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Transcriptome analysis of Control and FBXO38 knockdown in HCT116 and Hela cell lines

ABSTRACT: Transcriptome analysis of Control and FBXO38 knockdown in HCT116 and Hela cell lines

PROVIDER: PRJNA911795 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22715408_1.fastq.gz	Fastqsanger.gz
	SRR22715408_2.fastq.gz	Fastqsanger.gz
	SRR22715409_1.fastq.gz	Fastqsanger.gz
	SRR22715409_2.fastq.gz	Fastqsanger.gz
	SRR22715410_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of Control and FBXO38 knockdown in HCT116 and Hela cell lines

Project description:F-box only protein 38 (FBXO38), which belongs to SKP1-CUL1-F-box protein (SCF) family, exhibits the ability to mediate Lys48-linked poly-ubiquitination and subsequent proteasome degradations of PD-1.To investigate the effect of FBXO38 knockdown on transcription in tumor, we constructed control and FBXO38 knockdown by shRNA in Hela and HCT116 cell lines. We found that FBXO38 may interact with the immune pathway in the tumor.

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E3 ubiquitin ligase FBXO38 maintains antitumor function of NK cells through sustaining IL-15R signaling

Project description:Natural killer (NK) cells are the main innate antitumor effector cells and can be constrained in the tumor microenvironment (TME). It has been reported that E3 ligase FBXO38 accelerates PD-1 degradation of tumor-infiltrating T cells to unleash their cytotoxic function. In this study, we found that FBXO38 transcripts were significantly lower in intra-tumoral NK cells than in peri-tumoral regions using specimens from cancer patients in The Cancer Genome Atlas (TCGA). Conditional knock-out (cKO) of FBXO38 in NK cells accelerated tumor growth and increased tumor metastasis. However, FBXO38 deficiency did not show an effect on the cytotoxic function of tumor-infiltrating NK (TINK) cells, but decreased proliferation and survival of TINK cells. Mechanically, FBXO38 deficiency led to TINK cell hyporesponsiveness to IL-15 by reducing the expression of IL-15Rβ and IL-15Rγc, which accounted for the reduced expansion of FBXO38-deficient TINK cells in TME. Furthermore, human NK-92 cells proliferated more rapidly when FBXO38 was overexpressed and exerted greater antitumor efficacy in xenograft mouse models. Conversely, the removal of FBXO38 led to a dramatic decrease in NK-92 cell proliferation. In conclusion, our results suggest that FBXO38 strongly sustains NK cell expansion in the antitumor immunity response.

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