Ectonucleotidase activity driven by acid ectophosphatase in luminal A MCF-7 breast cancer cells.

Ectophosphatases catalyse the hydrolysis of phosphorylated molecules, such as phospho-amino acids, in the extracellular environment. Nevertheless, the hydrolysis of nucleotides in the extracellular environment is typically catalysed by ectonucleotidases. Studies have shown that acid ectophosphatase, or transmembrane-prostatic acid phosphatase (TM-PAP), a membrane-bound splice variant of prostatic acid phosphatase, has ecto-5'-nucleotidase activity.

Cerium oxide nanoparticles: Chemical properties, biological effects and potential therapeutic opportunities (Review).

The chemistry of pure cerium oxide (CeO) nanoparticles has been widely studied since the 1970s, especially for chemical catalysis. CeO nanoparticles have been included in an important class of industrial metal oxide nanoparticles and have been attributed a range of wide applications, such as ultraviolet absorbers, gas sensors, polishing agents, cosmetics, consumer products, high-tech devices and fuel cell conductors. Despite these early applications in the field of chemistry, the biological effects of CeO nanoparticles were only explored in the 2000s.

Primary colorectal diffuse large B-cell lymphoma: A report of eighteen cases in a tertiary care center.

Primary colorectal diffuse large B-cell lymphoma (DLBCL) is very rare colon malignancy. It is important to know the main demographic and clinical characteristics of these patients. We conducted a retrospective analysis of 18 patients diagnosed with primary colorectal DLBCL during a 17-year period at the National Cancer Institute of Brazil (INCA) between 2000 and 2018.

Primary diffuse large B-cell lymphoma of the head and neck in a Brazilian single-center study.

Objectives: Lymphomas represent around 10% of head and neck neoplasms, among which the diffuse large B-cell lymphoma (DLBCL) is the most common histologic subtype. In the present study, we characterized demographic parameters, anatomical sites, and survival rates of patients in a Brazilian cancer center.

Materials And Methods: Single-center retrospective epidemiological study of 243 head and neck DLBCL patients.

The pterocarpanquinone LQB‑118 compound induces apoptosis of cytarabine‑resistant acute myeloid leukemia cells.

Acute myeloid leukemia (AML) is a complex hematological disorder characterized by blockage of differentiation and high proliferation rates of myeloid progenitors. Anthracycline and cytarabine‑based therapy has remained the standard treatment for AML over the last four decades. Although this treatment strategy has increased survival rates, patients often develop resistance to these drugs.

Osteopontin‑c isoform inhibition modulates ovarian cancer cell cisplatin resistance, viability and plasticity.

Osteopontin (OPN) is upregulated in several types of tumor and has been associated with chemoresistance. However, the contribution of OPN splicing isoforms (OPN‑SIs) to chemoresistance requires further investigation. The present study aimed to evaluate the expression patterns of each tested OPN‑SI in cisplatin (CDDP)‑resistant ovarian carcinoma cell lines, focusing on the role of the OPN‑c isoform (OPNc) in drug resistance.

Galectin-3 mediates survival and apoptosis pathways during Trypanosoma cruzi-host cell interplay.

Neglected tropical diseases, such as Chagas disease caused by the protozoa Trypanosoma cruzi, affect millions of people worldwide but lack effective treatments that are accessible to the entire population, especially patients with the debilitating chronic phase. The recognition of host cells, invasion and its intracellular replicative success are essential stages for progression of the parasite life cycle and the development of Chagas disease. It is predicted that programmed cell death pathways (apoptosis) would be activated in infected cells, either via autocrine secretion or mediated by cytotoxic immune cells.

Expression of nuclear XIAP associates with cell growth and drug resistance and confers poor prognosis in breast cancer.

Evasion from apoptosis is one of the hallmarks of cancer. X-linked inhibitor of apoptosis protein (XIAP) is known to modulate apoptosis by inhibiting caspases and ubiquitinating target proteins. XIAP is mainly found at the cytoplasm, but recent data link nuclear XIAP to poor prognosis in breast cancer.

Unraveling survivin expression in chronic myeloid leukemia: Molecular interactions and clinical implications.

Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by the BCR-ABL oncoprotein, known to drive leukemogenesis by orchestrating multiple signaling pathways ultimately involved in cell survival. Despite successful response rates of CML patients to tyrosine kinase inhibitors (TKIs), resistance eventually arises due to BCR-ABL-dependent and independent mechanisms. Survivin is an inhibitor of apoptosis protein acting in the interface between apoptosis deregulation and cell cycle progression.

The LQB-223 Compound Modulates Antiapoptotic Proteins and Impairs Breast Cancer Cell Growth and Migration.

Drug resistance represents a major issue in treating breast cancer, despite the identification of novel therapeutic strategies, biomarkers, and subgroups. We have previously identified the LQB-223, 11a-N-Tosyl-5-deoxi-pterocarpan, as a promising compound in sensitizing doxorubicin-resistant breast cancer cells, with little toxicity to non-neoplastic cells. Here, we investigated the mechanisms underlying LQB-223 antitumor effects in 2D and 3D models of breast cancer.

[Corrigendum] The pterocarpanquinone LQB-118 induces apoptosis in acute myeloid leukemia cells of distinct molecular subtypes and targets FoxO3a and FoxM1 transcription factors.

Subsequent to the publication of the above article, the authors have realized that there were errors associated with Figs. 1c and 2b. In Fig.

FOXK2 Transcription Factor and Its Emerging Roles in Cancer.

Forkhead box (FOX) transcription factors compose a large family of regulators of key biological processes within a cell. FOXK2 is a member of FOX family, whose biological functions remain relatively unexplored, despite its description in the early nineties. More recently, growing evidence has been pointing towards a role of FOXK2 in cancer, which is likely to be context-dependent and tumour-specific.

Full-length osteopontin and its splice variants as modulators of chemoresistance and radioresistance (Review).

Osteopontin (OPN) is a matricellular phosphoglycoprotein overexpressed in several tumor types and can activate several aspects of cancer progression in solid and non‑solid tumors. In the present review, the roles of OPN in mediating resistance to chemotherapy and radiotherapy and their main associated signaling pathways were summarized and discussed. Furthermore, it was detailed how OPN expression may be able to modulate resistance to these therapies by controlling epithelial cell plasticity, stemness potential and cell survival.

IKZF1 deletion and co-occurrence with other aberrations in a child with chronic myeloid leukemia progressing to acute lymphoblastic leukemia.

Chronic myeloid leukemia (CML) is a rare disease in children. Different from that in adults, childhood CML involves transformative events occurring over a short time period. CML transformation to lymphoid blast phase (BP) is associated with copy number abnormalities, characteristic of BCR-ABL1 positive acute lymphoblastic leukemia, but not of CML in the chronic phase.

SUMOylation modulates FOXK2-mediated paclitaxel sensitivity in breast cancer cells.

The forkhead transcription factor FOXK2 plays a critical role in suppressing tumorigenesis and mediating cytotoxic drug action in breast cancer. However, the mechanism by which the biological function of FOXK2 is regulated remains poorly understood. Here, we investigated the role of SUMOylation in modulating FOXK2-mediated drug sensitivity.

11a-N-Tosyl-5-deoxi-pterocarpan, LQB-223, a novel compound with potent antineoplastic activity toward breast cancer cells with different phenotypes.

Unlabelled: Multidrug resistance is the major obstacle for successful treatment of breast cancer, prompting the investigation of novel anticancer compounds.

Purpose: In this study, we tested whether LQB-223, an 11a-N-Tosyl-5-deoxi-pterocarpan newly synthesized compound, could be effective toward breast cancer cells.

Methods: Human breast cell lines MCF-7, MDA-MB-231, HB4a and MCF-7 Dox(R) were used as models for this study.

In Vitro Methods for Studying the Mechanisms of Resistance to DNA-Damaging Therapeutic Drugs.

Most commonly used anticancer drugs exert their effects mainly by causing DNA damage. The enhancement in DNA damage response (DDR) is considered a key mechanism that enables cancer cells to survive through eliminating the damaged DNA lesions and thereby developing resistance to DNA-damaging agents. This chapter describes the four experimental approaches for studying DDR and genotoxic drug resistance, including the use of γ-H2AX and comet assays to monitor DNA damage and repair capacity as well as the use of clonogenic and β-galactosidase staining assays to assess long-term cell fate after DNA-damaging treatment.

FOXM1 targets XIAP and Survivin to modulate breast cancer survival and chemoresistance.

Drug resistance is a major hurdle for successful treatment of breast cancer, the leading cause of deaths in women throughout the world. The FOXM1 transcription factor is a potent oncogene that transcriptionally regulates a wide range of target genes involved in DNA repair, metastasis, cell invasion, and migration. However, little is known about the role of FOXM1 in cell survival and the gene targets involved.

Insights into a Critical Role of the FOXO3a-FOXM1 Axis in DNA Damage Response and Genotoxic Drug Resistance.

FOXO3a and FOXM1 are two forkhead transcription factors with antagonistic roles in cancer and DNA damage response. FOXO3a functions like a typical tumour suppressor, whereas FOXM1 is a potent oncogene aberrantly overexpressed in genotoxic resistant cancers. FOXO3a not only represses FOXM1 expression but also its transcriptional output.

FOXM1: an emerging master regulator of DNA damage response and genotoxic agent resistance.

FOXM1 is a transcription factor required for a wide spectrum of essential biological functions, including DNA damage repair, cell proliferation, cell cycle progression, cell renewal, cell differentiation and tissue homeostasis. Recent evidence suggests that FOXM1 also has a role in many aspects of the DNA damage response. Accordingly, FOXM1 drives the transcription of genes for DNA damage sensors, mediators, signal transducers and effectors.

The pterocarpanquinone LQB-118 induces apoptosis in acute myeloid leukemia cells of distinct molecular subtypes and targets FoxO3a and FoxM1 transcription factors.

Acute myeloid leukemia (AML) patients' outcome is usually poor, mainly because of drug resistance phenotype. The identification of new drugs able to overcome mechanisms of chemoresistance is essential. The pterocarpanquinone LQB-118 compound has been shown to have a potent cytotoxic activity in myeloid leukemia cell lines and patient cells.

FOXM1: A key oncofoetal transcription factor in health and disease.

Forkhead Box M1 (FOXM1) is a bona fide oncofoetal transcription factor, which orchestrates complex temporal and spatial gene expression throughout embryonic and foetal development as well as during adult tissue homeostasis and repair. Controlled FOXM1 expression and activity provides a balanced transcriptional programme to ensure proper growth and maturation during embryogenesis and foetal development as well as to manage appropriate homeostasis and repair of adult tissues. Conversely, deregulated FOXM1 upregulation likely affects cell migration, invasion, angiogenesis, stem cell renewal, DNA damage repair and cellular senescence, which impact tumour initiation, progression, metastasis, angiogenesis and drug resistance.

Phosphorylated Crkl reduction levels are associated with the lowest P-glycoprotein activity levels in cells from chronic myeloid leukemia patients.

ABCB1/P-glycoprotein (Pgp) and ABCG2/BCRP overexpression have been described as related to imatinib resistance in chronic myeloid leukemia (CML). We showed in CML cells from 55 patients that Pgp activity was more frequently detected than BCRP activity (p=0.0074).

Doxorubicin induces cell death in breast cancer cells regardless of Survivin and XIAP expression levels.

Breast cancer is the leading cause of deaths in women around the world. Resistance to therapy is the main cause of treatment failure and still little is known about predictive biomarkers for response to systemic therapy. Increasing evidence show that Survivin and XIAP overexpression is closely associated with chemoresistance and poor prognosis in breast cancer.