IST-MES2

Name: IST-MES2
Brand: Creative Bioarray

Cat.No.: CSC-6274W

Species: Homo sapiens (Human)

Source: Pleural Effusion

Morphology: grown as monolayer, epithelial-like

Culture Properties: Adherent

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Cat.No.

CSC-6274W

Description

established from the pleural effusion of a 71- year- old Caucasian man with pleural epithelioid mesothelioma

Species

Homo sapiens (Human)

Source

Pleural Effusion

Recommended Medium

DMEM + 10% FBS + 2mM L-Glutamine + 1% non-essential amino acids

Culture Properties

Adherent

Morphology

grown as monolayer, epithelial-like

Disease

Pleural Epithelioid Mesothelioma

Quality Control

Mycoplasma: negative in PCR assays
Viruses: PCR: HBV -, HCV -, HHV-8 -, HIV-1 -, HIV-2 -, HTLV-I/II -, MLV -, SMRV -

Storage and Shipping

ship in dry ice; store in liquid nitrogen

Synonyms

IST-Mes2; IST-MES-2; ISTMES2; IstMes2; Istituto Scientifico Tumori-Mesothelioma 2

Citation Guidance

If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

IST-MES2 is a continuously growing human malignant pleural mesothelioma (MPM) cell line established in 1997 from the pleural effusion of a 71-year-old Caucasian male patient with histologically confirmed pleural epithelioid mesothelioma. IST-MES2 exhibits an adherent, epithelial-like morphology with spindle-shaped cells that form a characteristic cobblestone-like pattern at confluence. Karyotypically, the cell line is hypodiploid and displays complex chromosomal alterations, including losses in chromosome arms 9p and 22q, which are commonly associated with mesothelioma pathogenesis.

IST-MES2 expresses canonical mesothelial markers including calretinin, WT-1, and cytokeratin, while lacking EGFR amplification. Notably, the cells also express stemness-associated markers such as CD24, ABCG2, and OCT4, rendering them valuable for investigating mechanisms of drug resistance and metastatic progression in MPM. The cell line constitutively produces IL-6 and TGF-β2, and exhibits positive immunoreactivity for CAM5.2 and HBME-1. IST-MES2 has a doubling time ranging from 37 to 87 hours and reaches exponential growth within 4-7 days post-plating. Importantly, IST-MES2 cells are non-tumorigenic in nude mice upon orthotopic pleural injection, distinguishing this epithelioid line from biphasic counterparts such as IST-MES3 and MM-B1, which readily form pleural tumors.

IST-MES2 serves as a robust in vitro model for studying MPM biology, asbestos-related oncogenesis, and therapeutic resistance. The line has been extensively utilized in preclinical screening of chemotherapeutics, targeted agents, and immunotherapies. Furthermore, the availability of multiple CRISPR-engineered knockout derivatives-targeting genes involved in O-GlcNAcylation (OGT), N-glycan branching (MGAT4C), core fucosylation (FUT8), O-glycosylation (C1GALT1), and glycosaminoglycan biosynthesis (XYLT2)-positions IST-MES2 as a versatile platform for dissecting the role of glycosylation and post-translational modifications in mesothelioma pathogenesis.

Identification of non-covalent inhibitors for the atypical peroxiredoxin PRDX5 as a therapeutic strategy in malignant pleural mesothelioma

bioRxiv | DOI | Paper 2026 | By Josep Monserrat, Floriane Montanari, Victor Laurent, Pierre-Benoit Ancey, Nicolas Jean, Cécilia Jeannu, Guimin Wang, Genshu You, Qiancheng Shen, Alice Mac Kain, Yacine Bareche, Loïc Herpin, Nadia Jeremiah, Roberta Codato, Alberto Romagnoni, Alex J. Cornish, Ekaterina Rozhavskaya, Lucia Pattarini, Constance Petit, Pierre-Joachim Zindy, Jinal Shukla, Sylvie Gomez, MOSAIC Consortium, Markus Eckstein, Almoatazbellah Youssef, Ulrich Keilholz, Markus Morkel, Krisztian Homicsko, Chiara Saglietti, Leilei Shi, Jian Zhang, Elodie Pronier

Background

This bioRxiv preprint identifies peroxiredoxin 5 (PRDX5) as a subtype-specific vulnerability in malignant pleural mesothelioma (MPM). Using MOSAIC single-cell and spatial transcriptomics, PRDX5 is upregulated in epithelioid MPM and correlates with resistance to oxidative/nitrosative stress. Machine-learning-guided pocket detection and virtual screening of 3.6 million compounds followed by biochemical validation yielded 36 non-covalent PRDX5 inhibitors, including sub-micromolar hits. The study nominates PRDX5 as a therapeutic target and provides chemical starting points for redox-modulating precision oncology in MPM.

Key Findings

PRDX5 is significantly upregulated in epithelioid malignant pleural mesothelioma (MPM) compared with sarcomatoid and biphasic subtypes, validated in an independent cohort where 97% of tumors expressed PRDX5 in >50% of cells and 73% showed moderate-to-strong staining. MPM cell lines resist peroxynitrite and H2O2 more than healthy mesothelial cells, correlating with basal PRDX5 expression. PRDX5-positive malignant cells are enriched for hypoxia, ROS detoxification, and RNS metabolism signatures, particularly in tumor cores. Using AlloDeep/AlloTango, the authors identified three putative allosteric pockets (G85, alpha3, alpha5) and virtually screened 3.6 million compounds. Biochemical testing of 452 candidates yielded 36 non-covalent inhibitors (8% hit rate), including 13 potent and 23 weakly active hits. G85 and alpha3 leads showed IC50 values of 4.46 µM and 9.81 µM, respectively, with an azetidine-containing scaffold. This establishes PRDX5 as a subtype-specific MPM target and provides new chemical tools for redox-modulating cancer therapy.

Contribution

Creative Bioarray provided the human malignant pleural mesothelioma cell lines IST-MES-1 and IST-MES-2, which were used for PRDX5 target validation, oxidative/nitrosative stress sensitivity assays, and protein expression analysis. These cell models were essential for confirming PRDX5-mediated stress resistance and supporting the therapeutic rationale.

Fig. 1. PRDX5 is highly expressed in epithelioid MPM patients.

FABP5 Silencing Affects Mesothelioma Cell Dynamics and Metabolism

Pleural mesothelioma (PM) poses a significant challenge in oncology due to its intricate molecular and metabolic landscape, chronic inflammation, and heightened oxidative stress, which contribute to its notorious resilience and clinical complexities. Given the pivotal role attributed to FABP5 and envisioning its potential as a therapeutic target in the context of innovative strategies against mesothelioma, we investigated the consequences of FABP5 silencing on the proliferation, apoptosis, and metabolism of both mesothelial and mesothelioma cells.

Inducing FABP5 silencing, using a pool of siRNA against FABP5 or a scrambled siRNA, as control (Fig. 1A), we observed a notable reduction in the proliferation rates of IstMes2 and MPP89, while the proliferation of normal mesothelial cells HMC35 remained unaffected (Fig. 1B). Remarkably, FABP5 silencing induced a significant increase in apoptosis, as evidenced by Annexin-V assay, in both mesothelioma cell lines IstMes2 and MPP89, while apoptosis levels in normal mesothelial cells remained unaltered (Fig. 1C). Further, we found FABP5 silencing triggered notable metabolic shifts in mesothelioma cells. Specifically, we observed a decrease in mitochondrial activity (Fig. 1D), accompanied by an increase in the ADP/ATP ratio (Fig. 1E) and the NAD/NADH ratio (Fig. 1F). In contrast, normal mesothelial cells exhibited no discernible changes in these metabolic parameters. Furthermore, FABP5 silencing led to a reduction in the abundance of lipid droplets (Fig. 1G) and a concurrent decrease in the mRNA expression levels of key enzymes involved in phospholipid biosynthesis CCTα, CHPT1, and CEPT1 (Fig. 1H). These findings underscore the potential therapeutic efficacy of targeting FABP5, revealing its intricate involvement in mesothelioma cell dynamics and metabolic pathways.