Tag Archives: type-publication

lncRNA SNHG11 Facilitates Prostate Cancer Progression through the Upregulation of IGF-1R Expression and by Sponging miR-184

Researchers investigated the functional role and molecular mechanisms of SNHG11 in prostate cancer (PCa) progression. It was revealed that the SNHG11 expression levels were significantly upregulated in PCa tissues, in comparison with those in adjacent normal tissues.
[International Journal of Molecular Sciences]
Xie, Q., Zhao, S., Kang, R., & Wang, X. (2021). lncRNA SNHG11 facilitates prostate cancer progression through the upregulation of IGF‑1R expression and by sponging miR‑184. International Journal of Molecular Medicine, 48(3), 1–11. https://doi.org/10.3892/ijmm.2021.5015 Cite
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Androgen Receptor Antagonists Produced by Streptomyces Overcome Resistance to Enzalutamide

From the natural product screening, the novel compound arabilin was isolated from Streptomyces sp. MK756-CF1. Unlike STK765173, arabilin could overcome resistance to enzalutamide.
[Journal of Antibiotics]
Imoto, M., Fujimaki, T., Saito, S., & Tashiro, E. (2021). Androgen receptor antagonists produced by Streptomyces overcome resistance to enzalutamide. The Journal of Antibiotics, 1–11. https://doi.org/10.1038/s41429-021-00453-y Cite
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Compromised Dental Cells Viability Following Teeth-Whitening Exposure

Researchers assessed the viability of dental cells following time-dependent carbamide peroxide teeth-whitening treatments using an in vitro dentin perfusion assay model.
[Scientific Reports]
Redha, O., Mazinanian, M., Nguyen, S., Son, D. O., Lodyga, M., Hinz, B., Odlyha, M., McDonald, A., & Bozec, L. (2021). Compromised dental cells viability following teeth-whitening exposure. Scientific Reports, 11(1), 15547. https://doi.org/10.1038/s41598-021-94745-w Cite
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Mkx Mediates Tenogenic Differentiation but Incompletely Inhibits the Proliferation of Hypoxic MSCs

qRT-PCR, western blot, and immunofluorescence staining were performed to evaluate the expression of Mkx and other tendon-associated markers in adipose-derived MSCs and bone marrow-derived MSCs under hypoxia condition.
[Stem Cell Research & Therapy]
Chen, G., Fan, D., Zhang, W., Wang, S., Gu, J., Gao, Y., He, L., Li, W., Zhang, C., Li, M., Zhang, Y., Liu, Z., & Hao, Q. (2021). Mkx mediates tenogenic differentiation but incompletely inhibits the proliferation of hypoxic MSCs. Stem Cell Research & Therapy, 12(1), 426. https://doi.org/10.1186/s13287-021-02506-3 Cite
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Donor-Derived CD7 Chimeric Antigen Receptor T Cells for T-Cell Acute Lymphoblastic Leukemia: First-in-Human, Phase I Trial

In this single-center, Phase I trial, we administered anti-CD7 chimeric antigen receptor (CAR) T cells, manufactured from either previous stem-cell transplantation donors or new donors, to patients with relapsed or refractory T-cell acute lymphoblastic leukemia, in single infusions at doses of 5 × 105 or 1 × 106 cells per kilogram of body weight.
[Journal of Clinical Oncology]
Pan, J., Tan, Y., Wang, G., Deng, B., Ling, Z., Song, W., Seery, S., Zhang, Y., Peng, S., Xu, J., Duan, J., Wang, Z., Yu, X., Zheng, Q., Xu, X., Yuan, Y., Yan, F., Tian, Z., Tang, K., … Feng, X. (2021). Donor-Derived CD7 Chimeric Antigen Receptor T Cells for T-Cell Acute Lymphoblastic Leukemia: First-in-Human, Phase I Trial. Journal of Clinical Oncology, JCO.21.00389. https://doi.org/10.1200/JCO.21.00389 Cite
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The Synergistic Anticancer Traits of Graphene Oxide Plus Doxorubicin Against BT474 and MCF7 Breast Cancer Stem Cells In Vitro

Different concentrations of doxorubicin (DOX), graphene oxide, and graphene oxide plus doxorubicin (GO-DOX) were subjected to MCF7 and BT474 human breast cancer cells at specified intervals.
[Applied Biochemistry and Biotechnology]
Ebrahimi, M., Teimouri, M., & Pooladi, M. (2021). The Synergistic Anticancer Traits of Graphene Oxide Plus Doxorubicin Against BT474 and MCF7 Breast Cancer Stem Cells In Vitro. Applied Biochemistry and Biotechnology. https://doi.org/10.1007/s12010-021-03623-8 Cite
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Hijacking TYRO3 from Tumor Cells via Trogocytosis Enhances NK-Cell Effector Functions and Proliferation

Investigators found that although NK cells did not express endogenous TYRO3 on the cell surface, activated NK cells rapidly acquired TYRO3 from tumor cells via trogocytosis in vitro and in vivo.
[Cancer Immunology Research]
Lu, T., Ma, R., Li, Z., Mansour, A. G., Teng, K.-Y., Chen, L., Zhang, J., Barr, T., Caligiuri, M. A., & Yu, J. (2021). Hijacking TYRO3 from tumor cells via trogocytosis enhances NK-cell effector functions and proliferation. Cancer Immunology Research. https://doi.org/10.1158/2326-6066.CIR-20-1014 Cite
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MASTL Regulates EGFR Signaling to Impact Pancreatic Cancer Progression

Based on a comprehensive investigation involving pancreatic cancer (PC) patient samples, murine models of PC progression, and loss and gain of function studies, researchers reported a previously undescribed critical role of microtubule-associated serine/threonine-protein kinase-like (MASTL) in promoting cancer malignancy and therapy resistance.
[Oncogene]
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PRMT1-Dependent Regulation of RNA Metabolism and DNA Damage Response Sustains Pancreatic Ductal Adenocarcinoma

Scientists employed an RNAi-based in vivo functional genomics platform to determine epigenetic vulnerabilities across a panel of patient-derived pancreatic ductal adenocarcinoma models.
[Nature Communications]
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Stress-Primed Secretory Autophagy Promotes Extracellular BDNF Maturation by Enhancing MMP9 Secretion

Brain-derived neurotrophic factor (BDNF) is essential for adult synaptic plasticity and its pathway is associated with major depression and posttraumatic stress disorder. Researchers found that stress-enhanced matrix metalloproteinase 9 (MMP9) secretion increased the cleavage of proBDNF to its mature form mBDNF.
[Nature Communications]
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Autoantibodies against NMDA Receptor 1 Modify Rather Than Cause Encephalitis

Investigators tested whether following immunization with a “cocktail” of 4 NMDAR1 peptides, induction of a spatially and temporally defined sterile encephalitis by diphtheria toxin-mediated ablation of pyramidal neurons would modify/aggravate the ensuing phenotype.
[Molecular Psychiatry]
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