STAT pathway in the regulation of zoledronic acid-induced apoptosis in chronic myeloid leukemia cells

Kiper, Hatice Demet; Kaymaz, Burçin Tezcanlı; Gökbulut, Aysun Adan; Selvi, Nur; Avci, Çığır Biray; Kosova, Buket; Iskender, Guniz; Yandım, Melis Kartal; Gündüz, Cumhur; Şahin, Fahri; Baran, Yusuf; Saydam, Güray

doi:10.1016/j.biopha.2013.04.006

Cited by 12 publications

(9 citation statements)

References 37 publications

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“…EGFR-TKIs inhibit phosphorylation of EGFR tyrosine kinase region, thus inhibiting downstream signaling pathways. Studies have found that the antitumor effect of ZA is associated with inhibition of the activation of Akt and STAT3 (38)(39)(40). Our study found that ZA can inhibit Akt and STAT3 protein phosphorylation and STAT3 protein expression in HCC827 cells, and the combined treatment obviously inhibited EGFR and downstream signaling of Akt, ERK1/2 and STAT3 protein phosphorylation and slightly inhibited STAT3 protein expression.…”

Section: Discussionsupporting

confidence: 57%

Zoledronic acid increases the antitumor effect of gefitinib treatment for non-small cell lung cancer with EGFR mutations

Feng

Liu

et al. 2016

Oncology Reports

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Abstract. Non-small cell lung cancer (NSCLC) patients with epithelial growth factor receptor (EGFR) mutations and bone metastases are often concurrently administered tyrosine kinase inhibitors (TKIs) and bisphosphonates. Yet, the effects and mechanisms of these agents are unclear. In the present study, we aimed to ascertain whether zoledronic acid (ZA) increases the antitumor effects of gefitinib treatment on NSCLC with EGFR mutations and the related mechanisms of action. The effects of ZA and gefitinib on NSCLC tumor cells with EGFR mutations (HCC827, HCC827 GR and H1975) in regards to proliferation, apoptosis, cell cycle and signaling pathways were detected. ZA increased the antitumor effects of gefitinib on NSCLC with EGFR activating mutations and TKI resistance in vitro. Gefitinib caused cell cycle arrest in the G0/G1 phase, ZA induced S phase accumulation and the effect of the combined treatment was neutralization. Combined treatment obviously inhibited STAT3 and/or p-STAT3 protein expression compared with treatment with each single drug in vitro and in vivo, and it also significantly inhibited TKI resistance NSCLC tumor growth in vivo. In conclusion, ZA increased the antitumor effects of gefitinib on NSCLC with EGFR activating mutations and TKI resistance by regulating the cell cycle, inducing caspase-3 expression and inhibiting STAT3 expression.

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Section: Discussionsupporting

confidence: 57%

Zoledronic acid increases the antitumor effect of gefitinib treatment for non-small cell lung cancer with EGFR mutations

Feng

Liu

et al. 2016

Oncology Reports

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“…In some cases, ZA does not exhibit explicit proliferative inhibition in the MDA-MB-231 breast cancer cell line. Nevertheless, evidence of the effects of ZA on the regulation of tumor cell apoptosis has been universally recognized [12][13][14] . Therefore, researchers have sought new strategies that combine ZA with other chemotherapeutic agents or nutraceuticals, including paclitaxel, doxorubicin, cisplatin, camellia sinensis and gemcitabine, to treat osteosarcoma, breast cancer and multiple myeloma [15][16][17] .…”

Section: Introductionmentioning

confidence: 99%

Synergistic suppression of human breast cancer cells by combination of plumbagin and zoledronic acid In vitro

et al. 2015

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“…For instance, decitabine has been shown to markedly inhibit the proliferation of HL-60 cells and to enhance the cytotoxicity of natural killer cells to HL-60 cells, which may be related to the STAT3 signaling pathway (106). Zoledronic acid and bortezomib can both inhibit the proliferation of K562 cells and induce apoptosis via the STAT3 signaling pathway (107,108). Chidamide has been shown to affect AML cell viability by inhibiting the JAK2/STAT3 signaling pathway (109).…”

Section: The Roles Of Stat3 In the Diagnosis Treatment And Prognosis Of Leukemiamentioning

confidence: 99%

Roles of STAT3 in leukemia (Review)

Yin

Zhang

et al. 2018

Int J Oncol

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Leukemia is a type of hematopoietic malignancy, and the incidence rate in the United States and European Union increases by an average of 0.6 to 0.7% annually. The incidence rate in China is approximately 5.17/100,000 individuals, and the mortality rate is 3.94/100,000 individuals. Leukemia is the most common tumor affecting children and adults under 35 years of age, and is one of the major diseases leading to the death of adolescents. Signal transducer and activator of transcription 3 (STAT3) is a vital regulatory factor of signal transduction and transcriptional activation, and once activated, the phosphorylated form of STAT3 (p-STAT3) is transferred into the nucleus to regulate the transcription of target genes, and plays important roles in cell proliferation, differentiation, apoptosis and other physiological processes. An increasing number of studies have confirmed that the abnormal activation of STAT3 is involved in the development of tumors. In this review, the roles of STAT3 in the pathogenesis, diagnosis, treatment and prognosis of leukemia are discussed in the aspects of cell proliferation, differentiation and apoptosis, with the aim to further clarify the roles of STAT3 in leukemia, and shed light into possible novel targets and strategies for clinical diagnosis and treatment.

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STAT pathway in the regulation of zoledronic acid-induced apoptosis in chronic myeloid leukemia cells

Cited by 12 publications

References 37 publications

Zoledronic acid increases the antitumor effect of gefitinib treatment for non-small cell lung cancer with EGFR mutations

Zoledronic acid increases the antitumor effect of gefitinib treatment for non-small cell lung cancer with EGFR mutations

Synergistic suppression of human breast cancer cells by combination of plumbagin and zoledronic acid In vitro

Roles of STAT3 in leukemia (Review)

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