References
- Boffo S, Damato A, Alfano L, et al. CDK9 inhibitors in acute myeloid leukemia. J Exp Clin Cancer Res. 2018;37:36.
- Chou J, Quigley DA, Robinson TM, et al. Transcription-Associated Cyclin-Dependent Kinases as Targets and Biomarkers for Cancer Therapy. Cancer Discov. 2020;10:351–370.
- Parua PK, Fisher RP. Dissecting the Pol II transcription cycle and derailing cancer with CDK inhibitors. Nat Chem Biol. 2020;16:716–724.
- Ghia P, Scarfo L, Perez S, et al. Efficacy and safety of dinaciclib vs ofatumumab in patients with relapsed/refractory chronic lymphocytic leukemia. Blood. 2017;129:1876–1878.
- Cidado J, Boiko S, Proia T, et al. AZD4573 Is a Highly Selective CDK9 Inhibitor That Suppresses MCL-1 and Induces Apoptosis in Hematologic Cancer Cells. Clin Cancer Res. 2020;26:922–934.
- Wu T, Qin Z, Tian Y, et al. Recent Developments in the Biology and Medicinal Chemistry of CDK9 Inhibitors: an Update. J Med Chem. 2020;63:13228–13257.
- Minzel W, Venkatachalam A, Fink A, et al. Small Molecules Co-targeting CKIalpha and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models. Cell. 2018;175:171–185 e125.
- Lam LT, Pickeral OK, Peng AC, et al. Genomic-scale measurement of mRNA turnover and the mechanisms of action of the anti-cancer drug flavopiridol. Genome Biol. 2001;2:RESEARCH0041.
- Lu H, Xue Y, Yu GK, et al. Compensatory induction of MYC expression by sustained CDK9 inhibition via a BRD4-dependent mechanism. Elife. 2015;4:e06535.
- Itkonen HM, Poulose N, Steele RE, et al. Inhibition of O-GlcNAc Transferase Renders Prostate Cancer Cells Dependent on CDK9. Mol Cancer Res. 2020;18:1512–1521.
- Hart GW. Nutrient regulation of signaling and transcription. J Biol Chem. 2019;294:2211–2231.
- Yang X, Qian K. Protein O-GlcNAcylation: emerging mechanisms and functions. Nat Rev Mol Cell Biol. 2017;18:452–465.
- Hanover JA, Krause MW, Love DC. Bittersweet memories: linking metabolism to epigenetics through O-GlcNAcylation. Nat Rev Mol Cell Biol. 2012;13:312–321.
- Itkonen HM, Loda M, Mills IG. O-GlcNAc Transferase - An Auxiliary Factor or a Full-blown Oncogene? Mol Cancer Res. 2021;19:555–564.
- Itkonen HM, Minner S, Guldvik IJ, et al. O-GlcNAc transferase integrates metabolic pathways to regulate the stability of c-MYC in human prostate cancer cells. Cancer Res. 2013;73:5277–5287.
- Itkonen HM, Urbanucci A, Martin SE, et al. High OGT activity is essential for MYC-driven proliferation of prostate cancer cells. Theranostics. 2019;9:2183–2197.
- Brian A, Lewis DL. O-GlcNAc Transferase Activity is Essential for RNA Pol II Pausing in a Human Cell-Free Transcription System. bioRxiv. 2020.
- N; Cancer Genome Atlas Research. The Molecular Taxonomy of Primary Prostate Cancer. Cell. 2015;163:1011–1025.
- Zhang D, Hu Q, Liu X, et al. Intron retention is a hallmark and spliceosome represents a therapeutic vulnerability in aggressive prostate cancer. Nat Commun. 2020;11:2089.
- Shen S, Park JW, Lu ZX, et al. rMATS: robust and flexible detection of differential alternative splicing from replicate RNA-Seq data. Proc Natl Acad Sci U S A. 2014;111:E5593–5601.
- Tan ZW, Fei G, Paulo JA, et al. O-GlcNAc regulates gene expression by controlling detained intron splicing. Nucleic Acids Res. 2020;48:5656–5669.
- Itkonen HM, Mills IG. N-linked glycosylation supports cross-talk between receptor tyrosine kinases and androgen receptor. PLoS One. 2013;8:e65016.
- Itkonen HM, Engedal N, Babaie E, et al. UAP1 is overexpressed in prostate cancer and is protective against inhibitors of N-linked glycosylation. Oncogene. 2015;34:3744–3750.
- Hu R, Dunn TA, Wei S, et al. Ligand-independent androgen receptor variants derived from splicing of cryptic exons signify hormone-refractory prostate cancer. Cancer Res. 2009;69:16–22.
- Paschalis A, Sharp A, Welti JC, et al. Alternative splicing in prostate cancer. Nat Rev Clin Oncol. 2018;15:663–675.
- Squires MS, Feltell RE, Wallis NG, et al. Biological characterization of AT7519, a small-molecule inhibitor of cyclin-dependent kinases, in human tumor cell lines. Mol Cancer Ther. 2009;8:324–332.
- Olson CM, Jiang B, Erb MA, et al. Pharmacological perturbation of CDK9 using selective CDK9 inhibition or degradation. Nat Chem Biol. 2018;14:163–170.
- Sharp A, Coleman I, Yuan W, et al. Androgen receptor splice variant-7 expression emerges with castration resistance in prostate cancer. J Clin Invest. 2019;129:192–208.
- Decker TM, Forne I, Straub T, et al. Analog-sensitive cell line identifies cellular substrates of CDK9. Oncotarget. 2019;10:6934–6943.
- Yoshida K, Sanada M, Shiraishi Y, et al. Frequent pathway mutations of splicing machinery in myelodysplasia. Nature. 2011;478:64–69.
- Barkovskaya A, Seip K, Prasmickaite L, et al. Inhibition of O-GlcNAc transferase activates tumor-suppressor gene expression in tamoxifen-resistant breast cancer cells. Sci Rep. 2020;10:16992.
- Dobin A, Davis CA, Schlesinger F, et al. STAR: ultrafast universal RNA-seq aligner. Bioinformatics. 2013;29:15–21.
- Love MI, Huber W, Anders S. Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2. Genome Biol. 2014;15:550.
- Chandrashekar DS, Bashel B, Balasubramanya SAH, et al. UALCAN: a Portal for Facilitating Tumor Subgroup Gene Expression and Survival Analyses. Neoplasia. 2017;19:649–658.
- Hu Q, Hutson A, Liu S, Morgan M, Liu Q. Bioconductor toolchain for reproducible bioinformatics pipelines using Rcwl and Rcwl Pipelines. Bioinformatics. 2001.