Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Vianey Gonzalez-Villasana has a total of 46 co-authors. Here are the top co-authors by number of shared publications:

  • Cristina Ivan

    Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, USA

    2 shared publications
  • Diana Reséndez-Pérez

    Facultad de Ciencias Biológicas, Departamento de Biología Celular y Genética, Universidad Autónoma de Nuevo León, San Nicolás de los Garza, Nuevo León, México

    2 shared publications
  • Ezequiel Viveros-Valdez

    Departamento de Química, Facultad de Ciencias Biológicas, Universidad Autónoma de Nuevo León, Av. Pedro de Alba S/N, San Nicolás de los Garza 66450, Nuevo León, Mexico

    2 shared publications
  • Imelda Noehmi Monroy-García

    Departamento de Ingeniería Química y Bioquímica, Tecnológico Nacional de México, Instituto Tecnológico de Los Mochis, Juan de Dios Bátiz y 20 de Noviembre, Los Mochis 81259, Sinaloa, Mexico

    2 shared publications
  • José Roberto Estupiñan-Jiménez

    Facultad de Ciencias Biológicas, Departamento de Biología Celular y Genética, Universidad Autónoma de Nuevo León, San Nicolás de los Garza, Nuevo León, México

    2 shared publications
  • Pablo E. Vivas-Mejia

    Department of Biochemistry, University of Puerto Rico, Medical Sciences Campus, San Juan 00936, Puerto Rico

    2 shared publications

Latest Publications

  • Open Access

    Inhibition of microRNA-660-5p decreases breast cancer progression through direct targeting of TMEM41B

    by Valeria Villarreal-García, José Roberto Estupiñan-Jiménez, Vianey Gonzalez-Villasana, Pablo E. Vivas-Mejía, Marienid Flores-Colón, Irma Estefanía Ancira-Moreno, Patricio Adrián Zapata-Morín, Claudia Altamirano-Torres, José Manuel Vázquez-Guillen, Cristina Rodríguez-Padilla, et al.

    Background: Breast cancer is the most prevalent cancer among women worldwide. Most breast cancer-related deaths result from metastasis and drug resistance. Novel therapies are imperative for targeting metastatic and drug-resistant breast cancer cells. Accumulating evidence suggests that dysregulated microRNAs (miRNAs) promote breast cancer progression, metastasis, and drug resistance. Compared with healthy breast tissue, miR-660-5p is notably overexpressed in breast cancer tumor tissues. However, the downstream effectors of miR-660-5p in breast cancer cells have not been fully elucidated. Our aim was to investigate the role of miR-660-5p in breast cancer cell proliferation, migration, invasion, and angiogenesis and to identify its potential targets. Results: Our findings revealed significant upregulation of miR-660-5p in MDA-MB-231 and MCF-7 cells compared with MCF-10 A cells. Furthermore, inhibiting miR-660-5p led to notable decreases in the proliferation, migration, and invasion of breast cancer cells, as well as angiogenesis, in HUVEC cells. Through bioinformatics analysis, we identified 15 potential targets of miR-660-5p. We validated TMEM41B as a direct target of miR-660-5p via Western blot and dual-luciferase reporter assays. Conclusions: Our study highlights the upregulation and involvement of miR-660-5p in breast cancer cell proliferation, migration, invasion, and angiogenesis. Additionally, we identified TMEM41B as a direct target of miR-660-5p in breast cancer cells.


  • Open Access

    MicroRNA‐1307‐3p contributes to breast cancer progression through PRM2

    by José Roberto Estupiñan‐Jiménez, Valeria Villarreal‐García, Vianey Gonzalez‐Villasana, Pablo E. Vivas‐Mejia, Jose Manuel Vazquez‐Guillen, Patricio Adrián Zapata‐Morin, Marienid Flores‐Colón, Claudia Altamirano‐Torres, Ezequiel Viveros‐Valdez, Cristina Ivan, et al.

    Background: Despite advances in screening and therapy, breast cancer (BC) remains the predominant cancer in women globally. Dysregulation of microRNAs (miRNAs) is pivotal in carcinogenesis across various cancers, including BC. Evidence indicates that miR‐1307‐3p is upregulated in BC tumors, yet its target genes are not fully elucidated. This study aimed to explore how miR‐1307‐3p regulates BC proliferation, migration, invasion, and angiogenesis and to identify potential target genes.Methods: Basal miR‐1307‐3p levels were quantified in BC cell lines MDA‐MB‐231 and MCF‐7, as well as MCF‐10A using quantitative real‐time reverse transcription‐PCR (RT‐qPCR). The impact of miR‐1307‐3p inhibition on BC cell proliferation, migration, invasion, and angiogenesis was assessed. Nine miRNA‐target prediction databases identified potential miR‐1307‐3p targets. Target expression was validated using RT‐qPCR, Western blot, and dual‐luciferase reporter assays. MiR‐1307‐3p was overexpressed in MDA‐MB‐231 and MCF‐7 compared to MCF‐10A.Results: Inhibiting miR‐1307‐3p significantly reduced BC cell proliferation, migration, invasion, and angiogenesis. Bioinformatics analysis identified 17 potential miR‐1307‐3p targets, with protamine 2 (PRM2) overexpression confirmed via Western blot and dual‐luciferase assays.Conclusion: MiR‐1307‐3p overexpression in BC promotes proliferation, migration, invasion, and angiogenesis. PRM2 emerges as a novel miR‐1307‐3p target in BC.


  • Open Access

    Antioxidant and Biological Activity of Mexican Madroño Fruit (Arbutus arizonica)

    by Imelda N. Monroy-García, Pilar Carranza-Rosales, Irma Edith Carranza-Torres, Lelie Denisse Castro-Ochoa, Vianey González-Villasana, Alma Rosa Islas-Rubio, Ezequiel Viveros-Valdez

    The fruit of the Mexican madroño (Arbutus arizonica) has been consumed since pre-Columbian times by North American tribes and native groups in Mexico. Despite this, reports on its chemical composition and biological activity are limited. This work aims to determine the antioxidant, antiproliferative, and digestive enzyme inhibition activities of the methanol amberlite-retained extract of Mexican madroño. Results showed that madroño fruit is rich in antioxidants: DPPH (EC50 = 0.89 ± 0.03 mg/mL), TEAC (1078 ± 4.9 μM/g), and hemolysis inhibition (IC50 = 358.07 μg/mL), with high phenolic and flavonoid content at 15.92 ± 3.2 mg GAE/g and 4.33 ± 0.3 mg CA/g, respectively. Using analytical chromatography, gallic acid, vanillic acid, chlorogenic acid, ferulic acid, quercetin, and rutin were quantified. The extract also showed α-glucosidase inhibition (IC50 = 3.1 ± 0.17 mg/mL), but no inhibition against α-amylase and lipase (>5 mg/mL), while showing antiproliferative activity against HeLa, HT-29, and MCF-7 cancer cell lines. These results point towards an interesting potential for the fruit of the A. arizonica as chemopreventive and hold potential for elaborating functional foods.


  • Open Access

    Mechanistic Insights about Sorafenib-, Valproic Acid- and Metformin-Induced Cell Death in Hepatocellular Carcinoma

    by Edgar Xchel Franco-Juárez, Vianey González-Villasana, María Elena Camacho-Moll, Luisa Rendón-Garlant, Patricia Nefertari Ramírez-Flores, Beatriz Silva-Ramírez, Katia Peñuelas-Urquides, Ethel Daniela Cabello-Ruiz, Fabiola Castorena-Torres, Mario Bermúdez de León

    Hepatocellular carcinoma (HCC) is among the main causes of death by cancer worldwide, representing about 80–90% of all liver cancers. Treatments available for advanced HCC include atezolizumab, bevacizumab, sorafenib, among others. Atezolizumab and bevacizumab are immunological options recently incorporated into first-line treatments, along with sorafenib, for which great treatment achievements have been reached. However, sorafenib resistance is developed in most patients, and therapeutical combinations targeting cancer hallmark mechanisms and intracellular signaling have been proposed. In this review, we compiled evidence of the mechanisms of cell death caused by sorafenib administered alone or in combination with valproic acid and metformin and discussed them from a molecular perspective.


  • Open Access

    A vicious circle in breast cancer: The interplay between inflammation, reactive oxygen species, and microRNAs

    by Valeria Villarreal-García, José Roberto Estupiñan-Jiménez, Pablo E. Vivas-Mejía, Vianey Gonzalez-Villasana, José Manuel Vázquez-Guillén, Diana Reséndez-Pérez

    Breast cancer (BC) is the most common cancer in women worldwide. This highly heterogeneous disease is molecularly stratified into luminal A, luminal B, HER2, triple-negative/basal-like, and normal-like subtypes. An important aspect in BC progression is the activation of inflammatory processes. The activation of CD8+/Th1, NK, and M1 tumor associated macrophages (TAMs), leads to tumor destruction. In contrast, an anti-inflammatory response mediated by CD4+/Th2 and M2 TAMs will favor tumor progression. Inflammation also stimulates the production of inflammatory mediators like reactive oxygen species (ROS). In chronic inflammation, ROS activates oxidative stress and endothelial dysfunction. In cancer, ROS plays a dual role with anti-tumorigenic and pro-tumorigenic effects in cell signaling pathways that control proliferation, survival, apoptosis, and inflammation. MicroRNAs (miRNAs), which are known to be involved in BC progression and inflammation, can be regulated by ROS. At the same time, miRNAs regulate the expression of genes modulating oxidative stress. In this review, we will discuss the interplay between inflammation, ROS, and miRNAs as anticancer and tumor promoter molecules in BC. A clear understanding of the role of miRNAs in the regulation of ROS production and inflammation, may lead to new opportunities for therapy in BC.


  • Open Access

    Biological Activities of Seven Medicinal Plants Used in Chiapas, Mexico

    by Liliana De La Cruz-Jiménez, Mario Alberto Hernández-Torres, Imelda N. Monroy-García, Catalina Rivas-Morales, María Julia Verde-Star, Vianey Gonzalez-Villasana, Ezequiel Viveros-Valdez

    Seven medicinal plants from Chiapas, Mexico, used by Native Americans were analyzed, aiming to improve the understanding of their medicinal properties through the evaluation of various biological activities, i.e., bactericidal, antioxidant, α-glucosidase inhibition, and toxicity, to provide a scientific basis for the management of infectious and hyperglycemic diseases in the Mexican southeast. Plant extracts were obtained from Cordia dodecandra, Gaultheria odorata, Heliotropium angiospermum, Justicia spicigera, Leucaena collinsii spp. collinsii, Tagetes nelsonii, and Talisia oliviformis through maceration techniques using methanol and chloroform (1:1). Minimum Inhibitory Concentration (MIC) was employed to determine the antibacterial activity against Staphylococcus aureus, Enterobacter faecalis, Escherichia coli, Enterobacter aerogenes, Enterobacter cloacae, Klebsiella pneumoniae, and Pseudomonas aeuroginosa. The antiradical/antioxidant activity was determined by the 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2’-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assays and antihemolytic activity using the 2,2’-Azobis(2-amidinopropane) dihydrochloride radical (APPH). The anti-α-glucosidase activity was evaluated in vitro through the chromogenic PNPG assay. The toxicity was assessed using the brine shrimp lethality assay. The highest antimicrobial activity was displayed by T. nelsonii, mainly against E. faecalis and P. aeuroginosa. The extracts of L. collinsii, J. spicigera, and T. nelsonii possess antioxidant properties with EC50 < 50 μg/mL. J. spicigera and T. nelsonii extracts showed the highest antihemolytic activity with IC50 < 14 μg/mL. T. nelsonii exhibited a remarkable inhibitor effect on the α-glucosidase enzyme and the greatest toxic effect on Artemia salina with IC50 = 193 ± 20 μg/mL and LD50 = 14 ± 1 μg/mL, respectively. According to our results, G. odorata, J. spicigera, T. nelsonii, and T. oliviformis extracts contained active antimicrobial compounds. At the same time, T. nelsonii stands to be a possible source of effective antineoplastic and antihyperglycemic compounds.