Tag Archives: prostate cells

Targeting a Splicing-Mediated Drug Resistance Mechanism in Prostate Cancer by Inhibiting Transcriptional Regulation by PKCβ1

PKCβ inhibition reduced total androgen receptor (AR) gene expression, thus reducing AR-V7 protein levels and sensitizing prostate cancer cells to current anti-androgen therapies.
[Oncogene]
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HER2 Mediates PSMA/mGluR1-Driven Resistance to the DS-7423 Dual PI3K/mTOR Inhibitor in PTEN Wild-Type Prostate Cancer Models

Scientists investigated the response of PTEN wild-type prostate cancer cell lines to the dual PI3K/mTOR inhibitor DS-7423 alone or in combination with HER2 inhibitors or mGluR1 inhibitors.
[Molecular Cancer therapeutics]
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MIRO2 Regulates Prostate Cancer Cell Growth via GCN1-Dependent Stress Signaling

Using human cell lines that represent androgen-independent or -sensitive prostate cancer, the authors showed that mitochondrial Rho GTPase 2 (MIRO2) depletion impaired cell growth, colony formation, and tumor growth in mice.
[Molecular Cancer Research]
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Prostate Cancer Cell Proliferation Is Influenced by LDL-Cholesterol Availability and Cholesteryl Ester Turnover

As cholesterol is a key substrate for de novo steroidogenesis in prostate cells, researchers hypothesized that castrate-resistant/advanced prostate cancer cell growth was influenced by the availability of extracellular, low-density lipoprotein (LDL)-derived, cholesterol, which was coupled to intracellular cholesteryl ester homeostasis.
[Cancer & Metabolism]
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Targeting Protein Arginine Methyltransferase 5 (PRMT5) Suppresses Radiation-Induced Neuroendocrine Differentiation and Sensitizes Prostate Cancer Cells to Radiation

Scientists performed transcriptomic analysis and confirmed that fractionated ionizing radiation (FIR)-induced neuroendocrine (NE)-like cells share some features of clinical NE prostate cancer, suggesting that FIR-induced NE differentiation represents a clinically-relevant model.
[Molecular Cancer therapeutics]
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Combined Effect of Heat Shock Protein Inhibitor Geldanamycin and Free Radicals on Photodynamic Therapy of Prostate Cancer

The authors found that the inhibition of Hsp90 could inhibit the overexpression of its client proteins such as anti-apoptotic proteins and androgen receptor, thereby improving the efficacy of photodynamic therapy and inducing prostate cancer cell apoptosis.
[Journal of Materials Chemistry B]
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MIRO2 Regulates Prostate Cancer Cell Growth via GCN1-Dependent Stress Signaling

Using human cell lines that represent androgen-independent or -sensitive prostate cancer, the authors showed that Mitochondrial Rho GTPase 2 (MIRO2) depletion impaired cell growth, colony formation and tumor growth in mice.
[Molecular Cancer Research]
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Inhibitory Effect of Roburic Acid in Combination with Docetaxel on Human Prostate Cancer Cells

The potential synergistic anticancer effect and the underlying mechanisms of roburic acid in combination with docetaxel on prostate cancer were investigated.
[Journal of Enzyme inhibition and Medicinal Chemistry]
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Epigenetic Loss of Heterogeneity from Low to High Grade Localized Prostate Tumors

Researchers sequenced the accessible chromatin regions of 14,424 single-cells from 18 flash-frozen prostate tumors and observed shared chromatin features among low-grade prostate cancer cells are lost in high-grade tumors.
[Nature Communications]
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The Opposing Action of Stromal Cell Proenkephalin and Stem Cell Transcription Factors in Prostate Cancer Differentiation

Researchers found that prostate cancer cells appeared to retain their responsiveness to stromal proenkephalin (PENK) signaling. PENK could induce differentiation to counter de-differentiation caused by stem cell transcription factor activation.
[BMC Cancer]
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LncRNA LINC00184 Promotes Docetaxel Resistance and Immune Escape via miR-105-5p/Pd-L1 Axis in Prostate Cancer

The authors explored the function and mechanism of LINC00184 in docetaxel resistance of prostate cancer and found that LINC00184 promoted docetaxel resistance and immune escape in prostate cancer cells by adsorption of miR-105-5p, resulting in upregulation of the expression of PD-L1.
[Immunobiology]
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