Casein kinase 1α inhibition reduces prostate cancer cells viability: Role of the autophagy mechanism.

Screening of drugs on cancer cell lines is a first step in the search for compounds leading to cancer cell death, providing the basis for follow-up investigations. Cell line-based drug sensitivity data can be used for predictive modeling, for example, in the context of drug repurposing. In this work, we report a machine learning framework for the systematic prediction of drug sensitivity based on transcriptomic data from cancer cell line screening. Three different categories of complementary classification models are introduced to predict cell line sensitivities to known drugs based on encoded gene expression profiles, predict activity of new drugs for given cell lines based on compound fingerprints, and predict responses of new cell lines to new drugs based on combined molecular representations and gene expression profiles. The models are found to have adequate predictive performance for cell-based data and are shown to be applicable to predict drug sensitivity for sarcoma cell lines, a rare form of cancer, for which data are limited. For the subset of sarcoma cell lines, tested drugs were also ranked based on cell line sensitivity rates. Taken together, our results suggest that the complementary machine learning models have potential for practical applications to search for new compounds for the treatment of different types of cancers including sarcoma.

Human papillomavirus-positive (HPV+) head and neck squamous cell carcinoma (HNSCC) generally has a better prognosis, but some cases are aggressive with poor outcomes. This study established KUSCC-192, a de novo HPV+ tonsillar cancer cell line, and evaluated its tumorigenicity. The HPV status in KUSCC-192 was assessed using RT-qPCR, RT-PCR, and FISH. Aggressive characteristics were compared with other HPV+ cell lines and HPV- cell lines. KUSCC-192 exhibited a mixed type with a predominantly diffused FISH pattern and a few dotted signals and lower E2 gene expression. These findings, combined with its aggressive features, suggest that the mixed type may contribute to the poor prognosis observed in 2%-30% of HPV+ HNSCC cases. KUSCC-192 is a valuable model to study aggressive HPV+ cancer behaviors. Further research is needed to explore the clinical significance of mixed-type HPV integration in HNSCC.

De novo establishment of a stable brain cell line from Cephalopholis sonnerati (tomato grouper) and transcriptomic dissection of its response to nervous necrosis virus (NNV) infection.

Synthesis and biological evaluation of novel fused pyridopyrimidine derivatives as topoisomerase I inhibitors and as potential antitumor agents: promising results in lung, ovary and gastric cancer.

Iodinated contrast agents decrease the activity of multidrug resistance protein, cell migration, and induce cell death in different tumor cell lines and glioblastoma spheroids.

The time dimension matters: Improving mode of action classification with live-cell imaging

Modeling acquired TKI resistance and effective combination therapeutic strategies in murine RET+ lung adenocarcinoma.

During the 2010 influenza season, the Therapeutic Goods Administration (TGA) reviewed adverse event (AE) signals of febrile convulsions in children following the administration of the seasonal Fluvax® trivalent vaccine. These AEs were attributed to nuclear factor kappa-beta (NF-κB) activation. In response, the TGA developed a method to detect NF-κB activation by vaccine samples. Complementary Toll-Like Receptor (TLR)-expressing reporter cell lines THP1-Blue and Ramos-Blue enabled detection of TLR1-9 activation using the QUANTI-Blue™ system following incubation with a panel of TLR agonists, tumour necrosis factor-alpha (TNF-α), or vaccine sample. Using TNF-α as a positive control and specific Toll-like receptor (TLR) agonists, specificity was confirmed for each cell line based on extracellular (THP1-Blue) or endosomal (Ramos-Blue) TLR expression. Agonists for each cell line demonstrated linearity within the working range, met precision criteria for repeatability and precision. The assay tested viral protein, messenger RNA (mRNA), and bacterial protein vaccines, met accuracy parameter of 80-120 % recovery of spiked controls. We established and validated a robust, sensitive and reliable analytical approach for detecting possible NF-κB activation by bioactive components in vaccines. This assay enables manufacturers and regulators to meet the growing demand for reliable impurity screening assays that support the characterization of vaccines activating the NF-κB pathway. Future studies must further characterise NF-κB activation by individual TLRs across a broader range of vaccines.

Development of a quality control panel based on patient-derived immortalized B-Lymphoblastoid cell lines for thalassemia genotyping.

DeepSTFSynergy: A multi-scale structural information fusion method for personalized drug combination prediction.

Here, we present a protocol to generate an allo-transplantable tumor in mouse models using the YUMM1.7 cell line. We describe steps for mouse breeding using syngeneic C57BL/6 and allogeneic BALB/c mice, injecting the YUMM1.7 melanoma cell line into mice, and collecting and dissociating the growing tumors into single cells. We then detail the procedures for injecting the cells into mice for the generation of an allo-transplantable tumor by progressive passaging into more mismatched hosts. For complete details on the use and execution of this protocol, please refer to Rokan et al.1.

Synthesis and evaluation of Urolithins derivatives as anticancer agents for hepatocellular carcinoma: In vitro, molecular docking, and dynamics simulations.

Polyhydroxylated steroids from the Vietnamese starfish Luidia maculata.

Identification of MA-104 cells as a novel continuous cell line for the direct primary isolation of lumpy skin disease virus.

The function and mechanism of LINC01583 on Osimertinib resistance in non-small cell lung cancer.

Berberine chloride (BRB), an isoquinoline alkaloid isolated from Berberis vulgaris, demonstrated significant anticancer activity against breast cancer. This study assessed the therapeutic effects of BRB on cell proliferation, cell-cycle progression, apoptosis, and metastasis in human (MDA-MB-231) and murine (4T1) triple-negative breast cancer cells. Cytotoxicity testing using a crystal violet assay showed IC₅₀ values of 40 µM for MDA-MB-231 and 10 µM for 4T1 after 48 h of treatment. BRB induced S-phase arrest in MDA-MB-231 and G2/M-phase arrest in 4T1 cells. It also induced late apoptosis in both cell lines, along with increased reactive oxygen species production and loss of mitochondrial membrane potential. Furthermore, BRB exhibited marked anti-metastatic potential by inhibiting cell adhesion, migration, and invasion. Scratch-wound and Transwell assays demonstrated a significant, concentration-dependent reduction in migratory capacity, while 3D spheroid assays confirmed strong suppression of invasive behavior. BRB also reduced adhesion to extracellular matrix components, particularly collagen IV. At the molecular level, BRB significantly downregulated MMP2 and MMP9 mRNA expression in both cell lines, supporting its role in inhibiting extracellular matrix remodeling and metastatic progression. Molecular docking simulations indicated that BRB has a favorable binding energy with multiple cancer-related targets, including MDM2-P53, BCL2, Caspases (3, 8, and 9), MCL1 complexes, and matrix metalloproteinases (MMP-2 and MMP-9). The compound maintained stable hydrogen bonds, ππ-stacking interactions, and hydrophobic contacts, often achieving higher docking scores than the co-crystallized ligand. Overall, the results suggest that BRB exerts multi-targeted anticancer effects by regulating processes such as proliferation, apoptosis, migration, and adhesion, indicating that BRB could be a promising candidate for breast cancer therapy.

As a frequently occurring malignant disorder in women, breast cancer (BC) is closely associated with circular RNAs (circRNAs) in mediating its pathological progression. Accumulating evidence suggests that hsa_circ_0001588 promotes BC via microRNA (miRNA) sponging. To investigate the expression dynamics, functional contributions, and molecular underpinnings of hsa_circ_0001588 in BC progression, focusing on its regulatory axis with miR-525-3p and KPNB1. Clinical BC tissues and cell lines were used to validate hsa_circ_0001588 expression via RT-qPCR. Cell proliferation was evaluated via MTT assay, whereas migration and invasion capacities were assessed using Transwell systems. Dual-luciferase reporter assays and RIP were implemented to validate the reciprocal interactions among hsa_circ_0001588, miR-525-3p, and KPNB1. Rescue strategies involving miR-525-3p inhibition or KPNB1 overexpression were thereafter executed to validate the regulatory axis. Hsa_circ_0001588 exhibited elevated expression in BC tissues and cell lines, demonstrating positive associations with advanced TNM staging and unfavorable prognosis. Depletion of hsa_circ_0001588 impaired proliferative, migratory, and invasive capacities, as well as EMT in cells. Mechanistically, hsa_circ_0001588 directly binds to miR-525-3p, relieving its repression on KPNB1. The inhibitory effects resulting from the knockdown of hsa_circ_0001588 can be reversed by either inhibiting miR-525-3p or overexpressing KPNB1. Hsa_circ_0001588 emerges as a critical regulator of BC malignancy by modulating the miR-525-3p/KPNB1 axis. Its overexpression correlates with poor prognosis, positioning it as a promising diagnostic marker and actionable therapeutic target. The online version contains supplementary material available at 10.1007/s10616-026-00920-0.

Differential metabolic responses to hydrogen peroxide-induced oxidative stress in parotid and submandibular gland acinar cell lines.

Variations in DNA repair gene expression and cyto-genotoxic evaluation of bisphenol S in Madin-Darby Bovine Kidney (MBDK) cell line.