Frequent Loss-of-Heterozygosity in CRISPR-Cas9–Edited Early Human Embryos

Scientists developed computational pipelines to assess single-cell genomics and transcriptomics datasets from OCT4 CRISPR-Cas9–targeted and control human preimplantation embryos
[Proceedings of the National Academy of Sciences of the United States of America]
Alanis-Lobato, G., Zohren, J., McCarthy, A., Fogarty, N. M. E., Kubikova, N., Hardman, E., Greco, M., Wells, D., Turner, J. M. A., & Niakan, K. K. (2021). Frequent loss-of-heterozygosity in CRISPR-Cas9–edited early human embryos. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.2004832117 Cite
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Loss-of-Function Genetic Screening Identifies ALDOA as an Essential Driver for Liver Cancer Cell Growth under Hypoxia

Scientists identified aldolase A (ALDOA), a key enzyme in glycolysis and gluconeogenesis, as an essential driver for HCC cell growth under hypoxia.
[Hepatology]
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Eltrombopag Improves Erythroid Differentiation in a Human Induced Pluripotent Stem Cell Model of Diamond Blackfan Anemia

Diamond Blackfan Anemia (DBA) iPSC lines were generated from blood mononuclear cells of DBA patients with inactivating mutations in RPS19 and subjected to hematopoietic differentiation to model disease phenotypes.
[Cells]
Qanash, H., Li, Y., Smith, R. H., Linask, K., Young-Baird, S., Hakami, W., Keyvanfar, K., Choy, J. S., Zou, J., & Larochelle, A. (2021). Eltrombopag Improves Erythroid Differentiation in a Human Induced Pluripotent Stem Cell Model of Diamond Blackfan Anemia. Cells, 10(4), 734. https://doi.org/10.3390/cells10040734 Cite
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AMPK Activation by ASP4132 Inhibits Non-small Cell Lung Cancer Cell Growth

In primary NSCLC cells and established cell lines ASP4132 potently inhibited cell growth, proliferation and cell cycle progression as well as cell migration and invasion.
[Cell Death & Disease]
Xia, Y., Zha, J., Sang, Y.-H., Yin, H., Xu, G., Zhen, J., Zhang, Y., & Yu, B. (2021). AMPK activation by ASP4132 inhibits non-small cell lung cancer cell growth. Cell Death & Disease, 12(4), 1–14. https://doi.org/10.1038/s41419-021-03655-2 Cite
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Loss of Splicing Factor IK Impairs Normal Skeletal Muscle Development

The authors show that the splicing factor IK contributes to normal skeletal muscle development in vivo and myogenic differentiation in vitro.
[BMC Biology]
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Efficient CRISPR/Cas9 Based Genome Editing of β-Globin Gene on Erythroid Cells from Homozygous β039-Thalassemia Patients

By CRISPR/Cas9 gene editing, scientists present the correction of the β039-thalassemia mutation, one of the most frequent in the Mediterranean area.
[Molecular Therapy-Methods & Clinical Development]
Cosenza, L. C., Gasparello, J., Romanini, N., Zurlo, M., Zuccato, C., Gambari, R., & Finotti, A. (2021). Efficient CRISPR/Cas9 based genome editing of β-globin gene on erythroid cells from homozygous β039-thalassemia patients. Molecular Therapy - Methods & Clinical Development, 0(0). https://doi.org/10.1016/j.omtm.2021.03.025 Cite
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Targeted Replacement of Full-Length CFTR in Human Airway Stem Cells by CRISPR/Cas9 for Pan-Mutation Correction in the Endogenous Locus

Scientists used CRISPR/Cas9 and two adeno-associated viruses carrying the two halves of the cystic fibrosis transmembrane conductance regulator (CFTR) cDNA to sequentially insert the full CFTR cDNA along with a truncated CD19 enrichment tag in upper airway basal stem cells and human bronchial basal stem cells.
[Molecular Therapy]
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AP-2alpha Regulates S-Phase and is a Marker for Sensitivity to PI3K-inhibitor Buparlisib in Colon Cancer

CRISPR-Cas9 and shRNA were used to eliminate TFAP2A expression in HCT116 and a panel of colon cancer cell lines.
[Molecular Cancer Research]
Beck, A. C., Cho, E., White, J. R., Paemka, L., Li, T., Gu, V. W., Thompson, D. T., Koch, K. E., Franke, C., Gosse, M., Wu, V. T., Landers, S. R., Pamatmat, A. J., Kulak, M. V., & Weigel, R. J. (2021). AP-2alpha Regulates S-phase and is a Marker for Sensitivity to PI3K-inhibitor Buparlisib in Colon Cancer. Molecular Cancer Research. https://doi.org/10.1158/1541-7786.MCR-20-0867 Cite
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Defective Metabolic Programming Impairs Early Neuronal Morphogenesis in Neural Cultures and an Organoid Model of Leigh Syndrome

Using patient-derived induced pluripotent stem cells and CRISPR/Cas9 engineering, investigators developed a human model of Leigh syndrom caused by mutations in the complex IV assembly gene SURF1.
[Nature Communications]
Inak, G., Rybak-Wolf, A., Lisowski, P., Pentimalli, T. M., Jüttner, R., Glažar, P., Uppal, K., Bottani, E., Brunetti, D., Secker, C., Zink, A., Meierhofer, D., Henke, M.-T., Dey, M., Ciptasari, U., Mlody, B., Hahn, T., Berruezo-Llacuna, M., Karaiskos, N., … Prigione, A. (2021). Defective metabolic programming impairs early neuronal morphogenesis in neural cultures and an organoid model of Leigh syndrome. Nature Communications, 12(1), 1929. https://doi.org/10.1038/s41467-021-22117-z Cite
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A Genome-Scale CRISPR Cas9 Dropout Screen Identifies Synthetically Lethal Targets in SRC-3 Inhibited Cancer Cells

Scientists indicated that combined SI-12 and SGI-1027 treatment could achieve stronger inhibition on triple-negative breast cancer organoid formation and growth than single treatment with either compound.
[Communications Biology]
Gilad, Y., Eliaz, Y., Yu, Y., Dean, A. M., Han, S. J., Qin, L., O’Malley, B. W., & Lonard, D. M. (2021). A genome-scale CRISPR Cas9 dropout screen identifies synthetically lethal targets in SRC-3 inhibited cancer cells. Communications Biology, 4(1), 1–17. https://doi.org/10.1038/s42003-021-01929-1 Cite
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Generation of PARP1 Gene Knockout Human Embryonic Stem Cell Line Using CRISPR/Cas9

To clarify the function of PARP1 in hESCs, scientists report a PARP1 knockout hESC line, generated by CRISPR/Cas9 mediated gene targeting. This cell line showed normal karyotype, pluripotent stem cell marker expression and differentiation potential in vitro.
[Stem Cell Research]
Li, Y., Li, J., Zhou, T., Pan, G., & Huang, K. (2021). Generation of PARP1 gene knockout human embryonic stem cell line using CRISPR/Cas9. Stem Cell Research, 53, 102288. https://doi.org/10.1016/j.scr.2021.102288 Cite
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