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A novel lncRNA lncRNA-AF339830 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE132888 | GEO | 2019/07/08

REPOSITORIES: GEO

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A novel lncRNA lncRNA-AK096729 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc

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2019-10-01 | GSE129950 | GEO

LncRNA GLCC1 promotes colorectal carcinogenesis and glucose metabolism by stabilizing c-Myc.

Project description:Long non-coding RNAs (lncRNAs) contribute to colorectal cancer (CRC). However, the role of lncRNAs in CRC metabolism, especially glucose metabolism remains largely unknown. In this study, we identify a lncRNA, GLCC1, which is significantly upregulated under glucose starvation in CRC cells, supporting cell survival and proliferation by enhancing glycolysis. Mechanistically, GLCC1 stabilizes c-Myc transcriptional factor from ubiquitination by direct interaction with HSP90 chaperon and further specifies the transcriptional modification pattern on c-Myc target genes, such as LDHA, consequently reprogram glycolytic metabolism for CRC proliferation. Clinically, GLCC1 is associated with tumorigenesis, tumor size and predicts poor prognosis. Thus, GLCC1 is mechanistically, functionally, and clinically oncogenic in colorectal cancer. Targeting GLCC1 and its pathway may be meaningful for treating patients with colorectal cancer.

| S-EPMC6677832 | biostudies-literature

A novel lncRNA lncRNA-AF339830 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc [RNA-Seq]

Project description:To elucidate whether lncRNA-AF339830 plays a role in colorectal cancer tumorigenesis, a RNA-seq analysis was performed to compare the gene expression profiles of lncRNA-AF339830 siRNA and control siRNA transfectants.

2019-07-08 | GSE119866 | GEO

A novel lncRNA lncRNA-AF339830 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc [ChIP-Seq]

Project description:To elucidate whether lncRNA-AF339830 plays a role in colorectal cancer tumorigenesis, a Chip-seq analysis was performed to compare the change of c-myc genome-wide binding of lncRNA-AF339830 siRNA and control siRNA transfectants.

2019-07-08 | GSE132887 | GEO

A novel lncRNA lncRNA-AK096729 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc

Project description:A novel lncRNA lncRNA-AK096729 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc

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A novel lncRNA lncRNA-AF339830 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc

Project description:A novel lncRNA lncRNA-AF339830 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc

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A novel lncRNA lncRNA-AF339830 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc [ChIP-Seq]

Project description:A novel lncRNA lncRNA-AF339830 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc [ChIP-Seq]

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A novel lncRNA lncRNA-AF339830 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc [RNA-Seq]

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CircECE1 activates energy metabolism in osteosarcoma by stabilizing c-Myc.

Project description:BackgroundOsteosarcoma (OS) is the most common malignant bone tumor and has a poor prognosis. The potential involvement of circular RNAs (circRNAs) in OS progression remains unexplored. Here, we report that CircECE1, a circular RNA derived from human ECE1, plays a critical role in energy metabolism in OS.MethodsThe RIP chip sequence assay was performed to confirm CircECE1, through overexpression or knockdown of CircECE1 to verify its function in 143B and U2OS. RNA immunoprecipitation and immunoprecipitation were used to verify CircECE1's regulation of protein c-Myc and co- immunoprecipitation was used to verified the competitive binding relationship between CircECE1 and SPOP. The influence of CircECE1 on energy metabolism was evaluated by seahorse experiment, western blot, and immunohistochemistry.ResultsWe found that CircECE1 is highly expressed in OS tissues and cells and that CircECE1 knockdown suppresses tumor proliferation and metastasis both in vitro and in vivo. Further, CircECE1 significantly promotes glucose metabolism in OS cells in vitro and in vivo. Mechanistically, CircECE1 interacts with c-Myc to prevent speckle-type POZ-mediated c-Myc ubiquitination and degradation. C-Myc inhibits thioredoxin binding protein (TXNIP) transcription and subsequently activates the Warburg effect.ConclusionsCircECE1 regulates the Warburg effect through the c-Myc/TXNIP axis. CircECE1 mediated signal transduction plays a important role in OS process and energy metabolism. These findings may identify novel targets for OS molecular therapy.

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Risk modification of colorectal adenoma by CYP7A1 polymorphisms and the role of bile acid metabolism in carcinogenesis.

Project description:Cholesterol 7?-hydroxylase (CYP7A1), the rate-limiting enzyme in the conversion of cholesterol to bile acids, is a postulated gene modifier of colorectal cancer risk and target for the therapeutic bile acid, ursodeoxycholic acid (UDCA). We investigated associations between CYP7A1 polymorphisms and fecal bile acids, colorectal adenoma (CRA), and UDCA efficacy for CRA prevention. Seven tagging, single-nucleotide polymorphisms (SNP) in CYP7A1 were measured in 703 (355 UDCA, 348 placebo) participants of a phase III chemoprevention trial, of which 495 had known baseline fecal bile acid concentrations. In the placebo arm, participants with two minor G(rs8192871) alleles (tag for a low activity promoter polymorphism at -204) had lower odds of high secondary bile acids (OR = 0.26, 95% CI: 0.10-0.69), and CRA at 3 years' follow-up (OR = 0.41, 95% CI: 0.19-0.89), than AA carriers. Haplotype construction from the six polymorphic SNPs showed participants with the third most common haplotype (C(rs10957057)C(rs8192879)G(rs8192877)T(rs11786580)A(rs8192871)G(rs13251096)) had higher odds of high primary bile acids (OR = 2.34, 95% CI: 1.12-4.89) and CRA (OR = 1.89, 95% CI: 1.00-3.57) than those with the most common CTACAG haplotype. Furthermore, three SNPs (rs8192877, rs8192871, and rs13251096) each modified UDCA efficacy for CRA prevention, and CCGTAG-haplotype carriers experienced 71% lower odds of CRA recurrence with UDCA treatment, an effect not present for other haplotypes (test for UDCA-haplotype interaction, P = 0.020). Our findings support CYP7A1 polymorphisms as determinants of fecal bile acids and risk factors for CRA. Furthermore, UDCA efficacy for CRA prevention may be modified by genetic variation in CYP7A1, limiting treatment benefit to a subgroup of the population.

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