chloroquine/sarcoom

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Chloroquine inhibits lytic replication of Kaposi's sarcoma-associated herpesvirus by disrupting mTOR and p38-MAPK activation.

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Lytic infection is essential for the persistent infection and pathogenesis of Kaposi's sarcoma-associated herpesvirus (KSHV), and inhibiting KSHV lytic replication may effectively prevent the occurrence of KSHV-related diseases. Chloroquine (CQ), a well-known antimalarial drug and autophagy

A metabolic synthetic lethal strategy with arginine deprivation and chloroquine leads to cell death in ASS1-deficient sarcomas.

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Sarcomas comprise a large heterogeneous group of mesenchymal cancers with limited therapeutic options. When treated with standard cytotoxic chemotherapies, many sarcomas fail to respond completely and rapidly become treatment resistant. A major problem in the investigation and treatment of sarcomas

Inhibition of endoplasmic reticulum stress-induced autophagy promotes the killing effect of X-rays on sarcoma in mice.

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Endoplasmic reticulum (ER) stress is a conserved cellular process for cells to clear unfolded or misfolded proteins and maintain cell homeostasis under stress conditions. Autophagy may act as a pro-survival strategy to cope with multiple stress conditions in tumor progression and distant metastasis.

Transport of a lysosomally targeted Rous sarcoma virus envelope glycoprotein involves transient expression on the cell surface.

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The details of intracellular transport pathways for glycosylated proteins remain incompletely described. We previously described a mutant Rous sarcoma virus envelope glycoprotein (gp), mu 26, with an altered membrane-spanning domain that was targeted to lysosomes after traversing the trans-Golgi.

A charged amino acid substitution within the transmembrane anchor of the Rous sarcoma virus envelope glycoprotein affects surface expression but not intracellular transport.

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Two point mutations were introduced by oligonucleotide-directed mutagenesis into the region of the Rous sarcoma virus envelope gene that encodes the hydrophobic transmembrane anchor of the receptor glycoprotein. Single-nucleotide substitutions ultimately converted a hydrophobic leucine, located

Chloroquine Enhances Rapamycin-induced Apoptosis in MG63 Cells.

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We previously showed that the use of autophagy inhibitors in combination with chemotherapy can enhance anticancer effects in sarcoma cell lines. In this study, we investigated the combined effect of the autophagy inhibitor chloroquine and the mTOR inhibitor rapamycin on MG63

VDR agonists down regulate PI3K/Akt/mTOR axis and trigger autophagy in Kaposi's sarcoma cells.

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The Kaposi's sarcoma-associated herpesvirus G protein-coupled receptor (KSHV/vGPCR) is a key molecule in the pathogenesis of Kaposi's sarcoma. We have previously shown that 1α,25(OH)₂D₃ or its less-calcemic analog TX 527 inhibits the proliferation of endothelial cells

Therapeutic potential of CPI-613 for targeting tumorous mitochondrial energy metabolism and inhibiting autophagy in clear cell sarcoma.

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Clear cell sarcoma (CCS) is an aggressive type of soft tissue tumor that is associated with high rates of metastasis. In the present study, we found that CPI-613, which targets tumorous mitochondrial energy metabolism, induced autophagosome formation followed by lysosome fusion in HS-MM CCS cells in

Macroautophagy is dispensable for growth of KRAS mutant tumors and chloroquine efficacy.

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Macroautophagy is a key stress-response pathway that can suppress or promote tumorigenesis depending on the cellular context. Notably, Kirsten rat sarcoma (KRAS)-driven tumors have been reported to rely on macroautophagy for growth and survival, suggesting a potential therapeutic approach of using

Mediation of reduction of spontaneous and experimental pulmonary metastases by ricin A-chain immunotoxin 45-2D9-RTA with potentiation by systemic monensin in mice.

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We developed a model to assess the therapeutic effects of the 45-2D9-ricin A-chain immunotoxin (RTA) on pulmonary metastases. The 45-2D9 mouse monoclonal antibody recognizes a Mr 74,000 glycoprotein highly expressed by rat fibroblasts transformed with the Kirsten sarcoma virus (transformed rat

Energy requirement for degradation of tumor-associated protein p53.

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A 53,000-dalton protein (p53) present in large amounts in several types of tumorigenic cells was rapidly degraded in nontumorigenic BALB/c 3T3 fibroblasts (t 1/2, approximately 0.5 h) but not in tumorigenic methylcholanthrene-induced mouse sarcoma cells (t 1/2, greater than 2 h). In 3T3 cells,

Replacement of the human insulin receptor transmembrane and cytoplasmic domains by corresponding domains of the oncogene product v-ros leads to accelerated internalization, degradation, and down-regulation.

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Internalization, degradation, and insulin-induced down-regulation of insulin receptors were studied comparatively in transformed Chinese hamster ovary (CHO) cell lines, CHO.T and CHO.IR.ros, respectively expressing either the wild-type human insulin receptor (hIR) or a mutated hybrid receptor in

Polycation-DNA complexes for gene delivery: a comparison of the biopharmaceutical properties of cationic polypeptides and cationic lipids.

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DNA plasmids formed particulate complexes with a variety of cationic polyamino acids and cationic lipids, which were used to transfect mammalian cells in culture. Complexation was studied by assaying for exclusion of ethidium using a fluorometric assay, which indicated that complexation with

Role of the MAPK/cJun NH2-terminal kinase signaling pathway in starvation-induced autophagy.

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Autophagy is required for cellular homeostasis and can determine cell viability in response to stress. It is established that MTOR is a master regulator of starvation-induced macroautophagy/autophagy, but recent studies have also implicated an essential role for the MAPK8/cJun NH2-terminal kinase 1

ARF, autophagy and tumor suppression.

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Autophagy plays a critical role in the initiation and progression of tumors. The exact nature of this role, however, is complex. Autophagy is suppressive to tumor initiation, and reduces genomic instability. Genes with key roles in autophagy are mutated in human cancer, and knockout mice for certain

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