Anticancer uses of non-oncology drugs have occasionally been found, but such discoveries have been serendipitous. We sought to create a public resource containing the growth-inhibitory activity of 4,518 drugs tested across 578 human cancer cell lines. We used PRISM (profiling relative inhibition simultaneously in mixtures), a molecular barcoding method, to screen drugs against cell lines in pools. An unexpectedly large number of non-oncology drugs selectively inhibited subsets of cancer cell lines in a manner predictable from the molecular features of the cell lines. Our findings include compounds that killed by inducing phosphodiesterase 3A-Schlafen 12 complex formation, vanadium-containing compounds whose killing depended on the sulfate transporter SLC26A2, the alcohol dependence drug disulfiram, which killed cells with low expression of metallothioneins, and the anti-inflammatory drug tepoxalin, which killed via the multidrug resistance protein ATP-binding cassette subfamily B member 1 (ABCB1). The PRISM drug repurposing resource (https://depmap.org/repurposing) is a starting point to develop new oncology therapeutics, and more rarely, for potential direct clinical translation.
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The PRISM Repurposing dataset, including screening data and all metadata, is available at the Cancer Dependency Map portal (https://depmap.org/repurposing). Raw and processed PRISM viability data are available from the Cancer Dependency Map portal (https://depmap.org/repurposing) and have been archived via figshare (https://doi.org/10.6084/m9.figshare.9393293). Interactive versions of Figs. 2a and 4 (with accompanying raw data) are also available on the Cancer Dependency Map portal; scatter plot source data are also deposited in figshare. The cell line features used for biomarker analysis are listed in Supplementary Table 10 and archived via figshare (https://doi.org/10.6084/m9.figshare.10277810). RNA-seq data have been deposited with the Gene Expression Omnibus (accession number GSE133299). All other data supporting the findings of this study are available from the corresponding author upon reasonable request.
Data analysis was performed in R v.3.5.1 using custom-made or publicly available R packages. Individual packages are explicitly cited in the manuscript. The custom code is available upon request and from GitHub (https://github.com/broadinstitute/repurposing).
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We thank C. Yu, W. Hahn, B. Wolpin, A. Bass, N. Gray, K. Stegmaier, E. Stover, T. Lewis, M. Mesleh, A. Burgin, S. Alper, G. Botta, M. Macaluso, P. Tsvetkov, X. Jin, K. Blakeslee, G. Ciolek and E. Lander for helpful scientific discussions. M. Passino, C. Zhu, K. Gore, M. Laird, C. Trapechio and E. Parikh generated the barcoded PRISM cell lines and performed the assays. K. Stumbraite assisted with STR fingerprinting. S. Johnson and J. Davis performed lysate processing and detection. S.E. Johnston and R. Singh provided analytical chemistry support. A. Vrcic, C. Sandland and S. Figueroa-Lazu assisted with compound management. G. Kugener and A. Gonzalez provided technical assistance. This study was supported in part by the Carlos Slim Foundation (Slim Initiative in Genomic Medicine for the Americas), the Next Generation Fund at the Broad Institute of MIT and Harvard (S.M.C.), the Conquer Cancer Foundation of ASCO Young Investigator Award (S.M.C.) and National Institutes of Health grants nos. U01 HG008699 (T.R.G and A.S.), U54 HL127366 (T.R.G and A.S.), KL2 TR002542 (S.M.C.) and K08 CA230220 (S.M.C.).
S.M.C., X.W., H.G., M.M., A.S. and T.R.G. receive research funding unrelated to this project from Bayer HealthCare. M.M. receives research funding from Ono and serves as a scientific advisory board and consultant for OrigiMed. M.M. has patents licensed to LabCorp and Bayer. M.M. and T.R.G. were formerly consultants and equity holders in Foundation Medicine, which was acquired by Roche. J.A.B. is an employee and shareholder of Vertex Pharmaceuticals. J.G.D. and A.T. consult for Tango Therapeutics. T.R.G. is a consultant to GlaxoSmithKline and is a founder of Sherlock Biosciences. Patent applications for the drug uses detailed in this manuscript have been filed. The other authors declare no competing interests.
Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
a, Lineage diversity of PRISM cell lines. The 489+ cancer cell lines tested span more than 23 tumor types. Lineages with fewer than 10 cell lines are listed on the right. b, Experimental protocol. Cell lines are grouped by doubling time into pools of approximately 25 cell lines. One pool is plated onto each assay plate. Compounds are transferred by pin transfer from a source compound plate (HTS and HTS002 screens), or cells are plated directly onto assay-ready plates generated by acoustic dispensing of compounds (MTS004, MTS005, and MTS006 screens). In either case, compound plates are shared by all replicates of each treatment condition. After incubation and lysis, all assay plates generated by a given compound plate are grouped and collapsed into 3 (HTS002, MTS005, and MTS006 screens) or 6 (HTS, MTS004 screens) detection plates so that each detection plate receives 1 or zero copies of each pool. Ten control barcodes are then spiked into each detection plate well (HTS002, MTS005, and MTS006 screens). Detection plates are amplified by PCR and detected using Luminex FLEXMAP 3D instruments. c, Data processing workflow. Median Fluorescence Intensity (MFI) values are calculated from fluorescence values for each replicate-condition-cell line combination and are log2-transformed. Assay plates wells are normalized, median-collapsed, and compared to the normalized medians of other assay plate wells in the same well position that have been dosed by the same compound plate. A robust z-score is calculated, and assay plate wells with a |z-score| > 5 are filtered. Strictly standardized mean differences (SSMD) are calculated between positive and negative control conditions for each cell line on each assay plate. Cell line-assay plate combinations with SSMD < 2 are filtered by a control-separation filter to generate the log MFI data matrix. In datasets with control barcodes added, data are normalized with respect to the median of control barcodes to generate the MFI normalized data matrix. Data are DMSO-normalized and pooling artifacts are corrected using ComBat to generate the log fold change data matrix. Up to 3 independently treated plates (range 1-3 based QC filtering) in one screen are median-collapsed to generate the collapsed log fold change data matrix.
a, Primary screen QC pass rate by pool. The fraction of treated assay plate-wells that pass the outlier filter is indicated. Cell line log MFI data are median-centered, and the medians of assay plate-wells are compared within each well-detection plate combination. Extreme outliers with |robust z-score| >5 are filtered. b, Primary screen QC pass rate by detection plate. c, Primary screen QC pass rate of assay plates. Overall pass rate was high (median 98.6%, minimum 83.8%). d, Secondary screen QC pass rate by pool. e, Secondary screen QC pass rate by detection plate. The pass rate is above 95% for 81% of detection plates. f, Secondary screen QC pass rate by plate-pool combinations. 3 replicate plates are combined for visualization. Overall pass rate was high (median 99.1%, mean 94.3%), where failures are almost exclusively coming from 7 detection plates, implying failure at final detection step. Across the screen, 5.7% of the pools are filtered out as outliers.
aa, Primary screen QC pass rate by cell line. SSMD of log MFI values is calculated between positive control and negative control treatments for each cell line on each plate. Data from cell line-plates with SSMD < 2 are filtered. b, Primary screen QC pass rate by detection plate. c, Primary screen QC pass rate of assay plates. Overall pass rate was high (median 99.2%, mean 94.3%). Some detection plates show higher failure rates for specific detection pools, implying failure at final detection step. The bulk of the filtered data was from two detection plate-detection pools (PREP013_X2 and PREP003_X1 in detection pool 8). d, Secondary screen QC pass rate by cell line. SSMD of log MFI values is calculated between positive control and negative control treatments for each cell line on each assay plate. Data from cell line-plates with SSMD < 2 are filtered. e, Secondary screen QC pass rate by detection plate. f, Secondary screen QC pass rate of assay plates. Overall pass rate was lower than primary (median 99.88%, mean 79.1%). Similar to the primary screen, the main mode of failure is platewise failures.
a, Number of individual cell assay well replicates (max n = 3) that pass QC filters in the primary screen, grouped by compound plate and cell line quality. 86% (497 out of 578) of the cell lines have at least one passing replicate for all compound plates. Identity of cell lines with lower quality data are listed at the bottom. b, Number of individual cell assay well replicates (max n = 3) that pass QC filters in the secondary screen. 95% (463 out of 489) of cell lines have at least 1 passing replicate on at least 85% (30 out of 35) of the compound plates.
a, Pairwise Pearson correlations between drug response AUCs of publicly available datasets. AUC values were recomputed for 84 compounds and 318 cell lines (median 236 cell lines per compound) over the same dose-range for each compound-cell line pair in all 3 datasets (GDSC, CTD2, REP), and capped at 1. The Pearson correlation across shared compound-cell line pairs of the datasets is above 0.6. 44.8% of cell line-compound pairs show inactivity (AUC > 0.8) in all three datasets (n = 16650 compound-cell line pairs). b, Pairwise Pearson correlations between drug response AUCs after removing inactive cell line-compound pairs. Pearson correlations were re-calculated after filtering out the inactive data points (AUC > 0.8 in at all three datasets) (n = 9188 compound-cell line pairs). c, Compound-wise correlation between publicly available datasets. Correlation between PRISM data and other datasets is similar to correlation between other datasets. Points represent Pearson correlations and error bars represent 95% confidence intervals computed using Fisher’s z-transform. GDSC vs. CTD2 is in blue and REP vs. GDSC/CTD2 is in red. The number of cell lines shared by all three datasets is shown after each drug name. Paired t-tests on compound-wise correlations show statistically significant (two-sided p-value: 0.012 and 0.014 for top and bottom, respectively) but small mean of differences (0.049 and 0.039 for top and bottom, respectively). The number of data points used to compute each correlation is given in the figure for each compound.
a, Cell line standard error estimates across vehicle-treated wells on PRISM plates treated with DMSO (n = 489 cell lines). Log fold change standard errors are estimated for each cell line using DMSO-only plates included in the MTS006 screen (n = 384 × 3 replicate wells for each cell line). b, Comparison of standard error estimates across screens. The error estimate calculation is repeated for each screen using DMSO wells on standard compound plates (n = 32 replicate wells per plate), except for MTS006, which uses DMSO-only plates (n = 384 replicate wells per plate). Higher noise levels are observed in the initial high-throughput screens HTS001 (n = 578 cell lines) and HTS002 (n = 489 cell lines) compared with the medium-throughput screens MTS004 (n = 578 cell lines), MTS005 (n = 489 cell lines), and MTS006 (n = 489 cell lines). Upper box limits, center lines, and lower box limits correspond to 75th, 50th, and 25th percentiles, respectively. Whiskers extend from the box limits to the most extreme value up to 1.5 IQR from the median. All cell lines are depicted as points, regardless of outlier status. c, Comparison of estimated standard error of vehicle control wells between high-throughput pharmacogenomic datasets. The average standard error across cell lines (n = 301 cell lines for PRISM versus CTD2 and n = 197 for PRISM versus GDSC) is indicated by dashed lines with standard deviation in parentheses. d, Relationship between drug selectivity and replicate reproducibility in PRISM. Average Pearson correlation between replicates for each compound, dose, and screen combination is stratified by mean bimodality coefficient. For comparison, the null distribution for randomly paired compounds is shown in blue.
a, SF295 cells were transduced with multiple guides targeting the MTF-1 gene. Following selection, genomic DNA was isolated, and the targeted region was amplified by PCR. Results from the NGS CRISPR assay are shown as percent indel formation. b, Differentially expressed genes in SF295 glioma cells following MTF-1 knockout by CRISPR/Cas9. Loss of MT1E, MT1X, and MT2A expression was observed upon MTF-1 knockout. Gene expression across three independent cell wells per cell line were measured by mRNA sequencing. Two-sided p-values for differential gene expression following MTF-1 knockout vs. parental cell line were calculated with DESeq2 and corrected for multiple hypothesis testing using the Benjamini-Hochberg method. c, Drug sensitivity of SF295 cells with and without MTF-1 knockout. MTF-1 does not alter sensitivity to control chemotherapeutic bortezomib. Mean viability across 3 independently treated wells is shown, with standard deviation indicated by error bars. d, Western immunoblot validation of SLC26A2 knockout in OVISE ovarian and A2058 melanoma cancer cell lines. The SLC26A2 protein is known to migrate across a range of molecular weights due to glycosylation. Results are representative of two independent experiments. e, OVISE cells were transduced with multiple guides targeting the SLC26A2 gene. Indel frequency at the SLC26A2 CRISPR Cas9 cut sites was assessed by NGS CRISPR assay. f, ABCB1 western blot with and without CRISPR knockout of ABCB1 in the LS1034 colon cancer cell line. Western blot was performed once. g, Percent indel formation at genomic cut site in LS1034 ABCB1 CRISPR knockout lines assessed by NGS CRISPR assay. h, Cellular viability of LS1034 CRISPR knockout lines after treatment with tepoxalin for 5 days. Mean viability across 3 independently treated wells is shown, with standard deviation indicated by error bars. Source data
a, ABCB1 western blot with and without overexpression of ABCB1 in the Kuramochi ovarian cancer cell line. Western blot was performed once with three independent samples. b, Cellular viability of Kuramochi wild type and ABCB1-overexpressing cells after treatment with tepoxalin for 8 days. Mean viability across 3 independently treated wells is shown, with standard deviation indicated by error bars. c, (Left) Single-agent dose-response curves for LS1034 cells treated with tepoxalin and zosuquidar for 5 days. Two replicates were averaged. (Middle) Dose response curves for tepoxalin in combination with varying doses of zosuquidar (indicated by different colors) for 5 days. Data are shown for tepoxalin doses above 470 nM (the range indicated by the vertical dashed lines above). (Right) Bliss synergy scores estimated for each dose combination, showing strong antagonism by zosuquidar at tepoxalin doses above ~5 μM. Two combinations were not tested (NT). d, Maximum synergy score is shown across several drug combinations measured in both LS1034 and REC1 cell lines. Both tariquidar and elacridar were strongly synergistic in combination with paclitaxel, while all MDR1 inhibitors tested were antagonistic in combination with tepoxalin. e, Cellular permeability study of tepoxalin and RWJ20142 in LS1034 colon cancer cell lines with and without ABCB1 knockout. Each indicated cell line or media-only control was treated with 20 μM tepoxalin or RWJ20142 for 3 hours. Tepoxalin and RWJ20142 concentrations in cell lysate or medium were determined by liquid chromatography-mass spectrometry. Mean viability across 3 independently treated wells is shown, with standard deviation indicated by error bars. Shaded dots indicate underlying data. f, Stability study of tepoxalin in three different vehicles over 72 hours. Percent of tepoxalin remaining is indicated at each timepoint. g, ABCB1 antagonism assay using calcein AM fluorescence. MDCKII cells were treated with indicated concentration of tepoxalin or RWJ20142. Mean percent ABCB1 inhibition across 3 replicates is shown. h, ABCB1 transport-based activity assay. Basolateral transport of the ABCB1 substrate loperamide was assessed using a monolayer of MDCK-ABCB1 cells in the presence of tepoxalin or RWJ20142. Mean percent ABCB1 inhibition across 2 replicates is shown. Source data
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Corsello, S.M., Nagari, R.T., Spangler, R.D. et al. Discovering the anticancer potential of non-oncology drugs by systematic viability profiling. Nat Cancer 1, 235–248 (2020). https://doi.org/10.1038/s43018-019-0018-6
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