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Long noncoding RNA TCONS_00027385 acts as a miR-874-5p sponge to suppress the progression of prostate cancer through regulating ASCC2 expression

ABSTRACT: Coal tar pitch (CTP) is a byproduct of cooking process which is used in making coatings, corrosion protection materials, and electrode. and it has been verified that Coal tar pitch extract (CTPE) constitutes polycyclic aromatic hydrocarbons (PAHs) (87.91%) and monocyclic aromatic hydrocarbons, heterocyclic compounds and alkenes (the remaining total is 12.09%) using gas chromatography/mass spectrometry (GC/MS). In this study, we determine the lncRNA expression profile in CTPE group and control group. The key lncRNAs were screen out by using microarray analysis in defferent group. The experiment is divided into two groups: 22RV1 cells as control group, 22RV1 cells induced with Robustanoids A. then perform lncRNAs chips by Arraystar Human lncRNAs chip (Arraystar).

ORGANISM(S): Homo sapiens

PROVIDER: GSE180612 | GEO | 2021/07/24

REPOSITORIES: GEO

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Project description:The polycyclic aromatic hydrocarbon (PAH), benzo[a]pyrene (BaP), was compared to dibenzo[def,p]chrysene (DBC) and combinations of three environmental PAH mixtures (coal tar, diesel particulate and cigarette smoke condensate) using a two stage, FVB/N mouse skin tumor model. DBC (4 nmol) was most potent, reaching 100% tumor incidence with a shorter latency to tumor formation, less than 20 weeks of 12-O-tetradecanoylphorbol-13-acetate (TPA) promotion compared to all other treatments. Multiplicity was 4 times greater than BaP (400 nmol). Both PAHs produced primarily papillomas followed by squamous cell carcinoma and carcinoma in situ. Diesel particulate extract (1 mg SRM 1650b; mix 1 ) did not differ from toluene controls and failed to elicit a carcinogenic response. Addition of coal tar extract (1 mg SRM 1597a; mix 2) produced a response similar to BaP. Further addition of 2 mg of cigarette smoke condensate (mix 3) did not alter the response of mix 2. PAH-DNA adducts measured in epidermis 12 h post initiation and analyzed by 32P post- labeling, did not correlate with tumor incidence. PAH dependent alteration in transcriptome of skin 12 h post initiation was assessed by microarray. Principal component analysis (sum of all treatments) of the 922 significantly altered genes (p<0.05), showed DBC and BaP to cluster distinct from PAH mixtures and each other. BaP and mixtures up-regulated phase 1 and 2 metabolizing enzymes while DBC did not. The carcinogenicity with DBC and two of the mixtures was much greater than would be predicted based on published Relative Potency Factors (RPFs). Gene expression was measured in mouse skin 12 hours after initiation with PAH carcinogens. The following initiation treatments were applied to mice (N=4 or 5 per biological replicates treatment); toluene vehicle control (200 M-NM-<l), BaP 400 nmol (100 M-NM-<g), DBC 4 nmol (1.2 M-NM-<g), or to mixtures of environmental PAH mixtures containing diesel particulate extract, coal tar extract, or cigarette smoke condensate.

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Long noncoding RNA TCONS_00027385 acts as a miR-874-5p sponge to suppress the progression of prostate cancer through regulating ASCC2 expression

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