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Fulvic acid exhibits antitumor effects in ovarian cancer cells by upregulating CYP1A1 expression

ABSTRACT: Fulvic acid exhibits antitumor effects in ovarian cancer cells by upregulating CYP1A1 expression

PROVIDER: PRJNA1065415 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27563711_1.fastq.gz	Fastqsanger.gz
	SRR27563711_2.fastq.gz	Fastqsanger.gz
	SRR27563712_1.fastq.gz	Fastqsanger.gz
	SRR27563712_2.fastq.gz	Fastqsanger.gz
	SRR27563713_1.fastq.gz	Fastqsanger.gz

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Fulvic acid exhibits antitumor effects in ovarian cancer cells by upregulating CYP1A1 expression

Project description:Humic substances are a mixture of natural organic macromolecular compounds, mainly fulvic acid (FA) (soluble in alkali, water, and acid) and humic acid (soluble in alkali but insoluble in water and acid). However, to the best of our knowledge, its antitumor effect remains indeterminate. Herein, we aimed to explore the effects and mechanisms of FA in ovarian cancer cells.

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Project description:In this project, we transfected MC38 cells with Flag-tagged Mbtps1 or vector control. After that, we performed immunoprecipitation–mass spectrometry analysis to search the interacting proteins of MBTPS1. In our study, We observed that the loss of membrane-bound transcription factor site-1 protease (MBTPS1) in tumor cells enhanced antitumor immunity and potentiated anti-PD-1 therapy. Mechanistic studies revealed that tumor cell-intrinsic MBTPS1 competed with USP13 for binding to STAT1, thereby disrupting USP13-dependent deubiquitination and stabilization of STAT1. MBTPS1 deficiency induced CXCR3+ CD8+ T cell infiltration by upregulating STAT1-transcribed chemokines including CXCL9, CXCL10 and CXCL11. Notably, the regulatory role of MBTPS1 in antitumor immunity operates independently of its classic function in cleaving membrane-bound transcription factors. Collectively, our results provide a theoretical basis for MBTPS1 as a potential immunotherapy target and also as a predictor of immunotherapy efficacy.

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PRMT5 inhibition by SCR-6920 leads to downregulation of HIF-1α and exhibits synergistic antitumor activity with bevacizumab in ovarian cancer

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Cancer SLC6A6-mediated taurine uptake impairs CD8+ T cell antitumor immunity by upregulating immune checkpoints [mouse RNA-Seq]

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Modulating the Response to Benzo[a]pyrene when CYP1A1 and CYP1B1 are Knocked Down

Project description:Benzo[a]pyrene is a Group 1 carcinogen. It undergoes metabolism in the liver through CYP1A1 and CYP1B1 enzymes. This study was conducted to investigate the response to benzo[a]pyrene in the liver when these enzymes are knocked down.

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PM2.5 leads to adverse pregnancy outcomes by inducing trophoblast oxidative stress and mitochondrial apoptosis via KLF9/CYP1A1 transcriptional axis

Project description:Epidemiological studies have demonstrated that fine particulate matter (PM2.5) is associated with adverse obstetric and postnatal metabolic health outcomes, but the mechanism remains unclear. This study aimed to investigate the toxicological pathways by which PM2.5 damaged placental trophoblasts in vivo and in vitro. We confirmed that PM2.5 induced adverse gestational outcomes such as increased fetal mortality rates, decreased fetal number and weight, damaged placental structure, and increased apoptosis of trophoblasts. Additionally, PM2.5 induced dysfunction of the trophoblast cell line HTR8/SVneo, including in its proliferation, apoptosis, invasion, migration and angiogenesis. Moreover, we comprehensively analyzed the transcriptional landscape of HTR8/SVneo cells exposed to PM2.5 through RNA-Seq and observed that PM2.5 triggered overexpression of pathways involved in oxidative stress and mitochondrial apoptosis to damage HTR8/SVneo cell biological functions through CYP1A1. Mechanistically, PM2.5 stimulated KLF9, a transcription factor identified as binding to CYP1A1 promoter region, which further modulated the CYP1A1-driven downstream phenotypes. Together, this study demonstrated that the KLF9/CYP1A1 axis played a crucial role in the toxic progression of PM2.5 induced adverse pregnancy outcomes, suggesting adverse effects of environmental pollution on pregnant females and putative targeted therapeutic strategies.

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Project description:Benzo[a]pyrene (BaP) is a prototypical polycyclic aromatic hydrocarbon (PAH) found in combustion processes. Cytochrome P450 1A1 and 1B1 enzymes (CYP1A1, CYP1B1) and other enzymes can activate PAHs to reactive oxygenated intermediates involved in mutagenesis and tumor initiation; also, CYP1 enzymes can detoxify PAHs. Cyp1(+/+) wild-type (WT) and Cyp1b1(-/-) knockout mice receiving oral BaP (12.5 mg/kg/day) remain healthy for >12 months. In contrast, we found that global knockout of the Cyp1a1 gene (1a1KO) results in proximal small intestine (PSI) adenocarcinoma within 8 to 12 weeks on this BaP regimen; striking compensatory increases in PSI CYP1B1 likely participate in initiation of adenocarcinoma in 1a1KO mice. Cyp1a1/1b1(-/-) double-knockout (DKO) mice on this BaP regimen show no PSI adenocarcinoma, but instead preputial gland duct (PGD) squamous cell carcinoma (SCC) occurs by 12 weeks. Herein we compare microarray expression of PGD genes in WT, 1a1KO and DKO mice at zero, 4, 8, 12, and 16 weeks of oral BaP; about four dozen genes up- or down-regulated during the most critical time-points were further verified by qRT-PCR. In DKO mice, CYP3A59 was unequivocally identified as the BaP-inducible and BaP-metabolizing best candidate responsible for initiation of BaP-induced SCC. Striking increases or decreases were found in 26 cancer-related genes plus eight Serpin genes in DKO, but not in 1a1KO or WT, mice on this BaP regimen; of the 26, eight were RAS-related oncogenes. The mechanism by which cancer-related genes are responsible for SCC tumor progression in the PGD remains to be elucidated. The tissue being tested is preputial gland duct of mice. Three genotypes (WT, Cyp1a1 KO and Cyp1a1/1b1 DKO) were compared with one another, at zero, 4, 8, 12 and 16 weeks of oral BaP. The five time-points within each genotype were also compared.

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