Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Colorectal cancer cells respond differentially to autophagy inhibition in vivo

ABSTRACT: Colorectal cancer cells respond differentially to autophagy inhibition in vivo

PROVIDER: PRJNA553764 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9667730_1.fastq.gz	Fastqsanger.gz
	SRR9667730_2.fastq.gz	Fastqsanger.gz
	SRR9667731_1.fastq.gz	Fastqsanger.gz
	SRR9667731_2.fastq.gz	Fastqsanger.gz
	SRR9667732_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Colorectal cancer cells respond differentially to autophagy inhibition in vivo

Project description:inhibition of autophagy in vivo had a substantial cell line-dependent impact on tumor growth of different CRC derived cell lines. RNA sequencing of WT and RAB21 KD tumors in a CAM model was used to determine the gene expression profile associated with these differential responses.

2019-07-11 | GSE134095 | GEO

Colorectal cancer cells respond differentially to autophagy inhibition in vivo.

Project description:Autophagy has both tumor-promoting and -suppressing effects in cancer, including colorectal cancer (CRC), with transformed cells often exhibiting high autophagic flux. In established tumors, autophagy inhibition can lead to opposite responses resulting in either tumor cell death or hyperproliferation. The functional mechanisms underlying these differences are poorly understood. The present study aimed to investigate the relationship between the autophagic capacities of CRC cells and their sensitivities to autophagy inhibition. All studied CRC cell lines showed high basal autophagic flux. However, only HCT116 and Caco-2/15 cells displayed regulated autophagic flux upon starvation. Knockdown of ATG5 (which disrupts autophagosome elongation) or RAB21 (which decreases autophagosome/lysosome fusion) had little effect on CRC cell proliferation in vitro. Nonetheless, inhibition of autophagy in vivo had a substantial cell line-dependent impact on tumor growth, with some cells displaying decreased (HCT116 and Caco-2/15) or increased (SW480 and LoVo) proliferation. RNA sequencing and Western blot analyses in hyperproliferative SW480 tumors revealed that the mTORC2 and AKT pathways were hyperactivated following autophagy impairment. Inhibition of either mTOR or AKT activities rescued the observed hyperproliferation in autophagy-inhibited SW480 and reduced tumor growth. These results highlight that autophagy inhibition can lead, in specific cellular contexts, to compensatory mechanisms promoting tumor growth.

| S-EPMC6683171 | biostudies-literature

Rectal cancer sub-clones respond differentially to neoadjuvant therapy

Project description:Rectal cancer sub-clones respond differentially to neoadjuvant therapy

| PRJNA563898 | ENA

Differentially expressed miRNAs in colorectal cancer

Project description:Differentially expressed miRNAs in colorectal cancer

| PRJNA658901 | ENA

Inhibition of Hedgehog Signaling Pathway Impairs Cancer Cell Growth via Promotion of Autophagy

Project description:Analysis of gene expression levels in response to inhibition of Hh signaling in ovarian and glioma cancer cells using a cDNA microarray technique. Microarray analyses revealed that differentially expressed genes (DEGs) in human cancer cells are enriched in the senescence and autophagy pathways in response to the inhibition of Hh signaling. Further investigations showed that inhibition of Hh signaling induced autophagy.. ES2 and H4 cells were treated with GANT61 (20 M-NM-<M for 32hr and 48hr) and control vehicle DMSO, respectively.

2014-06-15 | E-GEOD-54936 | biostudies-arrayexpress

Decoding differentially regulated epithelial and stromal pathways in colorectal cancer

Project description:Analysis of differentially expressed genes from dissected whole tissue and laser capture microdissected colorectal cancer tissue samples The analysis, in colorectal cancer tissues, of compartmental and whole tissue expression profiles as well as the significantly active pathways that were differentially deregulated between the epithelial and stromal compartments when compared alongside that of whole tissue dissection Comparison of tumor epithelium vs normal epithelium; tumor stroma vs normal stroma and tumor whole tissue vs normal whole tissue

2011-08-09 | E-GEOD-31279 | biostudies-arrayexpress

Tumor-intrinsic expression of the autophagy gene Atg16l1 suppresses anti-tumor immunity in colorectal cancer

Project description:The vast majority of colorectal cancer (CRC) patients fail to respond to immune checkpoint inhibitors (ICI). Understanding tumor-intrinsic determinants of immunotherapy resistance is critical to improve CRC patient outcomes. Here, we demonstrate that transcript levels of the core autophagy gene ATG16L1 are prognostic of poor outcome and predictive of ICI resistance in late-stage CRC. Deletion of Atg16l1 in murine CRC organoids markedly inhibited tumor growth in primary and metastatic niches in syngeneic hosts. ATG16L1 deficiency rendered CRC organoids more responsive to interferon (IFN) signaling and enhanced programmed cell death while decreasing tumor stem-like populations. IFN hypersensitivity consequently promoted cytotoxic anti-tumor immunity in vivo. In IMblaze370, a large phase III clinical trial of anti-PD-L1 in advanced metastatic CRC, low ATG16L1 levels identified patients with increased lymphocyte infiltration and improved outcome in a KRAS mutant setting. This work reveals autophagy as a clinically relevant immunosuppressive mechanism in CRC and provides a rationale for autophagy inhibition to boost immunotherapy responses in the clinic.

| EGAS00001005952 | EGA

Decoding differentially regulated epithelial and stromal pathways in colorectal cancer

2011-08-10 | GSE31279 | GEO

Tumor-intrinsic expression of the autophagy gene Atg16l1 suppresses anti-tumor immunity in colorectal cancer (bulk RNA-seq)

Project description:We utilized bulk RNA sequencing to assess intrinsic differences between wildtype and autophagy-defective (Atg16l1 deleted) AKPS colorectal cancer organoids in both untreated and IFN gamma treated conditions. AKPS mutations consist of loss-of-function in tumor suppressors Apc, Trp53, Smad4, and gain-of-function in oncogenic Kras(G12D).

2023-08-28 | GSE192513 | GEO

Differentially expressed SE-lncRNAs and mRNA in colorectal cancer

Project description:Differentially expressed SE-lncRNAs and mRNA in colorectal cancer

| PRJNA634378 | ENA