significantly higher in the metastatic tumors of patients surviving greater than 24 months, suggesting that increased ZFX expression confers a survival benefit to patients with stage IV metastatic breast cancer.

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ZFX Facilitates Cell Proliferation and Imatinib Resistance in Chronic Myeloid Leukemia Cells

Cited by 9 publications

References 28 publications

Circ_0000520 contributes to triple‐negative breast cancer progression through mediating the miR‐1296/ZFX axis

Circ_0000520 contributes to triple‐negative breast cancer progression through mediating the miR‐1296/ZFX axis

Homoharringtonine enhances the effect of imatinib on chronic myelogenous leukemia cells by downregulating ZFX

Expression of zinc-finger protein X-linked, ZFX, is associated with enhanced survival in patients with breast cancer.

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