Search bioRxiv⌕ Search

bioRxiv · 10.1101/2024.03.28.587184

Establishing the foundations for a data-centric AI approach for virtual drug screening through a systematic assessment of the properties of chemical data

Abstract

Researchers have adopted model-centric artificial intelligence (AI) approaches in cheminformatics by using newer, more sophisticated AI methods to take advantage of growing chemical libraries. It has been shown that complex deep learning methods outperform conventional machine learning (ML) methods in QSAR and ligand-based virtual screening1-3 but such approaches generally lack explanability. Hence, instead of developing more sophisticated AI methods (i.e., pursuing a model-centric approach), we wanted to explore the potential of a data-centric AI paradigm for virtual screening. A data-centric AI is an intelligent system that would automatically identify the right type of data to collect, clean and curate for later use by a predictive AI and this is required given the large volumes of chemical data that exist in chemical databases - PubChem alone has over 100 million unique compounds. However, a systematic assessment of the attributes and properties of suitable data is needed. We show here that it is not the result of deficiencies in current AI algorithms but rather, poor understanding and erroneous use of chemical data that ultimately leads to poor predictive performance. Using a new benchmark dataset of BRAF ligands that we developed, we show that our best performing predictive model can achieve an unprecedented accuracy of 99% with a conventional ML algorithm (SVM) using a merged molecular representation (Extended + ECFP6 fingerprints), far surpassing past performances of virtual screening platforms using sophisticated deep learning methods. Thus, we demonstrate that it is not necessary to resort to the use of sophisticated deep learning algorithms for virtual screening because conventional ML can perform exceptionally well if given the right data and representation. We also show that the common use of decoys for training leads to high false positive rates and its use for testing will result in an over-optimistic estimation of a models predictive performance. Another common practice in virtual screening is defining compounds that are above a certain pharmacological threshold as inactives. Here, we show that the use of these so-called inactive compounds lowers a models sensitivity/recall. Considering that some target proteins have a limited number of known ligands, we wanted to also observe how the size and composition of the training data impact predictive performance. We found that an imbalance training dataset where inactives outnumber actives led to a decrease in recall but an increase in precision, regardless of the model or molecular representation used; and overall, we observed a decrease in the models accuracy. We highlight in this study some of the considerations that one needs to take into account in future development of data-centric AI for CADD.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Chong, A., Phua, S.-X., Xiao, Y., Ng, W. Y., Li, H. Y., Goh, W. W. B.. 2024-03-31. Establishing the foundations for a data-centric AI approach for virtual drug screening through a systematic assessment of the properties of chemical data. https://doi.org/10.1101/2024.03.28.587184

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Tet2-Clonal Hematopoiesis Promotes Whereas Dnmt3a-CH Inhibits Breast Cancer Progression During Aging

Clonal hematopoiesis of indeterminate potential (CHIP) driven by somatic mutations in blood cells increases with age and is associated with adverse outcomes in cancer patients. How CHIP mutations influence solid tumor progression remains unclear. Using inducible murine models of Dnmt3a- or Tet2-mutant CHIP combined with orthotopic syngeneic breast cancer models, we demonstrate that upon aging Dnmt3a-mutant CHIP prevents whereas Tet2-mutant CHIP drives breast cancer progression. Dnmt3a-mutant immune infiltrates established interferon-mediated MHCIIhigh tumor-associated macrophages (TAMs) that supported cytotoxic CD8+ T cell-mediated tumor rejection. In contrast, Tet2-mutant TAMs exhibited an inflammatory, immunosuppressive phenotype characterized by increased IL-1 and CXCL2 production, reduced MHCII expression, and impaired T cell recruitment and activation. Therapeutic blockade of IL-1R1 or CXCR2 reduced tumor progression in aged Tet2-mutant CHIP mice and partially restored anti-tumor immunity. These findings establish that the effects of CHIP on cancer are mutation- and age-dependent and identify IL-1/CXCL2-driven inflammation as a therapeutic vulnerability of tumor-promoting Tet2-mutant CHIP.

cancer biology↗

Single Nucleus Profiling Reveals Rewired Tumor-Immune-Stromal Cell Communication in Plasmacytoid Urothelial Carcinoma

Plasmacytoid urothelial carcinoma (PUC) is an aggressive histologic subtype of bladder cancer associated with worse patient outcomes and therapeutic response compared to conventional urothelial carcinoma (CUC). While recent work has demonstrated metastatic lymph nodes from PUC tumors have an inflamed phenotype, how the tumor microenvironment (TME) and crosstalk between tumor, stromal, and immune cells in primary PUC bladder tumors differs from those in CUC remains poorly understood. The impact of these differences on response to immunotherapy is also unknown. To understand TME differences between CUC and PUC and their impact on cell signaling, we performed single nucleus RNA sequencing on PUC and CUC tumors, as well as Xenium spatial transcriptomics on a mixed CUC / PUC tumor. We identified increased signaling between PUC-enriched, CDH1-low urothelial cells, immunosuppressive lipid-associated macrophages, and SFRP2+/CTHRC1+ fibroblasts in PUC tumors compared to CUC. Spatial transcriptomics identified increased macrophage infiltration in PUC histology and colocalization of PUC tumor cells, immunosuppressive macrophages, and SFRP2+ fibroblasts. Taken together, this study delineates PUC architecture and demonstrates interplay CDH1-low tumor cells, EMT, and immunosuppressive macrophages, identifying possible therapeutic vulnerabilities in PUC.

cancer biology↗

The Phospholipase A2 Activity of Peroxiredoxin 6 Protects Hepatocarcinoma Cells Against Ferroptosis and Mitophagy Impairment

Peroxiredoxin 6 (PRDX6) is a moonlighting protein that plays a key role in regulating redox homeostasis and lipid metabolism through its unique dual peroxidase and calcium-independent phospholipase A2 (iPLA2) activities. Here, we generated a stable HepG2 cell line harboring a D140A mutation to selectively ablate iPLA2 activity, and we compared its phenotype with that of wild-type (WT) and PRDX6-knockout (KO) cells. D140A exhibited low ROS leves, similar to WT cells, confirming that oxidative stress is due to peroxidase deficiency. In contrast, D140A cells displayed higher lipid peroxidation than WT cells, though significantly lower than that of KO cells. Furthermore, the D140A mutant mirrored the KO phenotype regarding intracellular ferrous iron accumulation, impaired lipid droplet biogenesis, and the downregulation of the key ferroptosis regulator GPX4. Mechanistically, integrated proteomic, lipidomic, and enzymatic analyses revealed that a deficiency in iPLA2 activity of PRDX6 disrupted the release of key lipid species necessary for cell structure and signaling. Consequently, organelles involved in lipid synthesis and trafficking, such as peroxisomes, endoplasmic reticulum, mitochondria and lipid droplet, were affected. Specifically, we found that mitochondria exhibited a reduction in cristae and a diminished capacity for mitophagy and autophagy, which ultimately makes cells much more susceptible to erastin-induced ferroptotic cell death. Taken together, our findings demonstrate that PRDX6 iPLA2 activity uniquely coordinates organelle lipid homeostasis and mitophagy to protect cancer cells from ferroptotic cell death. Consequently, the use of iPLA2 inhibitors such as MJ33, which decreased PRDX6 iPLA2 activity to a level comparable to the mutant D140A, could represent a promising therapeutic strategy for inducing ferroptotic cell death in hepatocellular carcinoma.

cancer biology↗