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Article ; Online: Combinations of Calcitriol with Anticancer Treatments for Breast Cancer

Mariana Segovia-Mendoza / Janice García-Quiroz / Lorenza Díaz / Rocío García-Becerra

International Journal of Molecular Sciences, Vol 22, Iss 12741, p

An Update

2021 Volume 12741

Abstract: Preclinical, clinical, and epidemiological studies indicate that vitamin D3 (VD) deficiency is a risk factor for the development of breast cancer. Underlying mechanisms include the ability of calcitriol to induce cell differentiation, inhibit oncogenes ... ...

Abstract	Preclinical, clinical, and epidemiological studies indicate that vitamin D3 (VD) deficiency is a risk factor for the development of breast cancer. Underlying mechanisms include the ability of calcitriol to induce cell differentiation, inhibit oncogenes expression, and modify different signaling pathways involved in the control of cell proliferation. In addition, calcitriol combined with different kinds of antineoplastic drugs has been demonstrated to enhance their beneficial effects in an additive or synergistic fashion. However, a recognized adjuvant regimen based on calcitriol for treating patients with breast cancer has not yet been fully established. Accordingly, in the present work, we review and discuss the preclinical and clinical studies about the combination of calcitriol with different oncological drugs, aiming to emphasize its main therapeutic benefits and opportunities for the treatment of this pathology.
Keywords	breast cancer ; calcitriol ; drug combination ; efficacy ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-11-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Preclinical and clinical aspects of TNF-α and its receptors TNFR1 and TNFR2 in breast cancer

Isela Martínez-Reza / Lorenza Díaz / Rocío García-Becerra

Journal of Biomedical Science, Vol 24, Iss 1, Pp 1-

2017 Volume 8

Abstract: Abstract Breast cancer is the most common malignancy in women and a public health problem worldwide. Breast cancer is often accompanied by an inflammatory process characterized by the presence of proinflammatory cytokines such as tumor necrosis factor ( ... ...

Abstract	Abstract Breast cancer is the most common malignancy in women and a public health problem worldwide. Breast cancer is often accompanied by an inflammatory process characterized by the presence of proinflammatory cytokines such as tumor necrosis factor (TNF-α), which has important implications in the course of the disease. Inflammation has been described primarily as a favorable environment for tumor development. However, under certain conditions TNF-α can promote signals for activation, differentiation, survival or cell death, so the study of the variants of this cytokine, its receptors, the presence of polymorphisms and its implication in different phenotypes of breast cancer is necessary. Although the clinical application of TNF-α has been limited by its toxicity and side effects, preclinical and clinical studies have shown that these effects may partially be avoided via tumor-targeted delivery strategies. In this manner, TNF-α alone or combined with chemotherapy and radiotherapy can function as an adjuvant in the treatment of breast cancer.
Keywords	TNF-α ; TNFR1 ; TNFR2 ; Breast cancer ; Medicine ; R
Subject code	610
Language	English
Publishing date	2017-12-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Immunoendocrine Dysregulation during Gestational Diabetes Mellitus

Andrea Olmos-Ortiz / Pilar Flores-Espinosa / Lorenza Díaz / Pilar Velázquez / Carlos Ramírez-Isarraraz / Verónica Zaga-Clavellina

International Journal of Molecular Sciences, Vol 22, Iss 8087, p

The Central Role of the Placenta

2021 Volume 8087

Abstract: Gestational Diabetes Mellitus (GDM) is a transitory metabolic condition caused by dysregulation triggered by intolerance to carbohydrates, dysfunction of beta-pancreatic and endothelial cells, and insulin resistance during pregnancy. However, this ... ...

Abstract	Gestational Diabetes Mellitus (GDM) is a transitory metabolic condition caused by dysregulation triggered by intolerance to carbohydrates, dysfunction of beta-pancreatic and endothelial cells, and insulin resistance during pregnancy. However, this disease includes not only changes related to metabolic distress but also placental immunoendocrine adaptations, resulting in harmful effects to the mother and fetus. In this review, we focus on the placenta as an immuno-endocrine organ that can recognize and respond to the hyperglycemic environment. It synthesizes diverse chemicals that play a role in inflammation, innate defense, endocrine response, oxidative stress, and angiogenesis, all associated with different perinatal outcomes.
Keywords	inflammation ; cytokines ; adipokines ; antimicrobial peptides ; oxidative stress ; metabolic stress ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2021-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The Phytochemical α-Mangostin Inhibits Cervical Cancer Cell Proliferation and Tumor Growth by Downregulating E6/E7-HPV Oncogenes and KCNH1 Gene Expression

Lorenza Díaz / Samantha V. Bernadez-Vallejo / Rafael Vargas-Castro / Euclides Avila / Karla A. Gómez-Ceja / Rocío García-Becerra / Mariana Segovia-Mendoza / Heriberto Prado-Garcia / Galia Lara-Sotelo / Javier Camacho / Fernando Larrea / Janice García-Quiroz

International Journal of Molecular Sciences, Vol 24, Iss 3055, p

2023 Volume 3055

Abstract: Cervical cancer is the fourth most common cancer among women worldwide. The main factor associated with the onset and progression of this neoplasia is the human papillomavirus (HPV) infection. The HPV-oncogenes E6 and E7 are critical drivers of cellular ... ...

Abstract	Cervical cancer is the fourth most common cancer among women worldwide. The main factor associated with the onset and progression of this neoplasia is the human papillomavirus (HPV) infection. The HPV-oncogenes E6 and E7 are critical drivers of cellular transformation, promoting the expression of oncogenes such as KCNH1 . The phytochemical α-mangostin (AM) is a potent antineoplastic and antiviral compound. However, its effects on HPV oncogenes and KCNH1 gene expression remain unknown. This study evaluated the effects of AM on cell proliferation, cell cycle distribution and gene expression, including its effects on tumor growth in xenografted mice. AM inhibited cell proliferation in a concentration-dependent manner, being the most sensitive cell lines those with the highest number of HPV16 copies. In addition, AM promoted G1-cell cycle arrest in CaSki cells, while led to cell death in SiHa and HeLa cells. Of interest was the finding of an AM-dependent decreased gene expression of E6, E7 and KCNH1 both in vitro and in vivo, as well as the modulation of cytokine expression, Ki-67, and tumor growth inhibition. On these bases, we suggest that AM represents a good option as an adjuvant for the treatment and prevention of cervical cancer.
Keywords	α-mangostin ; cervical cancer ; KCNH1 ; HPV ; E6 ; E7 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Endothelium-Dependent Induction of Vasculogenic Mimicry in Human Triple-Negative Breast Cancer Cells Is Inhibited by Calcitriol and Curcumin

Gabriela Morales-Guadarrama / Edgar A. Méndez-Pérez / Janice García-Quiroz / Euclides Avila / Rocío García-Becerra / Alejandro Zentella-Dehesa / Fernando Larrea / Lorenza Díaz

International Journal of Molecular Sciences, Vol 23, Iss 14, p

2022 Volume 7659

Abstract: In highly aggressive tumors, cancer cells may form channel-like structures through a process known as vasculogenic mimicry (VM). VM is generally associated with metastasis, mesenchymal phenotype, and treatment resistance. VM can be driven by ... ...

Abstract	In highly aggressive tumors, cancer cells may form channel-like structures through a process known as vasculogenic mimicry (VM). VM is generally associated with metastasis, mesenchymal phenotype, and treatment resistance. VM can be driven by antiangiogenic treatments and/or tumor microenvironment-derived factors, including those from the endothelium. Curcumin, a turmeric product, inhibits VM in some tumors, while calcitriol, the most active vitamin D metabolite, exerts potent antineoplastic effects. However, the effect of these natural products on VM in breast cancer remains unknown. Herein, we studied the effect of both compounds on triple-negative breast cancer (TNBC) VM-capacity in a co-culture model. The process of endothelial cell-induced VM in two human TNBC cell lines was robustly inhibited by calcitriol and partially by curcumin. Calcitriol promoted TNBC cells’ morphological change from spindle-like to cobblestone-shape, while curcumin diminished VM 3D-structure. Notably, the treatments dephosphorylated several active kinases, especially those involved in the PI3K/Akt pathway. In summary, calcitriol and curcumin disrupted endothelium-induced VM in TNBC cells partially by PI3K/Akt inactivation and mesenchymal phenotype inhibition. Our results support the possible use of these natural compounds as adjuvants for VM inactivation in patients with malignant tumors inherently capable of forming VM, or those with antiangiogenic therapy, warranting further in vivo studies.
Keywords	co-culture ; tubulogenesis ; vascular mimicry ; breast cancer ; epithelial-to-mesenchymal transition ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2022-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Design, Synthesis and Preclinical Assessment of 99m Tc-iFAP for In Vivo Fibroblast Activation Protein (FAP) Imaging

Diana Trujillo-Benítez / Myrna Luna-Gutiérrez / Guillermina Ferro-Flores / Blanca Ocampo-García / Clara Santos-Cuevas / Gerardo Bravo-Villegas / Enrique Morales-Ávila / Pedro Cruz-Nova / Lorenza Díaz-Nieto / Janice García-Quiroz / Erika Azorín-Vega / Antonio Rosato / Laura Meléndez-Alafort

Molecules, Vol 27, Iss 264, p

2022 Volume 264

Abstract: Fibroblast activation protein (FAP) is expressed in the microenvironment of most human epithelial tumors. 68 Ga-labeled FAP inhibitors based on the cyanopyrrolidine structure (FAPI) are currently used for the detection of the tumor microenvironment by ... ...

Abstract	Fibroblast activation protein (FAP) is expressed in the microenvironment of most human epithelial tumors. 68 Ga-labeled FAP inhibitors based on the cyanopyrrolidine structure (FAPI) are currently used for the detection of the tumor microenvironment by PET imaging. This research aimed to design, synthesize and preclinically evaluate a new FAP inhibitor radiopharmaceutical based on the 99m Tc-((R)-1-((6-hydrazinylnicotinoyl)-D-alanyl) pyrrolidin-2-yl) boronic acid ( 99m Tc-iFAP) structure for SPECT imaging. Molecular docking for affinity calculations was performed using the AutoDock software. The chemical synthesis was based on a series of coupling reactions of 6-hidrazinylnicotinic acid (HYNIC) and D-alanine to a boronic acid derivative. The iFAP was prepared as a lyophilized formulation based on EDDA/SnCl 2 for labeling with 99m Tc. The radiochemical purity (R.P.) was verified via ITLC-SG and reversed-phase radio-HPLC. The stability in human serum was evaluated by size-exclusion HPLC. In vitro cell uptake was assessed using N30 stromal endometrial cells (FAP positive) and human fibroblasts (FAP negative). Biodistribution and tumor uptake were determined in Hep-G2 tumor-bearing nude mice, from which images were acquired using a micro-SPECT/CT. The iFAP ligand ( Ki = 0.536 nm, AutoDock affinity), characterized by UV-Vis, FT-IR, 1 H–NMR and UPLC-mass spectroscopies, was synthesized with a chemical purity of 92%. The 99m Tc-iFAP was obtained with a R.P. >98%. In vitro and in vivo studies indicated high radiotracer stability in human serum (>95% at 24 h), specific recognition for FAP, high tumor uptake (7.05 ± 1.13% ID/g at 30 min) and fast kidney elimination. The results found in this research justify additional dosimetric and clinical studies to establish the sensitivity and specificity of the 99m Tc-iFAP.
Keywords	fibroblast activation protein ; FAP inhibitors ; technetium-99m ; HYNIC-iFAP ; Organic chemistry ; QD241-441
Subject code	333
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Compartmentalized Innate Immune Response of Human Fetal Membranes against Escherichia coli Choriodecidual Infection

Andrea Olmos-Ortiz / Mayra Hernández-Pérez / Pilar Flores-Espinosa / Gabriela Sedano / Addy Cecilia Helguera-Repetto / Óscar Villavicencio-Carrisoza / María Yolotzin Valdespino-Vazquez / Arturo Flores-Pliego / Claudine Irles / Bruno Rivas-Santiago / Elsa Romelia Moreno-Verduzco / Lorenza Díaz / Verónica Zaga-Clavellina

International Journal of Molecular Sciences, Vol 23, Iss 2994, p

2022 Volume 2994

Abstract: An infectious process into the uterine cavity represents a major endangered condition that compromises the immune privilege of the maternal–fetal unit and increases the risk for preterm birth (PTB) and premature rupture of membranes (PROM). Fetal ... ...

Abstract	An infectious process into the uterine cavity represents a major endangered condition that compromises the immune privilege of the maternal–fetal unit and increases the risk for preterm birth (PTB) and premature rupture of membranes (PROM). Fetal membranes are active secretors of antimicrobial peptides (AMP), which limit bacterial growth, such as Escherichia coli . Nevertheless, the antibacterial responses displayed by chorioamniotic membranes against a choriodecidual E. coli infection have been briefly studied. The objective of this research was to characterize the profile of synthesis, activity, and spatial distribution of a broad panel of AMPs produced by fetal membranes in response to E. coli choriodecidual infection. Term human chorioamniotic membranes were mounted in a two independent compartment model in which the choriodecidual region was infected with live E. coli (1 × 10 5 CFU/mL). Amnion and choriodecidual AMP tissue levels and TNF-α and IL-1β secretion were measured by the enzyme-linked immunosorbent assay. The passage of bacterium through fetal membranes and their effect on structural continuity was followed for 24 h. Our results showed that E. coli infection caused a progressive mechanical disruption of the chorioamniotic membranes and an activated inflammatory environment. After the challenge, the amnion quickly (2–4 h) induced production of human beta defensins (HBD)-1, HBD-2, and LL-37. Afterwards (8–24 h), the amnion significantly produced HBD-1, HBD-2, HNP-1-3, S100A7, sPLA2, and elafin, whereas the choriodecidua induced LL-37 synthesis. Therefore, we noticed a temporal- and tissue-specific pattern regulation of the synthesis of AMPs by infected fetal membranes. However, fetal membranes were not able to contain the collagen degradation or the bacterial growth and migration despite the battery of produced AMPs, which deeply increases the risk for PTB and PROM. The mixture of recombinant HBDs at low concentrations resulted in increased bactericidal activity compared to each HBD alone in vitro, ...
Keywords	genitourinary infection ; innate defense ; innate immunity ; antimicrobial peptides ; beta defensins ; alpha defensins ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: α-Mangostin Synergizes the Antineoplastic Effects of 5-Fluorouracil Allowing a Significant Dose Reduction in Breast Cancer Cells

Galia Lara-Sotelo / Lorenza Díaz / Rocío García-Becerra / Euclides Avila / Heriberto Prado-Garcia / Gabriela Morales-Guadarrama / María de Jesús Ibarra-Sánchez / José Esparza-López / Fernando Larrea / Janice García-Quiroz

Processes, Vol 9, Iss 3, p

2021 Volume 458

Abstract: Breast cancer is the most common neoplasm and the leading cause of cancer death in women worldwide. Although 5-fluorouracil is a conventional chemotherapeutic agent for breast cancer treatment, its use may result in severe side effects. Thus, there is ... ...

Abstract	Breast cancer is the most common neoplasm and the leading cause of cancer death in women worldwide. Although 5-fluorouracil is a conventional chemotherapeutic agent for breast cancer treatment, its use may result in severe side effects. Thus, there is widespread interest in lowering 5-fluorouracil drawbacks, without affecting its therapeutic efficacy by the concomitant use with natural products. Herein, we aimed at evaluating whether α-mangostin, a natural antineoplastic compound, could increase the anticancer effect of 5-fluorouracil in different breast cancer cell lines, allowing for dose reduction. Cell proliferation was evaluated by sulforhodamine-B assays, inhibitory concentrations and potency were calculated by dose-response curves, followed by analysis of their pharmacological interaction by the combination-index method and dose-reduction index. Cell cycle distribution was evaluated by flow cytometry. Each compound inhibited cell proliferation in a dose-dependent manner, the triple negative breast cancer cells being the most sensitive. When 5-fluorouracil and α-mangostin were used concomitantly, synergistic antiproliferative effect was observed. The calculated dose-reduction index suggested that this combination exhibits therapeutic potential for reducing 5-fluorouracil dosage in breast cancer. Mechanistically, the cotreatment induced cell death in a greater extent than each drug alone. Therefore, α-mangostin could be used as a potent co-adjuvant for 5-fluorouracil in breast cancer.
Keywords	α-mangostin ; breast cancer ; combination index ; dose-reduction index ; 5-fluorouracil ; Chemical technology ; TP1-1185 ; Chemistry ; QD1-999
Subject code	610 ; 616
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: High Glucose Promotes Inflammation and Weakens Placental Defenses against E. coli and S. agalactiae Infection

Rodrigo Jiménez-Escutia / Donovan Vargas-Alcantar / Pilar Flores-Espinosa / Addy Cecilia Helguera-Repetto / Oscar Villavicencio-Carrisoza / Ismael Mancilla-Herrera / Claudine Irles / Yessica Dorin Torres-Ramos / María Yolotzin Valdespino-Vazquez / Pilar Velázquez-Sánchez / Rodrigo Zamora-Escudero / Marcela Islas-López / Caridad Carranco-Salinas / Lorenza Díaz / Verónica Zaga-Clavellina / Andrea Olmos-Ortiz

International Journal of Molecular Sciences, Vol 24, Iss 5243, p

Protective Role of Insulin and Metformin

2023 Volume 5243

Abstract: Placentas from gestational diabetes mellitus (GDM) patients undergo significant metabolic and immunologic adaptations due to hyperglycemia, which results in an exacerbated synthesis of proinflammatory cytokines and an increased risk for infections. ... ...

Abstract	Placentas from gestational diabetes mellitus (GDM) patients undergo significant metabolic and immunologic adaptations due to hyperglycemia, which results in an exacerbated synthesis of proinflammatory cytokines and an increased risk for infections. Insulin or metformin are clinically indicated for the treatment of GDM; however, there is limited information about the immunomodulatory activity of these drugs in the human placenta, especially in the context of maternal infections. Our objective was to study the role of insulin and metformin in the placental inflammatory response and innate defense against common etiopathological agents of pregnancy bacterial infections, such as E. coli and S. agalactiae , in a hyperglycemic environment. Term placental explants were cultivated with glucose (10 and 50 mM), insulin (50–500 nM) or metformin (125–500 µM) for 48 h, and then they were challenged with live bacteria (1 × 10 5 CFU/mL). We evaluated the inflammatory cytokine secretion, beta defensins production, bacterial count and bacterial tissue invasiveness after 4–8 h of infection. Our results showed that a GDM-associated hyperglycemic environment induced an inflammatory response and a decreased beta defensins synthesis unable to restrain bacterial infection. Notably, both insulin and metformin exerted anti-inflammatory effects under hyperglycemic infectious and non-infectious scenarios. Moreover, both drugs fortified placental barrier defenses, resulting in reduced E. coli counts, as well as decreased S. agalactiae and E. coli invasiveness of placental villous trees. Remarkably, the double challenge of high glucose and infection provoked a pathogen-specific attenuated placental inflammatory response in the hyperglycemic condition, mainly denoted by reduced TNF-α and IL-6 secretion after S. agalactiae infection and by IL-1β after E. coli infection. Altogether, these results suggest that metabolically uncontrolled GDM mothers develop diverse immune placental alterations, which may help to explain their increased ...
Keywords	hyperglycemia ; hypoglycemics ; inflammatory cytokines ; bacterial count ; bacterial invasiveness ; cytokine tolerization ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Mechanisms of Resistance to Endocrine Therapy in Breast Cancer

Javier Camacho / Lorenza Díaz / Rocío García-Becerra / Nancy Santos

International Journal of Molecular Sciences, Vol 14, Iss 1, Pp 108-

Focus on Signaling Pathways, miRNAs and Genetically Based Resistance

2012 Volume 145

Abstract: Breast cancer is the most frequent malignancy diagnosed in women. Approximately 70% of breast tumors express the estrogen receptor (ER). Tamoxifen and aromatase inhibitors (AIs) are the most common and effective therapies for patients with ERα-positive ... ...

Abstract	Breast cancer is the most frequent malignancy diagnosed in women. Approximately 70% of breast tumors express the estrogen receptor (ER). Tamoxifen and aromatase inhibitors (AIs) are the most common and effective therapies for patients with ERα-positive breast cancer. Alone or combined with chemotherapy, tamoxifen significantly reduces disease progression and is associated with more favorable impact on survival in patients. Unfortunately, endocrine resistance occurs, either de novo or acquired during the course of the treatment. The mechanisms that contribute to hormonal resistance include loss or modification in the ERα expression, regulation of signal transduction pathways, altered expression of specific microRNAs, balance of co-regulatory proteins, and genetic polymorphisms involved in tamoxifen metabolic activity. Because of the clinical consequences of endocrine resistance, new treatment strategies are arising to make the cells sensitive to tamoxifen. Here, we will review the current knowledge on mechanisms of endocrine resistance in breast cancer cells. In addition, we will discuss novel therapeutic strategies to overcome such resistance. Undoubtedly, circumventing endocrine resistance should help to improve therapy for the benefit of breast cancer patients.
Keywords	endocrine therapy ; breast cancer ; estrogen receptor ; hormonal resistance ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616 ; 610
Language	English
Publishing date	2012-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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