Escherichia coli is a highly diverse bacterial species that is canonically commensal; however, its genomic characteristics have enabled its evolution into pathogens capable of causing extraintestinal infections (ExPEC), which pose significant clinical challenges because of the variety of sites that can infect (mainly the urinary tract) and the multidrug resistance associated with these strains. The present study is aimed at characterizing ExPEC isolates recovered from the wards of a hospital in Sinaloa, Mexico, to establish their virulence and antimicrobial resistance profiles, as well as the phylogenetic group. Then, 200 Escherichia coli isolates and their antimicrobial susceptibility were confirmed by the VITEK‐2 automated system. Virulence factor genes and phylogenetic grouping were performed through endpoint and multiplex PCRs. Then, 59% of the strains produced extended‐spectrum β ‐lactamases (ESBLs), and 71.5% were classified as multidrug resistant (MDR), exhibiting high resistance rates to antibiotics such as amoxicillin, ampicillin, ciprofloxacin, and various cephalosporins. In this sense, 68.5% and 33% of the isolates were positive for the blaCTX-M1-8 and blaCTX-M9 genes, respectively, both associated with resistance to cefotaxime. Furthermore, 37% of the isolates harbored the blaOXA48 gene, which is linked to resistance to oxacillin‐type β ‐lactams. Moreover, 143 (71.5%) of them were classified as MDR. Regarding virulence, the distribution of toxin genes such as hlyA and vat was 16.5% and 24.5%, respectively. Adhesins papC and fimA were found in 62% and 34%, respectively. Additionally, the iron acquisition systems and outer membrane proteins such as iutA (74%), fyuA (63%), iroN (10%), agn43 (82%), and kpsmTII (34.5%) were present in the isolates. Phylogenetic analysis showed a predominance of group B2 (46%), followed by groups A (13.5%) and E (10.5%). These findings highlight the complexity and challenges posed by ExPEC strains in terms of antimicrobial resistance and virulence relevant to public health in hospital settings.

Cervical cancer remains a significant global health concern, impacting over half a million women annually. The primary cause is a persistent infection with hr-HPV, which disrupts various cellular processes crucial for normal function. This disruption leads to genetic instability, including changes in the expression of microRNAs and their corresponding host genes, with far-reaching consequences for cellular regulation. Researchers have widely utilized high-throughput technologies to analyze gene expression in cervical cancer, aiming to identify distinct molecular signatures of microRNAs and genes through genomic analysis. However, discrepancies among studies have been noted, possibly due to variations in sample collection, technological platforms, and data processing methods such as normalization and filtering. Therefore, it is essential to synthesize findings from diverse studies to comprehensively understand the molecular mechanisms of regulatory genetic networks involved in the initiation and progression of cervical cancer. This review examined the evidence detailing the role of microRNA signatures and their target genes in cervical carcinogenesis and disease advancement. The accumulated data suggest the presence of widespread regulatory genetic networks active in both precancerous and cancerous cervical cells, potentially acting as key drivers of this malignancy. Identifying these molecular genomic signatures could open new avenues for developing therapeutic strategies for cervical cancer, particularly in the realm of precision medicine.

Background: In recent years, the usage of metabolites obtained from plants in the synthesis of noble metal nanoparticles as reducing and stabilizing agents has been investigated, being polyphenols, such as anthocyanins and tannins highlighted due to the variety of beneficial effects that these compounds present in the human health. Objective: This study reports the use of hydrolysable tannins (HT) obtained from Rubus palmeri as a reducing and capping agent in the gold nanoparticles syntheses (AuNPs), as well as their cytotoxic effect on HeLa cell lines. Results: The obtained HT were identified as derivates of ellagic acid (Sanguiin H-6/Lambertianin A, Lambertianin C, and Lambertianin D). Furthermore, a successful synthesis occurred in a 1 mg/mL:1 mM (HT:HAuCl ₄ ) proportion rate at 30 °C, generating a single surface plasmon resonance (SPR) signal at 530 nm. The Fourier-transform infrared spectroscopy (FTIR) proved the interaction between the HT over the AuNPs surface. Additionally, the transmission electron microscopy (TEM) analysis set an average particle size of 22.2 nm and a prevalence of spheres. Moreover, the antioxidant assays showed a variation of two folds between the HT and the AuNPs-HT. Finally, the cytotoxic assay allowed us to establish an IC ₅₀ value at 16.52 µg/mL, indicating an cytotoxic effect in HeLa cells. Conclusion: The results reported herein demonstrate the function of HT in the photosynthesis of AuNPs, producing a colloid with cytotoxic effects on HeLa cells.

Background: In chemoresistance, a variety of oncogenic signaling pathways can be activated and interconnected to combat drug toxicity, making anticancer pharmacological strategies complex. Objective: This study aimed to generate a paclitaxel-chemoresistant cancer cell line scaffold and explore its mechanisms of chemoresistance. Materials and methods: Total RNAs from C-33A and C-33A RPTX (paclitaxel-resistant) cells were sequenced to determine the transcriptome of coding and long non-coding RNAs (lncRNAs). Enrichment analysis of differentially expressed genes (DEGs) was conducted. Flow cytometry was performed to analyze doxorubicin accumulation in C-33A RPTX cells. Results: C33-A RPTX cells achieved a resistance index of 55. 1332 genes were differentially expressed (log2 fold-change>1). Gene ontology (GO) analysis revealed that biological processes, such as angiogenesis and mesenchymal development, were altered, while the mainly altered cellular components were from the extracellular matrix (ECM). Meanwhile, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that signaling pathways, including PI3K/Akt, MAPK, Calcium, ECM-receptor, Rap1, EGFR tyrosine kinase inhibitor resistance, tight junction, and platinum drug resistance, were altered by coding RNAs or long non-coding RNAs (lncRNAs). Finally, the overexpression of the ABCB1 gene in C-33A RPTX cells correlated with a drug efflux phenotype, as evidenced by reduced cellular accumulation of the reporter drug doxorubicin. Alterations in signaling pathways recognized as relevant to chemoresistance and increased drug efflux, driven by changes in the expression patterns of coding RNAs and lncRNAs, may be cooperating to establish resistance to paclitaxel in C-33A RPTX cells. Conclusions: This C-33A RPTX model provides a new experimental platform to study the molecular mechanisms of chemoresistance in cervical cancer. The study integrates both coding and non-coding RNAs, revealing their coordinated alteration in chemoresistance-related signaling pathways. Thus, this dual-level analysis represents a novel systems-level insight into paclitaxel resistance. Beyond descriptive transcriptomics, this resistant model is proposed as a biological platform for testing novel antineoplastic compounds and exploring their mechanisms of action, giving it translational application.

With an incidence of over a half million cases every year, cervical cancer remains a major health problem for women worldwide. Epidemiologic and molecular studies have clearly confirmed a causal role of persistent infection with high-risk human papillomavirus in cervical carcinogenesis, affecting several cellular processes. During cervical cancer development, there is genetic instability including disrupted expression of microRNAs and host target genes, which may have multiple implications. Different studies have explored the gene expression profile in cervical cancer using high-throughput technologies, with the goal of identifying microRNA and/or gene molecular signatures from genomics analysis of cervical cancer. However, the results of some studies have been divergent, which may be due to differences in sample collection procedures, high-throughput platforms, data normalization, and filtering methods used in different protocols. Hence, it is imperative to integrate information about diagnostic or prognostic biomarkers from a variety of sources to characterize the molecular mechanisms of regulatory genetic networks in cervical cancer development and progression. In the present review, we analyze the evidence that describes the role of microRNA signatures and target genes in cervical carcinogenesis and cancer progression. The data reviewed support the existence of universal regulatory genetic networks, which operate in cervical pre-cancerous and cancer cells and may represent the main driving forces in this malignancy. This analysis will allow molecular genomic signatures to be put forward as therapeutic targets for cervical cancer, with potential applications in precision medicine.