BAX/BCL-XL gene expression ratio inversely correlates with disease progression in chronic myeloid leukemia

Gonzalez, Mariana Selena; Brasi, Carlos Daniel de; Bianchini, Michele; Gargallo, Patricia; Moiraghi, Beatriz; Bengió, Raquel; Larripa, Irene

doi:10.1016/j.bcmd.2010.07.011

Cited by 13 publications

(12 citation statements)

References 21 publications

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“…49 Mariana and Gonzalez suggest that Bax/Bcl-x L expression ratio may be a sensitive monitor of cancer progression and an early predictor for cancer patients. 50 In this study, we investigated at least three distinct parameters: absolute expression levels of Bax and Bcl-x L genes and the ratio of these pro and antiapoptotic proteins. Our results support the existence of a specific apoptotic mechanism in MCF-7 cells that increasing in Bax/Bcl-x L ratio causes the loss of cell viability and enhanced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Doxorubicin Changes Bax /Bcl-xL Ratio, Caspase-8 and 9 in Breast Cancer Cells

Sharifi¹,

Barar²,

Hejazi³

et al. 2015

Adv Pharm Bull

121

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Section: Discussionmentioning

confidence: 99%

Doxorubicin Changes Bax /Bcl-xL Ratio, Caspase-8 and 9 in Breast Cancer Cells

Sharifi¹,

Barar²,

Hejazi³

et al. 2015

Adv Pharm Bull

121

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“…In samples from CML patients, the levels of BAX are maintained but the ratio BAX/Bcl-X L varies during disease progression. Moreover, the level of Bcl-X L decreases when TKIs are used [ 65 ]. In addition, other molecules capable of counteracting the antiapoptotic effect, such as Bim, are expressed in low amounts in CML cells but their expression is increased when BCR–ABL is inhibited [ 66 ].…”

Section: Introductionmentioning

confidence: 99%

Multidrug resistance in chronic myeloid leukaemia: how much can we learn from MDR–CML cell lines?

2013

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The hallmark of CML (chronic myeloid leukaemia) is the BCR (breakpoint cluster region)–ABL fusion gene. CML evolves through three phases, based on both clinical and pathological features: a chronic phase, an accelerated phase and blast crisis. TKI (tyrosine kinase inhibitors) are the treatment modality for patients with chronic phase CML. The therapeutic potential of the TKI imatinib is affected by BCR–ABL dependent an independent mechanisms. Development of MDR (multidrug resistance) contributes to the overall clinical resistance. MDR involves overexpression of ABC -transporters (ATP-binding-cassette transporter) among other features. MDR studies include the analysis of cancer cell lines selected for resistance. CML blast crisis is accompanied by increased resistance to apoptosis. This work reviews the role played by the influx transporter OCT1 (organic cation transporter 1), by efflux ABC transporters, molecules involved in the modulation of apoptosis (p53, Bcl-2 family, CD95, IAPs (inhibitors of apoptosis protein)], Hh and Wnt/β-catenin pathways, cytoskeleton abnormalities and other features described in leukaemic cells of clinical samples and CML cell lines. An MDR cell line, Lucena-1, generated from K562 by stepwise exposure to vincristine, was used as our model and some potential anticancer drugs effective against the MDR cell line and patients’ samples are presented.

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“…The Bcl proteins family is comprised of two classes: anti-apoptotic proteins (e.g., Bcl-xl) and pro-apoptotic proteins (e.g., Bax). Bcl-xl has been proposed as an oncogene based on its ability to block cell apoptosis and trigger tumorigenesis, while other proteins, such as Bak, are inhibitors of cell apoptosis [ 24 ]. Importantly, other survival factors, such as Akt, can also suppress apoptosis in a transcription-independent manner by phosphorylating and inactivating components of the apoptotic machinery.…”

Section: Discussionmentioning

confidence: 99%

The milk-derived fusion peptide, ACFP, suppresses the growth of primary human ovarian cancer cells by regulating apoptotic gene expression and signaling pathways

Zhou¹,

Zhao²,

Tang³

et al. 2016

BMC Cancer

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BackgroundACFP is an anti-cancer fusion peptide derived from bovine milk protein. This study was to investigate the anti-cancer function and underlying mechanisms of ACFP in ovarian cancer.MethodsFresh ovarian tumor tissues were collected from 53 patients who underwent initial debulking surgery, and primary cancer cells were cultured. Normal ovarian surface epithelium cells (NOSECs), isolated from 7 patients who underwent surgery for uterine fibromas, were used as normal control tissue. Anti-viabilities of ACFP were assessed by WST-1 (water-soluble tetrazolium 1), and apoptosis was measured using a flow cytometry-based assay. Gene expression profiles of ovarian cancer cells treated with ACFP were generated by cDNA microarray, and the expression of apoptotic-specific genes, such as bcl-xl, bax, akt, caspase-3, CDC25C and cyclinB1, was assessed by real time PCR and western blot analysis.ResultsTreatment with ACFP inhibited the viability and promoted apoptosis of primary ovarian cancer cells but exhibited little or no cytotoxicity toward normal primary ovarian cells. Mechanistically, the anti-cancer effects of ACFP in ovarian cells were shown to occur partially via changes in gene expression and related signal pathways. Gene expression profiling highlighted that ACFP treatment in ovarian cancer cells repressed the expression of bcl-xl, akt, CDC25C and cyclinB1 and promoted the expression of bax and caspase-3 in a time- and dose-dependent manner.ConclusionsOur results suggest that ACFP may represent a potential therapeutic agent for ovarian cancer that functions by altering the expression and signaling of cancer-related pathways in ovarian cancer cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2281-6) contains supplementary material, which is available to authorized users.

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BAX/BCL-XL gene expression ratio inversely correlates with disease progression in chronic myeloid leukemia

Cited by 13 publications

References 21 publications

Doxorubicin Changes Bax /Bcl-xL Ratio, Caspase-8 and 9 in Breast Cancer Cells

Doxorubicin Changes Bax /Bcl-xL Ratio, Caspase-8 and 9 in Breast Cancer Cells

Multidrug resistance in chronic myeloid leukaemia: how much can we learn from MDR–CML cell lines?

The milk-derived fusion peptide, ACFP, suppresses the growth of primary human ovarian cancer cells by regulating apoptotic gene expression and signaling pathways

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