Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1519176 (PSA)
 5,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study aimed to analyze the expression, clinical significance of cyclin G2 (CCNG2) in prostate carcinoma, and the biological effect in its cell line by CCNG2 overexpression. Immunohistochemistry and Western blot were used to analyze CCNG2 protein expression in 85 cases of prostate cancer and normal tissues to study the relationship between CCNG2 expression and clinical factors. CCNG2 lentiviral vector and empty vector were, respectively, transfected into prostate cancer PC-3 cell line. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were used to detect the mRNA level and protein of CCNG2. MTT assay and cell cycle were also conducted as to the influence of the upregulated expression of CCNG2 that might be found on PC-3 cells biological effect. The level of CCNG2 protein expression was found to be significantly lower in prostate cancer tissue than normal tissues (P < 0.05). The level of CCNG2 protein expression was not correlated with age, PSA contention, and tumor size (P < 0.05), but it was correlated with lymph node metastasis, clinic stage, and Gleason score (P < 0.05). The result of biological function shown that PC-3 cell transfected CCNG2 had a lower survival fraction, more percentage of the G0/G1 phases, and lower CDK2 protein expression compared with PC-3 cell untransfected CCNG2 (P < 0.05). CCNG2 expression decreased in prostate cancer and correlated significantly with lymph node metastasis, clinic stage, and Gleason score, suggesting that CCNG2 may play important roles as a negative regulator to prostate cancer cell.
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PMID:Effect of cyclin G2 on proliferative ability of prostate cancer PC-3 cell. 2429 74

Recent data suggested that plasma Ghrelin O-Acyl Transferase enzyme (GOAT) levels could represent a new diagnostic biomarker for prostate cancer (PCa). In this study, we aimed to explore the diagnostic and prognostic/aggressiveness capacity of GOAT in urine, as well as to interrogate its putative pathophysiological role in PCa. We analysed urine/plasma levels of GOAT in a cohort of 993 patients. In vitro (i.e., cell-proliferation) and in vivo (tumor-growth in a xenograft-model) approaches were performed in response to the modulation of GOAT expression/activity in PCa cells. Our results demonstrate that plasma and urine GOAT levels were significantly elevated in PCa patients compared to controls. Remarkably, GOAT significantly outperformed PSA in the diagnosis of PCa and significant PCa in patients with PSA levels ranging from 3 to 10 ng/mL (the so-called PSA grey-zone). Additionally, urine GOAT levels were associated to clinical (e.g., Gleason-score, PSA levels) and molecular (e.g., CDK2/CDK6/CDKN2A expression) aggressiveness parameters. Indeed, GOAT overexpression increased, while its silencing/blockade decreased cell-proliferation in PCa cells. Moreover, xenograft tumors derived from GOAT-overexpressing PCa (DU145) cells were significantly higher than those derived from the mock-overexpressing cells. Altogether, our results demonstrate that GOAT could be used as a diagnostic and aggressiveness marker in urine and a therapeutic target in PCa.
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PMID:Clinical Utility of Ghrelin-O-Acyltransferase (GOAT) Enzyme as a Diagnostic Tool and Potential Therapeutic Target in Prostate Cancer. 3176 15

Prostate cancer (PC) is one of the most common cancers in males. MicroRNAs (miRNAs) are demonstrated to be involved in prostate cancer development and progression. Recently, miR-96 was identified to play a tumor promoting role in several tumors including PC, however, the underlying function of miR-96 in PC still need to be known. In the study, our results demonstrated that miR-96 was higher in prostate cancer tissues compared with adjacent normal tissues. Higher miR-96 was association with higher PSA level, lymph node metastasis, pathologic stage and distant metastasis in prostate cancer patients. Lose-of-function studies showed that down-regulated expression of miR-96 inhibited cell proliferation and cell cycle by regulating down-regulating CyclinA1, CDK2 and CDK4 expression in PC cells. Furthermore, we found that FOXF2 was a target of miR-96 in PC cells and miR-96 promoted cell proliferation by suppressing FOXF2 expression. Thus, these results showed that inhibition of miR-96 may be a target for prostate cancer treatment.
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PMID:Overexpression of miR-96 promotes cell proliferation by targeting FOXF2 in prostate cancer. 3196 4