Tag Archives: PTEN

Multiple Signaling Pathways Are Essential for Synapse Formation Induced by Synaptic Adhesion Molecules

To explore what signaling pathways may be involved, investigators employed heterologous synapse formation assays in which a synaptic adhesion molecule expressed in a nonneuronal cell induced pre- or postsynaptic specializations in cocultured neurons.
[Proceedings of the National Academy of Sciences of the United States of America]
Jiang, X., Sando, R., & Südhof, T. C. (2021). Multiple signaling pathways are essential for synapse formation induced by synaptic adhesion molecules. Proceedings of the National Academy of Sciences, 118(3). https://doi.org/10.1073/pnas.2000173118 Cite
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Oncogenic Activation of PI3K-AKT-mTOR Signaling Suppresses Ferroptosis via SREBP-Mediated Lipogenesis

Hyperactive mutation of PI3K-AKT-mTOR signaling protected cancer cells from oxidative stress and ferroptotic death through SREBP1/SCD1-mediated lipogenesis, and combination of mTORC1 inhibition with ferroptosis induction showed therapeutic promise in preclinical models.
[Proceedings of the National Academy of Sciences of the United States of America]
Yi, J., Zhu, J., Wu, J., Thompson, C. B., & Jiang, X. (2020). Oncogenic activation of PI3K-AKT-mTOR signaling suppresses ferroptosis via SREBP-mediated lipogenesis. Proceedings of the National Academy of Sciences, 117(49), 31189–31197. https://doi.org/10.1073/pnas.2017152117 Cite
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YY1-Mediated Long Non-Coding RNA Kcnq1ot1 Promotes the Tumor Progression by Regulating PTEN via DNMT1 in Triple Negative Breast Cancer

The authors identified the roles of YY1-mediated long non-coding RNA Kcnq1ot1 in TNBC.
[Cancer Gene Therapy]
Shen, B., Li, Y., Ye, Q., & Qin, Y. (2020). YY1-mediated long non-coding RNA Kcnq1ot1 promotes the tumor progression by regulating PTEN via DNMT1 in triple negative breast cancer. Cancer Gene Therapy, 1–14. https://doi.org/10.1038/s41417-020-00254-9 Cite
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Upregulation of PI3K/AKT/PTEN Pathway Is Correlated with Glucose and Glutamine Metabolic Dysfunction during Tamoxifen Resistance Development in MCF-7 Cells

The authors determined the molecular changes of PI3K/AKT/PTEN signaling pathway during tamoxifen-resistance development using gradually increased doses of tamoxifen in one model, while fixing tamoxifen treatment dose at 35 μM for several times in the second model.
[Scientific Reports]
Hamadneh, L., Abuarqoub, R., Alhusban, A., & Bahader, M. (2020). Upregulation of PI3K/AKT/PTEN pathway is correlated with glucose and glutamine metabolic dysfunction during tamoxifen resistance development in MCF-7 cells. Scientific Reports, 10(1), 21933. https://doi.org/10.1038/s41598-020-78833-x Cite
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An Autoregulatory Feedback Loop of miR-21/VMP1 Is Responsible for the Abnormal Expression of miR-21 in Colorectal Cancer Cells

Scientists found that the expression of miR-21 was negatively correlated with the expression of vacuole membrane protein-1 (VMP1) in colorectal cancer. Transcription of VMP1 activated either by small activating RNA or transcriptional activator GLI3 inhibited miR-21 expression through reducing its transcripts of VMP1-miR-21 and pri-miR-21, while no significant change in miR-21 expression after exogenous overexpression VMP1 in colorectal cancer cell HCT116.
[Cell Death & Disease]
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Enzalutamide Response in a Panel of Prostate Cancer Cell Lines Reveals a Role for Glucocorticoid Receptor in Enzalutamide Resistant Disease

Representative in vitro model systems that accurately model response to therapy and allow the identification of new targets are important for improving the treatment of prostate cancer. Scientists describe molecular characterization and drug testing in a panel of 20 prostate cancer cell lines.
[Scientific Reports]
Smith, R., Liu, M., Liby, T., Bayani, N., Bucher, E., Chiotti, K., Derrick, D., Chauchereau, A., Heiser, L., Alumkal, J., Feiler, H., Carroll, P., & Korkola, J. E. (2020). Enzalutamide response in a panel of prostate cancer cell lines reveals a role for glucocorticoid receptor in enzalutamide resistant disease. Scientific Reports, 10(1), 21750. https://doi.org/10.1038/s41598-020-78798-x Cite
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FRMD6 has Tumor Suppressor Functions in Prostate Cancer

In overexpression and CRISPR/Cas9 knockout experiments in prostate cancer cell lines, FRMD6 inhibited viability, proliferation, cell cycle progression, colony formation, 3D spheroid growth, and tumor xenograft growth in mice.
[Oncogene]
Haldrup, J., Strand, S. H., Cieza-Borrella, C., Jakobsson, M. E., Riedel, M., Norgaard, M., Hedensted, S., Dagnaes-Hansen, F., Ulhoi, B. P., Eeles, R., Borre, M., Olsen, J. V., Thomsen, M., Kote-Jarai, Z., & Sorensen, K. D. (2020). FRMD6 has tumor suppressor functions in prostate cancer. Oncogene, 1–14. https://doi.org/10.1038/s41388-020-01548-w Cite
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CDX2 Inhibits Epithelial–Mesenchymal Transition in Colorectal Cancer by Modulation of Snail Expression and β-Catenin Stabilization via Transactivation of PTEN Expression

A series of in vitro and in vivo experiments were conducted to reveal the role of caudal-related homoeobox transcription factor 2 (CDX2) in the invasion and metastasis of colorectal cancer.
[British Journal of Cancer]
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WDHD1 Is Essential for the Survival of PTEN-Inactive Triple-Negative Breast Cancer

To identify phosphatase and tensin homologue (PTEN) synthetic lethal interactions, TCGA analysis coupled with a whole-genome siRNA screen in isogenic PTEN-negative and -positive cells were performed. Among the candidate genes essential for the survival of PTEN-inactive TNBC cells, WDHD1 (WD repeat and high-mobility group box DNA-binding protein 1) expression was increased in the low vs. high PTEN TNBC samples.
[Cell Death & Disease]
Ertay, A., Liu, H., Liu, D., Peng, P., Hill, C., Xiong, H., Hancock, D., Yuan, X., Przewloka, M. R., Coldwell, M., Howell, M., Skipp, P., Ewing, R. M., Downward, J., & Wang, Y. (2020). WDHD1 is essential for the survival of PTEN-inactive triple-negative breast cancer. Cell Death & Disease, 11(11), 1–15. https://doi.org/10.1038/s41419-020-03210-5 Cite
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Senescence Reprogramming by TIMP1 Deficiency Promotes Prostate Cancer Metastasis

The authors identified the metalloproteinase inhibitor TIMP1 as a molecular switch that determines the effects of senescence in prostate cancer. Senescence driven either by PTEN deficiency or chemotherapy limited the progression of prostate cancer in mice.
[Cancer Cell]
Guccini, I., Revandkar, A., D’Ambrosio, M., Colucci, M., Pasquini, E., Mosole, S., Troiani, M., Brina, D., Sheibani-Tezerji, R., Elia, A. R., Rinaldi, A., Pernigoni, N., Rüschoff, J. H., Dettwiler, S., Marzo, A. M. D., Antonarakis, E. S., Borrelli, C., Moor, A. E., Garcia-Escudero, R., … Alimonti, A. (2020). Senescence Reprogramming by TIMP1 Deficiency Promotes Prostate Cancer Metastasis. Cancer Cell, 0(0). https://doi.org/10.1016/j.ccell.2020.10.012 Cite
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MiR-22, Regulated by MeCP2, Suppresses Gastric Cancer Cell Proliferation by Inducing a Deficiency in Endogenous S-Adenosylmethionine

Scientists revealed that the metabolic profiles in gastric cancer tissues were altered. S-adenosylmethionine, a universal methyl donor for histone and DNA methylation, which is specifically involved in the epigenetic maintenance of cancer cells, was found increased.
[Oncogenesis]
Tong, D., Zhang, J., Wang, X., Li, Q., Liu, L., Lu, A., Guo, B., Yang, J., Ni, L., Qin, H., Zhao, L., & Huang, C. (2020). MiR-22 , regulated by MeCP2, suppresses gastric cancer cell proliferation by inducing a deficiency in endogenous S-adenosylmethionine. Oncogenesis, 9(11), 1–16. https://doi.org/10.1038/s41389-020-00281-z Cite
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