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  • 1
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2020
    In:  Journal of Translational Medicine Vol. 18, No. 1 ( 2020-12)
    In: Journal of Translational Medicine, Springer Science and Business Media LLC, Vol. 18, No. 1 ( 2020-12)
    Abstract: Prostate cancer (PCa) is one of the most prevalent cancers that occur in men worldwide. Autophagy-related genes (ARGs) may play an essential role in multiple biological processes of prostate cancer. However, ARGs expression signature has rarely been used to investigate the association between autophagy and prognosis in PCa. This study aimed to identify and assess prognostic ARGs signature to predict overall survival (OS) and disease-free survival (DFS) in PCa patients. Methods First, a total of 234 autophagy-related genes were obtained from The Human Autophagy Database. Then, differentially expressed ARGs were identified in prostate cancer patients based on The Cancer Genome Atlas (TCGA) database. The univariate and multivariate Cox regression analysis was performed to screen hub prognostic ARGs for overall survival and disease-free survival, and the prognostic model was constructed. Finally, the correlation between the prognostic model and clinicopathological parameters was further analyzed, including age, T status, N status, and Gleason score. Results The OS-related prognostic model was constructed based on the five ARGs (FAM215A, FDD, MYC, RHEB, and ATG16L1) and significantly stratified prostate cancer patients into high- and low-risk groups in terms of OS (HR = 6.391, 95% CI = 1.581– 25.840, P  〈  0.001). The area under the receiver operating characteristic curve (AUC) of the prediction model was 0.84. The OS-related prediction model values were higher in T3-4 than in T1-2 (P = 0.008), and higher in Gleason score   〉  7 than  ≤ 7 (P = 0.015). In addition, the DFS-related prognostic model was constructed based on the 22 ARGs (ULK2, NLRC4, MAPK1, ATG4D, MAPK3, ATG2A, ATG9B, FOXO1, PTEN, HDAC6, PRKN, HSPB8, P4HB, MAP2K7, MTOR, RHEB, TSC1, BIRC5, RGS19, RAB24, PTK6, and NRG2), with AUC of 0.85 (HR = 7.407, 95% CI = 4.850–11.320, P  〈  0.001), which were firmly related to T status (P  〈  0.001), N status (P = 0.001), and Gleason score (P  〈  0.001). Conclusions Our ARGs based prediction models are a reliable prognostic and predictive tool for overall survival and disease-free survival in prostate cancer patients.
    Type of Medium: Online Resource
    ISSN: 1479-5876
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2118570-0
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  • 2
    In: Current Molecular Medicine, Bentham Science Publishers Ltd., Vol. 23 ( 2023-05-22)
    Abstract: Alpinetin, a natural flavonoid, has been shown to have anticancer effects on many tumors. This study investigated the antitumor effect of alpinetin on renal clear cell carcinoma (ccRCC). Methods: Network Pharmacology analysis was carried out on the targets and molecular mechanisms of alpinetin treating ccRCC. The Annexin V PE/7-AAD kit was used to detect apoptosis. Flow cytometry and Cell Counting Kit-8 (CCK-8) were used to detect cell proliferation and cycle. A 24-well transwell chamber and the ibidi scratch insertion performed cell migration analysis. The protein expression of the target molecule was detected by Western blotting. Nude mouse tumorigenesis assays were used to determine the in vivo antitumor effects of alpinetin. Results: The network pharmacology revealed that GAPDH, HRAS, SRC, EGFR, and AKT1 are the main targets of alpinetin in treating ccRCC, with the PI3K/AKT signaling pathway being the main pathway of action. We found that alpinetin could significantly inhibit the proliferation and migration of ccRCC cells by inducing apoptosis. In addition, alpinetin also inhibited the cycle progression of ccRCC cells by blocking them in the G1 phase. Furthermore, in vivo and in vitro, alpinetin could inhibit the activation of an important pathway involved in the proliferation and migration of ccRCC cells, namely the PI3K/Akt pathway. Conclusion: Alpinetin can inhibit the growth of ccRCC cells by inhibiting the activation of the PI3K/Akt pathway and can be a potential anti-cancer drug for ccRCC.
    Type of Medium: Online Resource
    ISSN: 1566-5240
    Language: English
    Publisher: Bentham Science Publishers Ltd.
    Publication Date: 2023
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  • 3
    Online Resource
    Online Resource
    Hindawi Limited ; 2020
    In:  BioMed Research International Vol. 2020 ( 2020-05-18), p. 1-10
    In: BioMed Research International, Hindawi Limited, Vol. 2020 ( 2020-05-18), p. 1-10
    Abstract: Background . Prostate adenocarcinoma (PRAD) is a common malignant tumor in elderly men. Our research uses The Cancer Gene Atlas (TCGA) database to find potential related genes for predicting the prognosis of patients with PRAD. Methods . We downloaded gene expression profiles and clinical sample information from TCGA for 490 patients with PRAD (patient age: 41-78 years). We calculated stromal and immune scores using the ESTIMATE algorithm to predict the level of stromal and immune cell infiltration. We categorized patients with PRAD in TCGA into high and low score arrays according to their median immune/stromal scores and identified differentially expressed genes (DEGs) that were significantly correlated with the prognosis of PRAD. Then, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed. The association between DEGs and overall survival was investigated by weighted Kaplan–Meier survival analysis and multivariate analysis. Furthermore, the protein-protein interaction network (PPI) of DEGs was constructed using the STRING tool. Finally, the hub genes were identified by analyzing the degree of association of PPI networks. Results . We found that 8 individual DEGs, C6, S100A12, MLC1, PAX5, C7, FAM162B, CAMK1G, and TCEAL5, were significantly predictive of favorable overall survival and one DEG, EPYC, was associated with poor overall survival. GO and KEGG pathway analyses revealed that the DEGs were associated with immune responses. Moreover, 30 hub genes were obtained using the PPI network of DEGs: ITGAM, CD4, CD3E, IL-10, LCP2, ITGB2, ZAP-70, C3, CCL19, CXCL13, CXCL9, BTK, CCL21, CD247, CD28, CD3D, FCER1G, PTPRC, TYROBP, CCR5, ITK, CCL13, CCR1, CCR2, CD79B, CYBB, IL2RG, JAK3, PLCG2, and CD19. These prominent nodes had the most associations with other genes, indicating that they might play crucial roles in the prognosis of PRAD. Conclusions . We extracted a list of genes associated with the prostate adenocarcinoma microenvironment, which might contribute to the prediction and interpretation of PRAD prognosis.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2698540-8
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  • 4
    In: Experimental Cell Research, Elsevier BV, Vol. 403, No. 2 ( 2021-06), p. 112614-
    Type of Medium: Online Resource
    ISSN: 0014-4827
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 1466780-0
    SSG: 12
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  • 5
    In: Cancer Control, SAGE Publications, Vol. 30 ( 2023-12), p. 107327482311557-
    Abstract: Recent evidence suggests that the Ki-67 labeling index is associated with lymph node metastasis and the prognosis of papillary thyroid carcinoma (PTC). Methods We retrospectively evaluated the clinicopathological features of consecutive PTC patients between Jan 2019 and Oct 2020 in our medical center. The molecular analysis was also conducted by using the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) program. The Chi-square test was performed for the comparison of variables between patients with central lymph node metastasis (CLNM) and not. Besides, univariate and stepwise multivariate logistic regression analyses were further used to determine the risk factors for CLNM in PTC. Results Our results showed that male gender (odd ratio (OR) = 3.02; 95% CI: 1.81-5.04), tumor size 〉 1 cm (OR = 2.81; 95% CI: 1.84-4.29), multifocality (OR = 2.08; 95% CI: 1.31-3.30, and Ki-67 labeling index ( 〉 3% and ≤5%: OR = 1.20; 95% CI: .73-1.97; 〉 5%: OR = 3.85; 95% CI: 1.62-9.14) were independent risk factors for CLNM. After excluding the patients with harvested central lymph nodes 〈 3, increased Ki-67 labeling index was still associated with the number of CLNM and the lymph node ratio. Additionally, the expression level of Ki-67 was significantly correlated with a higher N stage and worse disease-free survival in TCGA and validated GSE60542 datasets. Conclusions Higher Ki-67 labeling index ( 〉 5%) is significantly associated with the CLNM in PTC patients, like other indicators of the male gender, larger tumor size, and multifocality. Besides, the Ki-67 was also determined to be associated with CLNM and DFS in PTC patients, which may act as an important molecular marker in PTC.
    Type of Medium: Online Resource
    ISSN: 1073-2748 , 1526-2359
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2023
    detail.hit.zdb_id: 2004182-2
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  • 6
    Online Resource
    Online Resource
    Wiley ; 2021
    In:  Cell Biology International Vol. 45, No. 12 ( 2021-12), p. 2510-2520
    In: Cell Biology International, Wiley, Vol. 45, No. 12 ( 2021-12), p. 2510-2520
    Abstract: Previous studies in our lab suggest that nitrogen permease regulator 2‐like (NPRL2) upregulation in prostate cancer is associated with malignant behavior and poor prognosis. However, the underlying mechanisms of NPRL2 dysregulation remain poorly understood. This study aimed to explore the transcription factors (TFs) contributing to NPRL2 dysregulation in prostate cancer. Potential TFs were identified using prostate tissue/cell‐specific chromatin immunoprecipitation (ChIP)‐seq data collected in the Cistrome Data Browser and Signaling Pathways Project. Dual‐luciferase assay and ChIP‐qPCR assay were conducted to assess the binding and activating effect of TFs on the gene promoter. Cell Counting Kit‐8 and colony formation assays were performed to assess cell proliferation. Results showed that E2F1 is a TF that bound to the NPRL2 promoter and activated its transcription. NPRL2 inhibition significantly alleviated E2F1 enhanced cell proliferation. Kaplan–Meier survival analysis indicated that E2F1 upregulation was associated with unfavorable progression‐free survival and disease‐specific survival. FOXO1 interacted and E2F1 in both PC3 and LNCaP cells and weakened the binding of E2F1 to the NPRL2 promoter. Functionally, FOXO1 overexpression significantly slowed the proliferation of PC3 and LNCaP cells and also decreased E2F1 enhanced cell proliferation. In summary, this study revealed a novel FOXO1/E2F1‐NPRL2 regulatory axis in prostate cancer. E2F1 binds to the NPRL2 promoter and activates its transcription, while FOXO1 interacts with E2F1 and weakens its transcriptional activating effects. These findings help expand our understanding of the prostate cancer etiology and suggest that the FOXO1/E2F1‐NPRL2 signaling axis might be a potential target.
    Type of Medium: Online Resource
    ISSN: 1065-6995 , 1095-8355
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1462519-2
    SSG: 12
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  • 7
    In: Infection and Drug Resistance, Informa UK Limited, Vol. Volume 16 ( 2023-04), p. 2089-2096
    Type of Medium: Online Resource
    ISSN: 1178-6973
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2023
    detail.hit.zdb_id: 2494856-1
    SSG: 15,3
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