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http://localhost:1200/science/current/signaling - Success
```rss
<![CDATA[Contents | Science Signaling 15, 756 | Current Issue]]>
https://www.science.org/toc/signaling/current
RSSHubi@diygod.me (DIYgod)en-UShttps://www.science.org/apple-touch-icon.png<![CDATA[Contents | Science Signaling 15, 756 | Current Issue]]>
https://www.science.org/toc/signaling/current
Thu, 20 Oct 2022 23:25:56 GMT5<![CDATA[Rerouting the drug response: Overcoming metabolic adaptation in KRAS-mutant cancers]]>
Abstract
Mutations in guanosine triphosphatase KRAS are common in lung, colorectal, and pancreatic cancers. The constitutive activity of mutant KRAS and its downstream signaling pathways induces metabolic rewiring in tumor cells that can promote resistance to existing therapeutics. In this review, we discuss the metabolic pathways that are altered in response to treatment and those that can, in turn, alter treatment efficacy, as well as the role of metabolism in the tumor microenvironment (TME) in dictating the therapeutic response in KRAS-driven cancers. We highlight metabolic targets that may provide clinical opportunities to overcome therapeutic resistance and improve survival in patients with these aggressive cancers.
]]>
Tue, 18 Oct 2022 00:00:00 GMThttps://www.science.org/doi/10.1126/scisignal.abj3490
https://www.science.org/doi/10.1126/scisignal.abj3490
<![CDATA[Fusobacterium nucleatum induces proliferation and migration in pancreatic cancer cells through host autocrine and paracrine signaling]]>
A tumorigenic infection
The tumor-associated microbiome can contribute to tumor development and progression. Udayasuryan et al. found that Fusobacterium nucleatum—an oral commensal that can become an opportunistic pathogen—promotes tumor progression–associated activity in pancreatic ductal adenocarcinoma (PDAC) cells. Infection with various subspecies of F. nucleatum induced the release of cytokines that promoted proliferation, migration, and invasion in human PDAC cell lines but not in normal human pancreatic epithelial cells. Proliferation was prevented with an antibody that blocks one of the secreted cytokines, GM-CSF. The findings reveal a host-microbe interaction that may promote progression in PDAC and that may therefore inform clinical strategies for prognosis and therapeutic intervention.
Abstract
The tumor microbiome is increasingly implicated in cancer progression and resistance to chemotherapy. In pancreatic ductal adenocarcinoma (PDAC), high intratumoral loads of Fusobacterium nucleatum correlate with shorter survival in patients. Here, we investigated the potential mechanisms underlying this association. We found that F. nucleatum infection induced both normal pancreatic epithelial cells and PDAC cells to secrete increased amounts of the cytokines GM-CSF, CXCL1, IL-8, and MIP-3α. These cytokines increased proliferation, migration, and invasive cell motility in both infected and noninfected PDAC cells but not in noncancerous pancreatic epithelial cells, suggesting autocrine and paracrine signaling to PDAC cells. This phenomenon occurred in response to Fusobacterium infection regardless of the strain and in the absence of immune and other stromal cells. Blocking GM-CSF signaling markedly limited proliferative gains after infection. Thus, F. nucleatum infection in the pancreas elicits cytokine secretion from both normal and cancerous cells that promotes phenotypes in PDAC cells associated with tumor progression. The findings support the importance of exploring host-microbe interactions in pancreatic cancer to guide future therapeutic interventions.
]]>
Tue, 18 Oct 2022 00:00:00 GMThttps://www.science.org/doi/10.1126/scisignal.abn4948
https://www.science.org/doi/10.1126/scisignal.abn4948
<![CDATA[Taking mitochondria to heart]]>
Abstract
Long-chain fatty acids redirect the uptake of mitochondria released from adipocytes from macrophages to the heart.
The heparan sulfate–dependent transfer of mitochondria from adipocytes to resident macrophages in adipose tissue promotes metabolic homeostasis. This process is disrupted by a high-fat diet, which induces the systemic release of oxidatively damaged mitochondria from adipocytes that are taken up by the heart. Borcherding et al. found that a diet enriched in long-chain fatty acids promoted this diversion of mitochondria from adipose tissue macrophages to the heart. Analysis of mice expressing an adipocyte-specific mitochondrial reporter revealed that mitochondria were transferred not only to macrophages but also to other cell types in adipose tissue, such as endothelial cells and neutrophils, in a tissue-specific manner. Mitochondrial transfer from adipocytes to other cell types, in particular to macrophages, was reduced by a high-fat diet based on lard, which consists of long-chain fatty acids. Treatment of BV2 macrophage-like cells with long-chain fatty acids decreased the uptake of purified mitochondria and the biomass of the mitochondria that were taken up. Long-chain fatty acids inhibited a heparan sulfate–dependent mechanism of mitochondrial uptake by macrophages. In mice, feeding with the lard-based, high-fat diet increased the release of adipocyte-derived mitochondria into the circulation and the appearance of these mitochondria in heart tissue. These effects of the lard-based, high-fat diet were not observed with a high-fat diet based on hydrogenated coconut oil (which consists primarily of medium-chain fatty acids), a high-sucrose or -cornstarch diet, or aging. Thus, dietary intake of long-chain fatty acids prevents macrophages in adipose tissue from taking up mitochondria released by adipocytes and redirects these mitochondria to be taken up by the heart.
]]>Tue, 18 Oct 2022 00:00:00 GMThttps://www.science.org/doi/10.1126/scisignal.adf2995
https://www.science.org/doi/10.1126/scisignal.adf2995
```
github-actions[bot]
commented
2 years ago 
TonyRL
Routes
Full routes
Related documentation
https://docs.rsshub.app/en/journal.html#science-magazine
What is expected?
get an xml
What is actually happening?
unable to get xml
Deployment information
RSSHub demo (https://rsshub.app)
Deployment information (for self-hosted)
Node version: v16.18.0 Git Hash: f095eaf
Additional info
This is not a duplicated issue