STAT3 in the systemic inflammation of cancer cachexia

Weight loss is diagnostic of cachexia, a debilitating syndrome contributing mightily to morbidity and mortality in cancer. Most research has probed mechanisms leading to muscle atrophy and adipose wasting in cachexia; however cachexia is a truly systemic phenomenon. Presence of the tumor elicits an inflammatory response and profound metabolic derangements involving not only muscle and fat, but also the hypothalamus, liver, heart, blood, spleen and likely other organs. This global response is orchestrated in part through circulating cytokines that rise in conditions of cachexia. Exogenous Interleukin-6 (IL6) and related cytokines can induce most cachexia symptomatology, including muscle and fat wasting, the acute phase response and anemia, while IL-6 inhibition reduces muscle loss in cancer. Although mechanistic studies are ongoing, certain of these cachexia phenotypes have been causally linked to the cytokine-activated transcription factor, STAT3, including skeletal muscle wasting, cardiac dysfunction and hypothalamic inflammation. Correlative studies implicate STAT3 in fat wasting and the acute phase response in cancer cachexia. Parallel data in non-cancer models and disease states suggest both pathological and protective functions for STAT3 in other organs during cachexia. STAT3 also contributes to cancer cachexia through enhancing tumorigenesis, metastasis and immune suppression, particularly in tumors associated with high prevalence of cachexia. This review examines the evidence linking STAT3 to multi-organ manifestations of cachexia and the potential and perils for targeting STAT3 to reduce cachexia and prolong survival in cancer patients

Assembly annotation report

GO annotation report of the Saltugilia assembly using Annotate as part of the Trinity pipeline

Plastid_gene_alignments

MAFFT gene alignments for 80 plastid protein coding genes, as well as a concatenated alignment in both .phy and .nex formats. Genes were sequenced using MYbaits targeted exon capture baits, sequenced on Illumina platform, and analyzed using HybPiper

Nuclear_gene_alignments

MAFFT gene alignments for 89 putatively single copy nuclear genes, with a concatenated file in both .phy and .nex formats. Genes were sequenced using MYbaits exon capture kit, sequenced on Illumina platform, and then analyzed using HybPiper

de novo assemblies for each taxa and a master reference for the genus

This includes de novo assembly of a "master reference" using all reads in the study, then filtered assemblies for each taxa using a 1 TPM threshold

73 gene data set for 112 asterids

73 plastid genes for 112 accessions of asterids focusing on the lamiid

Gene partitions

List of the starting and stopping positions of the concatenated 73 plastid genes

GSK3 phylogenetic tree

Maximum Likelihood phylogenetic tree produced by RAxML 7.3.0 analysis of GSK3 land plant matrix with the GTRCAT model of evolutio

GSK3 gene expression

Gene expression data for GSK3 homologs in select seed plants. Gene expression levels are measured by normalized reads per kilobase per million (RPKM) values per tissue, except for Arabidopsis genes where they are measured by normalized microarray signal intensities per tissue. Gene expression levels in root, stem, seedling, leaf, flower/cone (during pre-meiotic, post-meiotic, and post-anthetic developmental stages), and fruit/seed of each species, are provided

Land Plant GSK3 matrix

MAFFT translation alignment of 445 plant genes encoding homologs of GSK3