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At present, cancers have been causing deadly fears to humans and previously unpredictable losses to health. Especially, lung cancer is one of the most common causes of cancer-related mortality accounting for approximately 15% of all cancer cases worldwide. While Non-Small Cell Lung Carcinomas (NSCLCs) makes up to 80% of lung cancer cases. The patient compliance has been weakening because of serious drug resistance and adverse drug effects. Therefore, there is an urgent need for the development of novel structural agents to inhibit NSCLCs. Nitrogen-containing heterocyclic compounds exhibit wide range of biological properties, especially antitumor activity. We reviewed some deadly defects of clinical medicines for the lung cancer therapy and importance of nitrogen based heterocyclic derivatives against NSCLCs. Nitrogen heterocycles exhibit significant antitumor activity against NSCLCs. Nitrogen heterocyclic hybrids could be developed as multi-target-directed NSCLC inhibitors and it is believed that the review is significant for rational designs and new ideas in the development of nitrogen heterocyclic-based drugs.
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http://dx.doi.org/10.2174/1389557519666190312152358 | DOI Listing |
EMBO J
September 2025
Department of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University; Frontier Science Center for Immunology and Metabolism, Taikang Center for Life and Medical Sciences; Wuhan University, Wuhan, 430071, China.
Inadequate antigen presentation by MHC-I in tumor microenvironment (TME) is a common immune escape mechanism. Here, we show that glycine decarboxylase (GLDC), a key enzyme in glycine metabolism, functions as an inhibitor of MHC-I expression in EGFR-activated tumor cells to induce immune escape by a mechanism independent of its enzymatic activity. Upon EGFR activation, GLDC is phosphorylated by SRC and subsequently translocated to the nucleus in human NSCLC cells.
View Article and Find Full Text PDFOncogene
September 2025
Department of Molecular Medicine and Biochemistry, Akita University Graduate School of Medicine, Akita, Japan.
Forkhead-box-protein P3 (FOXP3) is a key transcription factor in T regulatory cells (Tregs). However, its expression and significance in non-immune stromal cells in the tumor microenvironment remain unclear. Here, we demonstrated FOXP3 expression in stromal fibroblasts of mouse and human gastrointestinal tumors.
View Article and Find Full Text PDFBiochem Pharmacol
September 2025
Department of Biosciences, JIS University, 81, Nilgunj Road, Agarpara, Kolkata, West Bengal 700109, India. Electronic address:
The malignant manifestation of breast cancer is driven by complex molecular alterations that extend beyond genetic mutations to include epigenetic dysregulation. Among these, DNA methylation is a critical and reversible epigenetic modification that significantly influences breast cancer initiation, progression, and therapeutic resistance. This process, mediated by DNA methyltransferases (DNMTs), involves the addition of methyl groups to cytosine residues within CpG dinucleotides, resulting in transcriptional repression of genes.
View Article and Find Full Text PDFEur J Med Chem
September 2025
Shanghai Frontiers Science Center of Drug Target Identification and Delivery, National Key Laboratory of Innovative Immunotherapy, School of Pharmaceutical Sciences, Shanghai Jiao Tong University, Shanghai, 200240, China; State Key Laboratory of Innovative Immunotherapy, Central Research Institute,
Overexpression of protein lysine methyltransferase G9a, which catalyzes mono- and di-methylation of histone H3K9 and non-histone proteins, is closely associated with poor prognosis and metastasis of various cancers. Here, we designed and synthesized a series of novel G9a inhibitors bearing 2-tetrahydroisoquinoline substituted quinazoline scaffold. Among them, compound 31 with 2-dioxole fused tetrahydroisoquinoline exhibited the most potent inhibitory effects against G9a with an IC value of 0.
View Article and Find Full Text PDFPathol Res Pract
September 2025
Department of Biotechnology, Delhi Technological University, India. Electronic address:
The intricate interplay between cancer and autoimmune diseases (ADs) is rooted in immune dysregulation, where genetic susceptibility, chronic inflammation, epigenetic modifications, and immunosuppressive therapies contribute to tumorigenesis. The dualistic nature of immune activation complicates therapeutic strategies, as immune checkpoint inhibitors and other immune-stimulatory therapies may exacerbate underlying ADs, leading to immune-related adverse events (irAEs), including organ toxicity, dermatologic reactions, and disease flares. Conversely, immunosuppressive treatments aimed at controlling ADs can compromise anti-tumor immunity and reduce the efficacy of cancer therapies.
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