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BACKGROUND: Breast cancer (BC) is one of the most common cancers among women. Since diverse features can be collected, how to stably select the powerful ones for accurate BC diagnosis remains challenging. METHODS: A hybrid framework is designed for successively investigating both feature ranking (FR) stability and cancer diagnosis effectiveness. Specifically, on 4 BC datasets (BCDR-F03, WDBC, GSE10810 and GSE15852), the stability of 23 FR algorithms is evaluated via an advanced estimator (S), and the predictive power of the stable feature ranks is further tested by using different machine learning classifiers. RESULTS: Experimental results identify 3 algorithms achieving good stability ([Formula: see text]) on the four datasets and generalized Fisher score (GFS) leading to state-of-the-art performance. Moreover, GFS ranks suggest that shape features are crucial in BC image analysis (BCDR-F03 and WDBC) and that using a few genes can well differentiate benign and malignant tumor cases (GSE10810 and GSE15852). CONCLUSIONS: The proposed framework recognizes a stable FR algorithm for accurate BC diagnosis. Stable and effective features could deepen the understanding of BC diagnosis and related decision-making applications.
Assuntos
Neoplasias da Mama , Feminino , Humanos , Neoplasias da Mama/diagnóstico , Algoritmos , Aprendizado de MáquinaRESUMO
INTRODUCTION: Dendritic cells (DC) are involved in immune recognition, response and immunomodulation mechanisms related to the onset of cancer. OBJECTIVE: To explore DCs mechanism in the inhibition of autophagy in hepatoma cells. METHODS: Human peripheral blood mononuclear cells were isolated by Ficoll density gradient centrifugation and induced into DCs, which were co-cultured with HepG2 cells by Transwell migration assay. HepG2 cell activity was determined using the CCK8 assay. LC3 autophagy index expression was measured with Western blot analysis, and the expression and secretion of cytokines, with qRT-PCR and ELISA. RESULTS: In the co-culture system, DCs were able to reduce HepG2 cells viability; IL-2, IL-12, IL-10 and IFN-γ expression in DCs was also significantly inhibited, although IL-2 and IFN-γ were still expressed 0.6 and 0.53 more than in the control group. CONCLUSION: DCs can regulate autophagy in hepatocellular carcinoma cells. The mechanism may be related to the synthesis and release of cytokines such as IL-2, IL-12 and IFN-γ by DCs.
INTRODUCCIÓN: Las células dendríticas (CD) están involucradas en el reconocimiento, respuesta y modulación inmunológicos relacionados con la aparición del cáncer. OBJETIVO: Explorar el mecanismo de las CD en la inhibición de la autofagia de las células del hepatoma. MÉTODOS: Células mononucleares de sangre periférica humana se aislaron mediante centrifugación en gradiente de densidad de Ficoll y se indujeron en CD, las cuales fueron cocultivadas con células HepG2 por ensayo de migración Transwell. La actividad de las células HepG2 se determinó mediante ensayo CCK8. La expresión del índice de autofagia LC3 se midió con análisis de transferencia Western y la expresión y secreción de citocinas mediante qRT-PCR y ELISA. RESULTADOS: En el sistema de cocultivo, las CD redujeron la viabilidad de HepG2; la expresión de IL-2, IL-12, IL-10 e IFN-γ en CD también se inhibió significativamente, si bien IL-2 e IFN-γ aún se expresaron 0.6 y 0.53 más que en el grupo de control. CONCLUSIÓN: Las CD pueden regular la autofagia de las células del carcinoma hepatocelular. El mecanismo puede estar relacionado con la síntesis y liberación de citocinas como IL-2, IL-12 e IFN-γ por parte de las CD.
Assuntos
Carcinoma , Leucócitos Mononucleares , Humanos , Leucócitos Mononucleares/metabolismo , Interleucina-2/metabolismo , Interleucina-12/metabolismo , Citocinas , Autofagia , Células Dendríticas/metabolismo , Carcinoma/metabolismoRESUMO
Neurogenesis contributes to poststroke recovery. Long noncoding RNAs (lncRNAs) participate in the regulation of stem cell self-renewal and differentiation. However, the role of lncRNAs in stroke-induced neurogenesis remains unknown. In this study, we found that H19 was the most highly upregulated lncRNA in neural stem cells (NSCs) of the subventricular zone (SVZ) of rats subjected to focal cerebral ischemia. Deletion of H19 suppressed cell proliferation, promoted cell death, and blocked NSC differentiation. RNA sequencing analysis revealed that genes deregulated by H19 knockdown were those that are involved in transcription, apoptosis, proliferation, cell cycle, and response to hypoxia. H19 knockdown significantly increased the transcription of cell cycle-related genes including p27, whereas overexpression of H19 substantially reduced expression of these genes through the interaction with chromatin remodeling proteins EZH2 and SUZ12. Moreover, H19 regulated neurogenesis-related miRNAs. Inactivation of H19 in NSCs of ischemic rats attenuated spontaneous functional recovery after stroke. Collectively, our data provide novel insights into the epigenetic regulation of lncRNAs in stroke-induced neurogenesis.
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Neurogênese/genética , RNA Longo não Codificante/genética , Acidente Vascular Cerebral/genética , Acidente Vascular Cerebral/patologia , Animais , Diferenciação Celular/fisiologia , Proteína Potenciadora do Homólogo 2 de Zeste/genética , Proteína Potenciadora do Homólogo 2 de Zeste/metabolismo , Epigênese Genética , Masculino , MicroRNAs , Células-Tronco Neurais/metabolismo , Células-Tronco Neurais/patologia , Neurônios/metabolismo , Neurônios/patologia , Complexo Repressor Polycomb 2/genética , Complexo Repressor Polycomb 2/metabolismo , RNA Longo não Codificante/metabolismo , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos , Ratos Wistar , Acidente Vascular Cerebral/metabolismo , Regulação para CimaRESUMO
AIMS/HYPOTHESIS: Diabetic peripheral neuropathy (DPN) is one of the major complications of diabetes, which contributes greatly to morbidity and mortality. There is currently no effective treatment for this disease. Exosomes are cell-derived nanovesicles and play an important role in intercellular communications. The present study investigated whether mesenchymal stromal cell (MSC)-derived exosomes improve neurological outcomes of DPN. METHODS: Exosomes were isolated from the medium of cultured mouse MSCs by ultracentrifugation. Diabetic mice (BKS.Cg-m+/+Leprdb/J, db/db) at the age of 20 weeks were used as DPN models. Heterozygous mice (db/m) of the same age were used as the control. MSC-exosomes were administered weekly via the tail vein for 8 weeks. Neurological function was evaluated by testing motor and sensory nerve conduction velocities, and thermal and mechanical sensitivity. Morphometric analysis was performed by myelin sheath staining and immunohistochemistry. Macrophage markers and circulating cytokines were measured by western blot and ELISA. MicroRNA (miRNA) array and bioinformatics analyses were performed to examine the exosomal miRNA profile and miRNA putative target genes involved in DPN. RESULTS: Treatment of DPN with MSC-exosomes markedly decreased the threshold for thermal and mechanical stimuli and increased nerve conduction velocity in diabetic mice. Histopathological analysis showed that MSC-exosomes markedly augmented the density of FITC-dextran perfused blood vessels and increased the number of intraepidermal nerve fibres (IENFs), myelin thickness and axonal diameters of sciatic nerves. Western blot analysis revealed that MSC-exosome treatment decreased and increased M1 and M2 macrophage phenotype markers, respectively. Moreover, MSC-exosomes substantially suppressed proinflammatory cytokines. Bioinformatics analysis revealed that MSC-exosomes contained abundant miRNAs that target the Toll-like receptor (TLR)4/NF-κB signalling pathway. CONCLUSIONS/INTERPRETATION: MSC-derived exosomes alleviate neurovascular dysfunction and improve functional recovery in mice with DPN by suppression of proinflammatory genes.
Assuntos
Neuropatias Diabéticas/metabolismo , Exossomos/metabolismo , Células-Tronco Mesenquimais/citologia , Animais , Células Cultivadas , Diabetes Mellitus Experimental , Modelos Animais de Doenças , Imuno-Histoquímica , Macrófagos/citologia , Macrófagos/metabolismo , Masculino , Células-Tronco Mesenquimais/metabolismo , Camundongos , MicroRNAs/metabolismo , Nervo Isquiático/fisiologia , Vasa Nervorum/citologia , Vasa Nervorum/metabolismoRESUMO
Pancreatic ductal adenocarcinoma (PDAC) is the most prevalent and aggressive form of pancreatic cancer. Gemcitabine (GEM), the firstline treatment for PDAC, which alleviates symptoms and enhances the quality of life of patients. However, it is prone to lead to the development of drug resistance during treatment. Interferon (IFN)γ exhibits antitumor and immunomodulatory properties. The present study aimed to explore the impact of IFNγ on the viability, migration and apoptosis of GEMresistant pancreatic cancer cells. Firstly, a GEMresistant pancreatic cancer cell line, named PANC1/GEM, was constructed. Hematoxylin and eosin staining analyzed the cell morphology, whereas reverse transcriptionquantitative PCR (RTqPCR) assessed the expression levels of the drugresistance genes multidrug resistanceassociated protein (MRP) and breast cancer resistance protein (BCRP). The MTT assay and cell counting techniques were used to determine the appropriate concentration of IFNy and its effects on cell viability. The IFNγinduced apoptosis of PANC1/GEM cells was assessed using an Apoptosis Detection Kit, whereas the impact of IFNγ on the migration of these cells was evaluated using a woundhealing assay. The MTT assay revealed a resistance index of 22.4 in the PANC1/GEM cell line. RTqPCR indicated that, compared with in wildtype cells, the PANC1/GEM resistant strain exhibited lower MRP and higher BCRP mRNA expression levels. The optimal concentration of IFNγ for affecting PANC1/GEM cells was determined to be 0.3 µg/ml. At this concentration, IFNγ induced PANC1/GEM cell apoptosis, along with a notable reduction in migration. Following treatment of PANC1/GEM cells with IFNγ, MRP expression increased whereas BCRP mRNA expression decreased, indicating a reversal in their drugresistance gene expression. In conclusion, IFNγ exhibited antitumor immune properties by upregulating MRP and downregulating BCRP expression, reversing drugresistance gene expression, and reducing cell viability and migration, while promoting apoptosis in PANC1/GEM cells. IFNγ could potentially serve as a treatment option for patients with GEMresistant pancreatic cancer.
Assuntos
Carcinoma Ductal Pancreático , Neoplasias Pancreáticas , Humanos , Gencitabina , Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/genética , Desoxicitidina/farmacologia , Qualidade de Vida , Resistencia a Medicamentos Antineoplásicos/genética , Linhagem Celular Tumoral , Proteínas de Neoplasias/metabolismo , Neoplasias Pancreáticas/tratamento farmacológico , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/metabolismo , Carcinoma Ductal Pancreático/tratamento farmacológico , Carcinoma Ductal Pancreático/genética , Carcinoma Ductal Pancreático/metabolismo , Apoptose , RNA MensageiroRESUMO
Small extracellular vesicles (sEVs) have the ability to transfer genetic material between cells, but their role in mediating HBV infection and regulating M1 macrophages to promote immune evasion remains unclear. In this study, we utilized PMA + LPS + IFN-γ to induce THP-1 into M1 macrophages. We then extracted sEVs from HepG2.2.15 cell and treated the M1 macrophages with these sEVs. QPCR detection revealed the presence of HBV-DNA in the M1 macrophages. Additionally, RT-qPCR and WB analysis demonstrated a significantly decreased in the expression of TLR4, NLRP3, pro-caspase-1, caspase-1p20, IL-1ß and IL-18 in the M1 macrophages (P < 0.05). Furthermore, RT-qPCR results displayed high expression levels of that miR-146a and FEN-1 in the sEVs derived from HepG2.2.15 cells (P < 0.01). RT -qPCR and WB analysis showed that these sEVs enhanced the expression of FEN-1 or miR-146a in the M1 macrophages through miR-146a or FEN-1 (P < 0.05), while simultaneously reducing the expression of TLR4, NLRP3, caspase-1p20, IL-1ß and IL-18 in the M1 macrophages (P < 0.05). In summary, our findings indicate that sEVs loaded with HBV inhibit the inflammatory function of M1 macrophages and promote immune escape. Additionally, miR-146a and FEN-1 present in the sEVs play a crucial role in this process.
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Vesículas Extracelulares , Vírus da Hepatite B , Hepatite B , Evasão da Resposta Imune , Macrófagos , MicroRNAs , Humanos , Vesículas Extracelulares/metabolismo , Vesículas Extracelulares/imunologia , Vírus da Hepatite B/imunologia , Macrófagos/imunologia , Macrófagos/metabolismo , Macrófagos/virologia , MicroRNAs/genética , MicroRNAs/metabolismo , Células Hep G2 , Hepatite B/virologia , Hepatite B/imunologia , Hepatite B/metabolismo , Receptor 4 Toll-Like/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Interleucina-18/metabolismo , Células THP-1RESUMO
This study examined exosomal hepatitis B virus (HBV)-DNA levels in chronic HBV infection (CHB). Patients were grouped according to the European Association for the Study of the Liver classification (1: HBV-DNA-positive CHB, normal alanine aminotransferase [ALT]; 2: HBV-DNA-positive CHB, elevated ALT; 3: HBV-DNA-negative HBeAb-positive CHB, normal ALT; 4: HBV-DNA-positive HBeAg-negative HBeAb-positive CHB, elevated ALT; 5: HBV-DNA-negative, HBcAb-positive; 6: HBV-negative, normal ALT). Exosomes were isolated, comparative analysis of exosomes and serum HBV-DNA. The HBV-DNA content was lower in exosomes than in serum for groups 1, 2, and 4 (all P < 0.05). In the groups negative for serum HBV-DNA (groups 3 and 5), the exosomal HBV-DNA levels were higher than the serum HBV-DNA levels (all P < 0.05). The exosomal and serum HBV-DNA levels were correlated in groups 2 (R 2 = 0.84) and 4 (R 2 = 0.98). The exosomal HBV-DNA levels were correlated with total bilirubin (R 2 = 0.94), direct bilirubin (R 2 = 0.82), and indirect bilirubin (R 2 = 0.81) in group 5 (all P < 0.05). In patients with CHB and negative for serum HBV-DNA, exosomal HBV-DNA was detectable and could be used to monitor the treatment effects. Exosomal HBV-DNA could be used in patients with a high suspicion of HBV infection but negative for serum HBV-DNA.
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AIM: Hepatitis B virus (HBV) is a major cause of a variety of liver diseases. Existing antiviral drugs cannot eradicate HBV from our body, and the main reason is unclear on the molecular mechanism of HBV replication. Flap endonuclease 1 (FEN1) can repair relaxed circular DNA (HBV rcDNA) to covalently closed circular DNA (HBV cccDNA) that promotes HBV DNA replication, while its specific regulatory detail remains unclear. In addition, miR-146a is close related to regulation in HBV replication. This study aims to explore whether miR-146a regulates HBV cccDNA formation through FEN1. MAIN METHODS: We investigated the expression of miR-146a, FEN1 and HBV copies in HBV stable replication cell line HepG2.2.15 and its parent cell line HepG2 transfected miR-146a and FEN1 plasmid by qRT-PCR and western blot, to identify the cooperation of Argonaute-2 (Ago2) and miR-146a by Ago2 siRNA and Ago2 RNA Binding Protein Immunoprecipitation (RIP). KEY FINDINGS: Compared with the control group, we found that the expression of miR-146a was significantly up-regulated in HepG2.2.15, and the expression of FEN1 and HBV copies were also significantly up-regulated. On contrary, the expression of target gene of miR-146a, interleukin-1 receptor-associated kinase 1 (IRAK1) and tumor necrosis factor receptor-associated factor-6 (TRAF6), was significantly decreased in HepG2.2.15. With the use of Ago2 siRNA and then Ago2 RIP, we found that Ago2 performed as a carrier for miR-146a to promote HBV replication. SIGNIFICANCE: The results suggest a novel miR-146a â FEN1 â HBV DNA regulatory axis in HBV replication life. Ago2 cooperates with miR-146a to regulate the transcription and expression level of FEN1 protein through the downstream target gene IRAK1/TRAF6, and to promote HBV replication.
Assuntos
Proteínas Argonautas/genética , Vírus da Hepatite B/fisiologia , MicroRNAs/genética , Replicação Viral/genética , DNA Circular/genética , DNA Viral/genética , Endonucleases Flap/genética , Células Hep G2 , Humanos , Quinases Associadas a Receptores de Interleucina-1/genética , Peptídeos e Proteínas de Sinalização Intracelular/genéticaRESUMO
Resumen Introducción: Las células dendríticas (CD) están involucradas en el reconocimiento, respuesta y modulación inmunológicos relacionados con la aparición del cáncer. Objetivo: Explorar el mecanismo de las CD en la inhibición de la autofagia de las células del hepatoma. Métodos: Células mononucleares de sangre periférica humana se aislaron mediante centrifugación en gradiente de densidad de Ficoll y se indujeron en CD, las cuales fueron cocultivadas con células HepG2 por ensayo de migración Transwell. La actividad de las células HepG2 se determinó mediante ensayo CCK8. La expresión del índice de autofagia LC3 se midió con análisis de transferencia Western y la expresión y secreción de citocinas mediante qRT-PCR y ELISA. Resultados: En el sistema de cocultivo, las CD redujeron la viabilidad de HepG2; la expresión de IL-2, IL-12, IL-10 e IFN-γ en CD también se inhibió significativamente, si bien IL-2 e IFN-γ aún se expresaron 0.6 y 0.53 más que en el grupo de control. Conclusión: Las CD pueden regular la autofagia de las células del carcinoma hepatocelular. El mecanismo puede estar relacionado con la síntesis y liberación de citocinas como IL-2, IL-12 e IFN-γ por parte de las CD.
Abstract Introduction: Dendritic cells (DC) are involved in immune recognition, response and immunomodulation mechanisms related to the onset of cancer. Objective: To explore DCs mechanism in the inhibition of autophagy in hepatoma cells. Methods: Human peripheral blood mononuclear cells were isolated by Ficoll density gradient centrifugation and induced into DCs, which were co-cultured with HepG2 cells by Transwell migration assay. HepG2 cell activity was determined using the CCK8 assay. LC3 autophagy index expression was measured with Western blot analysis, and the expression and secretion of cytokines, with qRT-PCR and ELISA. Results: In the co-culture system, DCs were able to reduce HepG2 cells viability; IL-2, IL-12, IL-10 and IFN-γ expression in DCs was also significantly inhibited, although IL-2 and IFN-γ were still expressed 0.6 and 0.53 more than in the control group. Conclusion: DCs can regulate autophagy in hepatocellular carcinoma cells. The mechanism may be related to the synthesis and release of cytokines such as IL-2, IL-12 and IFN-γ by DCs.
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MicroRNA-146a (miR-146a) regulates multiple immune diseases. However, the role of miR-146a in diabetic peripheral neuropathy (DPN) has not been investigated. We found that mice (db/db) with type 2 diabetes exhibited substantial downregulation of miR-146a in sciatic nerve tissue. Systemic administration of miR-146a mimics to diabetic mice elevated miR-146a levels in plasma and sciatic nerve tissue and substantially increased motor and sensory nerve conduction velocities by 29 and 11%, respectively, and regional blood flow by 50% in sciatic nerve tissue. Treatment with miR-146a mimics also considerably decreased the response in db/db mice to thermal stimuli thresholds. Histopathological analysis showed that miR-146a mimics markedly augmented the density of fluorescein isothiocyanate-dextran-perfused blood vessels and increased the number of intraepidermal nerve fibers, myelin thickness, and axonal diameters of sciatic nerves. In addition, miR-146a treatment reduced and increased classically and alternatively activated macrophage phenotype markers, respectively. Analysis of miRNA target array revealed that miR-146a mimics greatly suppressed expression of many proinflammatory genes and downstream related cytokines. Collectively, our data indicate that treatment of diabetic mice with miR-146a mimics robustly reduces DPN and that suppression of hyperglycemia-induced proinflammatory genes by miR-146a mimics may underlie its therapeutic effect.
Assuntos
Diabetes Mellitus Tipo 2/complicações , Neuropatias Diabéticas/prevenção & controle , MicroRNAs/fisiologia , Animais , Citocinas/genética , Quinases Associadas a Receptores de Interleucina-1/genética , Ativação de Macrófagos , Masculino , Camundongos , Bainha de Mielina/fisiologia , NF-kappa B/fisiologia , Fluxo Sanguíneo Regional , Nervo Isquiático/irrigação sanguínea , Nervo Isquiático/fisiologia , Fator 6 Associado a Receptor de TNF/genéticaRESUMO
Chronic hepatitis B virus (HBV) infection is a worldwide problem and HBV reactivation following anticancer chemotherapy has become an emerging clinical challenge. However, the mechanisms of HBV reactivation following chemotherapy remain unclear. Epirubicin is an anthracycline drug used in chemotherapy to treat numerous types of malignancy, including breast cancer, acute leukemia, malignant lymphoma, lung cancer, ovarian cancer and stomach cancer. Epirubicin acts by intercalating DNA strands and inhibiting DNA and RNA synthesis. In this study, it was demonstrated that epirubicin directly upregulated the levels of in vitro HBV replication in a concentration-dependent manner. Exposure to epirubicin for 24 h induced >11- and 6-fold increases in the levels of intracellular and secreted HBV DNA, respectively. In concordance with the elevated levels of HBV DNA, the expression levels of HBV pregenomic RNA, intracellular HBV surface and HBV core antigens, and secreted HBV e antigen were significantly increased by treatment with 0.5 µM epirubicin. Notably, epirubicin promoted cellular excretion of HBV nucleocapsids, which are closely associated with the pathological effects of HBV, including acute liver failure. In conclusion, epirubicin exhibited a direct stimulatory effect on HBV replication and this may be a novel mechanism of HBV reactivation following cytotoxic anticancer chemotherapy.
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Antineoplásicos/farmacologia , Epirubicina/farmacologia , Vírus da Hepatite B/fisiologia , Ativação Viral/efeitos dos fármacos , Replicação Viral/efeitos dos fármacos , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , DNA Viral/metabolismo , Tratamento Farmacológico , Vírus da Hepatite B/efeitos dos fármacos , Humanos , Nucleocapsídeo/metabolismo , RNA Viral/metabolismo , Regulação para Cima/efeitos dos fármacos , Vírion/metabolismoRESUMO
HBV infections leads to severe public health problems around the world, especially in China. Improved understanding of the molecular mechanisms of HBV reverse transcription is fundamental for optimization of treatment and solution to drug-resistance. Recently, the main structural basis involved in the process of HBV reverse transcription and the cis-elements were revealed by means of biochemistry and genetics. The entire process of reverse transcription is completed mainly through the first template switch mediated by the P- epsilon structure; the second template switch mediated by 5E/3E and M structure; and the third template switch mediated by 5' r / 3' r structure. The important structure and the cis-elements involved in this process are the focus of this review, at the same time, an overview of the progress in relevent studies is demonstrated to show the whole picture of the HBV reverse process.
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Vírus da Hepatite B/genética , Hepatite B/virologia , Transcrição Reversa , Animais , Vírus da Hepatite B/enzimologia , Vírus da Hepatite B/metabolismo , Humanos , RNA Viral/genética , DNA Polimerase Dirigida por RNA/genética , DNA Polimerase Dirigida por RNA/metabolismo , Proteínas Virais/genética , Proteínas Virais/metabolismoRESUMO
The relax circle DNA (rcDNA) sequence and the covalently closed circle DNA (cccDNA) sequence in hepatitis B virus (HBV) are crucial regions for HBV infections. To analyze mutations in rcDNA and cccDNA, DNA sequencing is often used, although it is time-consuming and expensive. Herein, we report a simple, economic, albeit accurate allele-specific polymerase chain reaction (AS-PCR) to detect mutations in these regions of HBV. This method can be extensively used to screen for mutations at specific positions of HBV genome.
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DNA Circular/genética , DNA Viral/genética , Vírus da Hepatite B/genética , Mutação Puntual , Reação em Cadeia da Polimerase/métodos , Virologia/métodos , Alelos , Custos e Análise de Custo , Programas de Rastreamento/métodos , Reação em Cadeia da Polimerase/economia , Sensibilidade e Especificidade , Virologia/economiaRESUMO
In the binuclear title molecule, [Zn(2)(C(9)H(7)NO(4))Cl(2)(C(12)H(8)N(2))(2)], the two metal centres are bridged by a 2,6-dimethylpyridine-3,5-dicarboxylate ligand. The binuclear unit is extended to form a two-dimensional supramolecular motif via pi-pi stacking interactions between neighbouring phenanthroline rings.