Identifying regulators of aberrant stem cell and differentiation activity in colorectal cancer using a dual endogenous reporter system.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
12 Mar 2024
Historique:
received: 02 02 2023
accepted: 21 02 2024
medline: 13 3 2024
pubmed: 13 3 2024
entrez: 13 3 2024
Statut: epublish

Résumé

Aberrant stem cell-like activity and impaired differentiation are central to the development of colorectal cancer (CRC). To identify functional mediators of these key cellular programs, we engineer a dual endogenous reporter system by genome-editing the SOX9 and KRT20 loci of human CRC cell lines to express fluorescent reporters, broadcasting aberrant stem cell-like and differentiation activity, respectively. By applying a CRISPR screen targeting 78 epigenetic regulators with 542 sgRNAs to this platform, we identify factors that contribute to stem cell-like activity and differentiation in CRC. Perturbation single cell RNA sequencing (Perturb-seq) of validated hits nominate SMARCB1 of the BAF complex (also known as SWI/SNF) as a negative regulator of differentiation across an array of neoplastic colon models. SMARCB1 is a dependency and required for in vivo growth of human CRC models. These studies highlight the utility of biologically designed endogenous reporter platforms to uncover regulators with therapeutic potential.

Identifiants

pubmed: 38472198
doi: 10.1038/s41467-024-46285-w
pii: 10.1038/s41467-024-46285-w
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2230

Subventions

Organisme : U.S. Department of Defense (United States Department of Defense)
ID : CA201084

Informations de copyright

© 2024. The Author(s).

Références

Jackson, A. L. et al. Widespread siRNA “off-target” transcript silencing mediated by seed region sequence complementarity. RNA 12, 1179–1187 (2006).
pubmed: 16682560 pmcid: 1484447 doi: 10.1261/rna.25706
Boettcher, M. & McManus, M. T. Choosing the right tool for the job: RNAi, TALEN, or CRISPR. Mol. Cell 58, 575–585 (2015).
pubmed: 26000843 pmcid: 4441801 doi: 10.1016/j.molcel.2015.04.028
Mohr, S. E., Smith, J. A., Shamu, C. E., Neumuller, R. A. & Perrimon, N. RNAi screening comes of age: improved techniques and complementary approaches. Nat. Rev. Mol. Cell Biol. 15, 591–600 (2014).
pubmed: 25145850 pmcid: 4204798 doi: 10.1038/nrm3860
Wang, T., Wei, J. J., Sabatini, D. M. & Lander, E. S. Genetic screens in human cells using the CRISPR-Cas9 system. Science 343, 80–84 (2014).
pubmed: 24336569 doi: 10.1126/science.1246981
Shalem, O. et al. Genome-scale CRISPR-Cas9 knockout screening in human cells. Science 343, 84–87 (2014).
pubmed: 24336571 doi: 10.1126/science.1247005
Takeda, D. Y. et al. A somatically acquired enhancer of the androgen receptor is a noncoding driver in advanced prostate cancer. Cell 174, 422–432.e413 (2018).
pubmed: 29909987 pmcid: 6046260 doi: 10.1016/j.cell.2018.05.037
Barretina, J. et al. The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity. Nature 483, 603–607 (2012).
pubmed: 22460905 pmcid: 3320027 doi: 10.1038/nature11003
Chen, S. et al. Genome-wide CRISPR screen in a mouse model of tumor growth and metastasis. Cell 160, 1246–1260 (2015).
pubmed: 25748654 pmcid: 4380877 doi: 10.1016/j.cell.2015.02.038
Tsherniak, A. et al. Defining a cancer dependency map. Cell 170, 564–576.e516 (2017).
pubmed: 28753430 pmcid: 5667678 doi: 10.1016/j.cell.2017.06.010
Behan, F. M. et al. Prioritization of cancer therapeutic targets using CRISPR–Cas9 screens. Nature 568, 511–516 (2019).
pubmed: 30971826 doi: 10.1038/s41586-019-1103-9
Cowley, G. S. et al. Parallel genome-scale loss of function screens in 216 cancer cell lines for the identification of context-specific genetic dependencies. Sci. Data 1, 140035 (2014).
pubmed: 25984343 pmcid: 4432652 doi: 10.1038/sdata.2014.35
Olivieri, M. et al. A genetic map of the response to DNA damage in human cells. Cell 182, 481–496.e421 (2020).
pubmed: 32649862 pmcid: 7384976 doi: 10.1016/j.cell.2020.05.040
Yu, C. et al. Genome-wide CRISPR-cas9 knockout screening identifies GRB7 as a driver for MEK inhibitor resistance in KRAS mutant colon cancer. Oncogene 41, 191–203 (2022).
pubmed: 34718347 doi: 10.1038/s41388-021-02077-w
Ford, K., McDonald, D. & Mali, P. Functional genomics via CRISPR-Cas. J. Mol. Biol. 431, 48–65 (2019).
pubmed: 29959923 doi: 10.1016/j.jmb.2018.06.034
Bock, C. et al. High-content CRISPR screening. Nat. Rev. Methods Prim. 2, 8 (2022).
doi: 10.1038/s43586-021-00093-4
Cortez, J. T. et al. CRISPR screen in regulatory T cells reveals modulators of Foxp3. Nature 582, 416–420 (2020).
pubmed: 32499641 pmcid: 7305989 doi: 10.1038/s41586-020-2246-4
Tang, W. et al. A genome-wide RNAi screen for Wnt/beta-catenin pathway components identifies unexpected roles for TCF transcription factors in cancer. Proc. Natl Acad. Sci. USA 105, 9697–9702 (2008).
pubmed: 18621708 pmcid: 2453074 doi: 10.1073/pnas.0804709105
Firestein, R. et al. CDK8 is a colorectal cancer oncogene that regulates β-catenin activity. Nature 455, 547–551 (2008).
pubmed: 18794900 pmcid: 2587138 doi: 10.1038/nature07179
Wan, C. et al. Genome-scale CRISPR-Cas9 screen of Wnt/β-catenin signaling identifies therapeutic targets for colorectal cancer. Sci. Adv. 7, eabf2567 (2021).
pubmed: 34138730 pmcid: 8133758 doi: 10.1126/sciadv.abf2567
Kaelin, W. G. Jr. Common pitfalls in preclinical cancer target validation. Nat. Rev. Cancer 17, 425–440 (2017).
pubmed: 28524181 doi: 10.1038/nrc.2017.32
Hanahan, D. Hallmarks of cancer: new dimensions. Cancer Discov. 12, 31–46 (2022).
pubmed: 35022204 doi: 10.1158/2159-8290.CD-21-1059
de Sousa, E. M. F. & de Sauvage, F. J. Cellular plasticity in intestinal homeostasis and disease. Cell Stem Cell 24, 54–64 (2019).
doi: 10.1016/j.stem.2018.11.019
de The, H. Differentiation therapy revisited. Nat. Rev. Cancer 18, 117–127 (2018).
pubmed: 29192213 doi: 10.1038/nrc.2017.103
Liang, X. et al. An enhancer-driven stem cell-like program mediated by SOX9 blocks intestinal differentiation in colorectal cancer. Gastroenterology 162, 209–222 (2022).
pubmed: 34571027 doi: 10.1053/j.gastro.2021.09.044
Calnek, D. & Quaroni, A. Differential localization by in situ hybridization of distinct keratin mRNA species during intestinal epithelial cell development and differentiation. Differentiation 53, 95–104 (1993).
pubmed: 7689500 doi: 10.1111/j.1432-0436.1993.tb00649.x
Dow, L. E. et al. Apc restoration promotes cellular differentiation and reestablishes crypt homeostasis in colorectal cancer. Cell 161, 1539–1552 (2015).
pubmed: 26091037 pmcid: 4475279 doi: 10.1016/j.cell.2015.05.033
Clevers, H. Wnt/beta-catenin signaling in development and disease. Cell 127, 469–480 (2006).
pubmed: 17081971 doi: 10.1016/j.cell.2006.10.018
Shimokawa, M. et al. Visualization and targeting of LGR5(+) human colon cancer stem cells. Nature 545, 187–192 (2017).
pubmed: 28355176 doi: 10.1038/nature22081
Stewart-Ornstein, J. & Lahav, G. Dynamics of CDKN1A in single cells defined by an endogenous fluorescent tagging toolkit. Cell Rep. 14, 1800–1811 (2016).
pubmed: 26876176 pmcid: 5154611 doi: 10.1016/j.celrep.2016.01.045
Bala, P. et al. Aberrant cell state plasticity mediated by developmental reprogramming precedes colorectal cancer initiation. Sci. Adv. 9, eadf0927 (2023).
pubmed: 36989360 pmcid: 10058311 doi: 10.1126/sciadv.adf0927
Ng, J. M. & Yu, J. Promoter hypermethylation of tumour suppressor genes as potential biomarkers in colorectal cancer. Int. J. Mol. Sci. 16, 2472–2496 (2015).
pubmed: 25622259 pmcid: 4346847 doi: 10.3390/ijms16022472
Weisenberger, D. J. et al. CpG island methylator phenotype underlies sporadic microsatellite instability and is tightly associated with BRAF mutation in colorectal cancer. Nat. Genet. 38, 787–793 (2006).
pubmed: 16804544 doi: 10.1038/ng1834
Audia, J. E. & Campbell, R. M. Histone modifications and cancer. Cold Spring Harb. Perspect. Biol. 8, a019521 (2016).
pubmed: 27037415 pmcid: 4817802 doi: 10.1101/cshperspect.a019521
Dixit, A. et al. Perturb-Seq: dissecting molecular circuits with scalable single-cell RNA profiling of pooled genetic screens. Cell 167, 1853–1866.e1817 (2016).
pubmed: 27984732 pmcid: 5181115 doi: 10.1016/j.cell.2016.11.038
Reynolds, S., Rajagopal, S. & Chakrabarty, S. Differentiation-inducing effect of retinoic acid, difluoromethylornithine, sodium butyrate and sodium suramin in human colon cancer cells. Cancer Lett. 134, 53–60 (1998).
pubmed: 10381130 doi: 10.1016/S0304-3835(98)00242-0
Wester, R. A. et al. Retinoic acid signaling drives differentiation toward the absorptive lineage in colorectal cancer. iScience 24, 103444 (2021).
pubmed: 34877501 pmcid: 8633980 doi: 10.1016/j.isci.2021.103444
Qian, Y., Xia, S. & Feng, Z. Sox9 mediated transcriptional activation of FOXK2 is critical for colorectal cancer cells proliferation. Biochem. Biophys. Res. Commun. 483, 475–481 (2017).
pubmed: 28007600 doi: 10.1016/j.bbrc.2016.12.119
Mertens, S. et al. Drug-repurposing screen on patient-derived organoids identifies therapy-induced vulnerability in KRAS-mutant colon cancer. Cell Rep. 42, 112324 (2023).
pubmed: 37000626 doi: 10.1016/j.celrep.2023.112324
He, X. et al. Patient-derived organoids as a platform for drug screening in metastatic colorectal cancer. Front. Bioeng. Biotechnol. 11, 1190637 (2023).
pubmed: 37284236 pmcid: 10239948 doi: 10.3389/fbioe.2023.1190637
Agarwal, N. et al. TRIM28 is a transcriptional activator of the mutant TERT promoter in human bladder cancer. Proc. Natl Acad. Sci. USA 118, e2102423118 (2021).
pubmed: 34518220 pmcid: 8463889 doi: 10.1073/pnas.2102423118
Blanco, M. A. et al. Chromatin-state barriers enforce an irreversible mammalian cell fate decision. Cell Rep. 37, 109967 (2021).
pubmed: 34758323 doi: 10.1016/j.celrep.2021.109967
Sykes, D. B. et al. Inhibition of dihydroorotate dehydrogenase overcomes differentiation blockade in acute myeloid leukemia. Cell 167, 171–186.e115 (2016).
pubmed: 27641501 pmcid: 7360335 doi: 10.1016/j.cell.2016.08.057
Wang, E. et al. Surface antigen-guided CRISPR screens identify regulators of myeloid leukemia differentiation. Cell Stem Cell 28, 718–731.e716 (2021).
pubmed: 33450187 pmcid: 8145876 doi: 10.1016/j.stem.2020.12.005
Yan, F. et al. KAT6A and ENL form an epigenetic transcriptional control module to drive critical leukemogenic gene-expression programs. Cancer Discov. 12, 792–811 (2022).
pubmed: 34853079 pmcid: 8916037 doi: 10.1158/2159-8290.CD-20-1459
Fearon, E. R. & Vogelstein, B. A genetic model for colorectal tumorigenesis. Cell 61, 759–767 (1990).
pubmed: 2188735 doi: 10.1016/0092-8674(90)90186-I
Kinzler, K. W. & Vogelstein, B. Lessons from hereditary colorectal cancer. Cell 87, 159–170 (1996).
pubmed: 8861899 doi: 10.1016/S0092-8674(00)81333-1
Morin, P. J. et al. Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC. Science 275, 1787–1790 (1997).
pubmed: 9065402 doi: 10.1126/science.275.5307.1787
Barker, N. & Clevers, H. Mining the Wnt pathway for cancer therapeutics. Nat. Rev. Drug Discov. 5, 997–1014 (2006).
pubmed: 17139285 doi: 10.1038/nrd2154
Cancer Genome Atlas, N. Comprehensive molecular characterization of human colon and rectal cancer. Nature 487, 330–337 (2012).
doi: 10.1038/nature11252
Cheng, X., Xu, X., Chen, D., Zhao, F. & Wang, W. Therapeutic potential of targeting the Wnt/beta-catenin signaling pathway in colorectal cancer. Biomed. Pharmacother. 110, 473–481 (2019).
pubmed: 30530050 doi: 10.1016/j.biopha.2018.11.082
Firestein, R. et al. CDK8 is a colorectal cancer oncogene that regulates beta-catenin activity. Nature 455, 547–551 (2008).
pubmed: 18794900 pmcid: 2587138 doi: 10.1038/nature07179
Major, M. B. et al. New regulators of Wnt/beta-catenin signaling revealed by integrative molecular screening. Sci. Signal 1, ra12 (2008).
pubmed: 19001663 doi: 10.1126/scisignal.2000037
Lebensohn, A. M. et al. Comparative genetic screens in human cells reveal new regulatory mechanisms in WNT signaling. Elife 5, e21459 (2016).
pubmed: 27996937 pmcid: 5257257 doi: 10.7554/eLife.21459
Schmidt, R. et al. CRISPR activation and interference screens decode stimulation responses in primary human T cells. Science 375, eabj4008 (2022).
pubmed: 35113687 pmcid: 9307090 doi: 10.1126/science.abj4008
Wiersma, M. et al. Protein kinase Msk1 physically and functionally interacts with the KMT2A/MLL1 methyltransferase complex and contributes to the regulation of multiple target genes. Epigenetics Chromatin 9, 52 (2016).
pubmed: 27895715 pmcid: 5106815 doi: 10.1186/s13072-016-0103-3
Huang, Y. C. et al. The epigenetic factor Kmt2a/Mll1 regulates neural progenitor proliferation and neuronal and glial differentiation. Dev. Neurobiol. 75, 452–462 (2015).
pubmed: 25284327 doi: 10.1002/dneu.22235
Meyer, C. et al. The MLL recombinome of acute leukemias in 2017. Leukemia 32, 273–284 (2018).
pubmed: 28701730 doi: 10.1038/leu.2017.213
Grinat, J. et al. The epigenetic regulator Mll1 is required for Wnt-driven intestinal tumorigenesis and cancer stemness. Nat. Commun. 11, 6422 (2020).
pubmed: 33349639 pmcid: 7752919 doi: 10.1038/s41467-020-20222-z
Mashtalir, N. et al. A structural model of the endogenous human BAF complex informs disease mechanisms. Cell 183, 802–817.e824 (2020).
pubmed: 33053319 pmcid: 7717177 doi: 10.1016/j.cell.2020.09.051
Tang, Z., Kang, B., Li, C., Chen, T. & Zhang, Z. GEPIA2: an enhanced web server for large-scale expression profiling and interactive analysis. Nucleic Acids Res. 47, W556–w560 (2019).
pubmed: 31114875 pmcid: 6602440 doi: 10.1093/nar/gkz430
Yao, B. et al. PRMT1-mediated H4R3me2a recruits SMARCA4 to promote colorectal cancer progression by enhancing EGFR signaling. Genome Med. 13, 58 (2021).
pubmed: 33853662 pmcid: 8048298 doi: 10.1186/s13073-021-00871-5
Rago, F. et al. Exquisite Sensitivity to Dual BRG1/BRM ATPase Inhibitors Reveals Broad SWI/SNF Dependencies in Acute Myeloid Leukemia. Mol. Cancer Res. 20, 361–372 (2022).
pubmed: 34799403 doi: 10.1158/1541-7786.MCR-21-0390
Lee, D. et al. The bromodomain inhibitor PFI-3 sensitizes cancer cells to DNA damage by targeting SWI/SNF. Mol. Cancer Res 19, 900–912 (2021).
pubmed: 33208498 doi: 10.1158/1541-7786.MCR-20-0289
Xiao, L. et al. Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer. Nature 601, 434–439 (2022).
pubmed: 34937944 doi: 10.1038/s41586-021-04246-z
Wang, X., Haswell, J. R. & Roberts, C. W. Molecular pathways: SWI/SNF (BAF) complexes are frequently mutated in cancer-mechanisms and potential therapeutic insights. Clin. Cancer Res. 20, 21–27 (2014).
pubmed: 24122795 doi: 10.1158/1078-0432.CCR-13-0280
Wilson, B. G. et al. Epigenetic antagonism between polycomb and SWI/SNF complexes during oncogenic transformation. Cancer Cell 18, 316–328 (2010).
pubmed: 20951942 pmcid: 2957473 doi: 10.1016/j.ccr.2010.09.006
Roberts, C. W., Galusha, S. A., McMenamin, M. E., Fletcher, C. D. & Orkin, S. H. Haploinsufficiency of Snf5 (integrase interactor 1) predisposes to malignant rhabdoid tumors in mice. Proc. Natl Acad. Sci. USA 97, 13796–13800 (2000).
pubmed: 11095756 pmcid: 17655 doi: 10.1073/pnas.250492697
Wang, X. et al. SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation. Nat. Genet 49, 289–295 (2017).
pubmed: 27941797 doi: 10.1038/ng.3746
Alver, B. H. et al. The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers. Nat. Commun. 8, 14648 (2017).
pubmed: 28262751 pmcid: 5343482 doi: 10.1038/ncomms14648
Parisian, A. D. et al. SMARCB1 loss interacts with neuronal differentiation state to block maturation and impact cell stability. Genes Dev. 34, 1316–1329 (2020).
pubmed: 32912900 pmcid: 7528703 doi: 10.1101/gad.339978.120
Sekiguchi, F. et al. Genetic abnormalities in a large cohort of Coffin-Siris syndrome patients. J. Hum. Genet 64, 1173–1186 (2019).
pubmed: 31530938 doi: 10.1038/s10038-019-0667-4
Zhu, Z. et al. Mitotic bookmarking by SWI/SNF subunits. Nature 618, 180–187 (2023).
pubmed: 37225980 pmcid: 10303083 doi: 10.1038/s41586-023-06085-6
Mora-Blanco, E. L. et al. Activation of beta-catenin/TCF targets following loss of the tumor suppressor SNF5. Oncogene 33, 933–938 (2014).
pubmed: 23435428 doi: 10.1038/onc.2013.37
Knutson, S. K. et al. Durable tumor regression in genetically altered malignant rhabdoid tumors by inhibition of methyltransferase EZH2. Proc. Natl Acad. Sci. USA 110, 7922–7927 (2013).
pubmed: 23620515 pmcid: 3651445 doi: 10.1073/pnas.1303800110
Labun, K. et al. CHOPCHOP v3: expanding the CRISPR web toolbox beyond genome editing. Nucleic Acids Res 47, W171–W174 (2019).
pubmed: 31106371 pmcid: 6602426 doi: 10.1093/nar/gkz365
Hao, Y. et al. Integrated analysis of multimodal single-cell data. Cell 184, 3573–3587.e3529 (2021).
pubmed: 34062119 pmcid: 8238499 doi: 10.1016/j.cell.2021.04.048
Papalexi, E. et al. Characterizing the molecular regulation of inhibitory immune checkpoints with multimodal single-cell screens. Nat. Genet 53, 322–331 (2021).
pubmed: 33649593 pmcid: 8011839 doi: 10.1038/s41588-021-00778-2
Spisak, S. et al Identifying regulators of aberrant stem cell and differentiation activity in colorectal cancer using a dual endogenous reporter system. Endogenous_Reporter. https://doi.org/10.5281/zenodo.10658567 (2024).
Haber, A. L. et al. A single-cell survey of the small intestinal epithelium. Nature 551, 333–339 (2017).
pubmed: 29144463 pmcid: 6022292 doi: 10.1038/nature24489

Auteurs

Sandor Spisak (S)

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Institute of Molecular Life Sciences, HUN-REN Research Centre for Natural Sciences, Budapest, Hungary.

David Chen (D)

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada.

Pornlada Likasitwatanakul (P)

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Department of Medicine, Harvard Medical School, Boston, MA, USA.
Broad Institute of Massachusetts Institute of Technology (MIT) and Harvard University, Cambridge, MA, USA.
Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.

Paul Doan (P)

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Broad Institute of Massachusetts Institute of Technology (MIT) and Harvard University, Cambridge, MA, USA.

Zhixin Li (Z)

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Broad Institute of Massachusetts Institute of Technology (MIT) and Harvard University, Cambridge, MA, USA.

Pratyusha Bala (P)

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Broad Institute of Massachusetts Institute of Technology (MIT) and Harvard University, Cambridge, MA, USA.

Laura Vizkeleti (L)

Department of Bioinformatics, Faculty of Medicine, Semmelweis University, 1094, Budapest, Hungary.

Viktoria Tisza (V)

Institute of Molecular Life Sciences, HUN-REN Research Centre for Natural Sciences, Budapest, Hungary.

Pushpamali De Silva (P)

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.

Marios Giannakis (M)

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Department of Medicine, Harvard Medical School, Boston, MA, USA.
Broad Institute of Massachusetts Institute of Technology (MIT) and Harvard University, Cambridge, MA, USA.
Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Boston, MA, USA.

Brian Wolpin (B)

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Department of Medicine, Harvard Medical School, Boston, MA, USA.
Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Boston, MA, USA.

Jun Qi (J)

Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA.

Nilay S Sethi (NS)

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA. nilay_sethi@dfci.harvard.edu.
Department of Medicine, Harvard Medical School, Boston, MA, USA. nilay_sethi@dfci.harvard.edu.
Broad Institute of Massachusetts Institute of Technology (MIT) and Harvard University, Cambridge, MA, USA. nilay_sethi@dfci.harvard.edu.
Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Boston, MA, USA. nilay_sethi@dfci.harvard.edu.

Classifications MeSH