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The gene expression change of RNF31 depletion in MCF-7 cells

ABSTRACT: RNF31 is atypical E3 ligase, which is highly expressed in human breast cancers. In order to understand the effect of RNF31 depletion effect in breast cancers, we knocked down the expression of RNF31 in MCF-7 cells. We aim to find the significantly changed pathways and cell biology behavior.

ORGANISM(S): Homo sapiens

PROVIDER: GSE46010 | GEO | 2014/02/06

SECONDARY ACCESSION(S): PRJNA196872

REPOSITORIES: GEO

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The gene expression change of RNF31 depletion in MCF-7 cells

Project description:RNF31 is atypical E3 ligase, which is highly expressed in human breast cancers. In order to understand the effect of RNF31 depletion effect in breast cancers, we knocked down the expression of RNF31 in MCF-7 cells. We aim to find the significantly changed pathways and cell biology behavior. 100uM RNF31 siRNA was applied to transfect the MCF-7 cells, while 100uM siControl was used as the control. Cells were cultured in DMEM red medium with 10% of FBS. Seventy two hours of post transfection, the total RNA was extracted to perform RNA expression analysis.

2014-02-06 | E-GEOD-46010 | biostudies-arrayexpress

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Project description:Tumor escape mechanisms for immunotherapy include deficiencies in antigen presentation, diminishing adaptive CD8+ T cell antitumor activity. Although innate NK cells are triggered by loss of MHC class I, their response is often inadequate. To increase tumor susceptibility to both innate and adaptive immune elimination, we performed parallel genome-wide CRISPR-Cas9 screens. This identified all components, RNF31, RBCK1, and SHARPIN, of the linear ubiquitination chain assembly complex (LUBAC). Genetic and pharmacologic ablation of RNF31, an E3 ubiquitin ligase, strongly sensitized melanoma, breast and colorectal cancer cells to both NK and CD8+ T cell killing. This occurred in a TNF-dependent manner, causing loss of A20 and non-canonical IKK complexes from TNF Receptor Complex I. Corroborating this preclinically, a small molecule RNF31 inhibitor sensitized human colon carcinoma organoids to TNF and greatly enhanced immune bystander killing of antigen-loss and antigen presentation machinery-deficient tumor cells. These results merit exploration of RNF31 inhibition as a clinical pharmacological opportunity for immunotherapy-refractory cancers.

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