Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal cell cancer (RCC) is one of the most common malignant tumors of the urinary system. MicroRNA-454 (miR-454) has been reported to play an important role in various cancer progressions, such as hepatocellular carcinoma, breast cancer and glioblastoma. Nevertheless, its effect on RCC still remains unknown. We aimed to investigate the biological function and underlying mechanisms of miR-454 in RCC. The expressions of miR-454 and MECP2 in RCC tissues were assessed using data from TCGA database and our own clinical samples. Functional experiments Cell Counting Kit-8 (CCK-8), colony formation, wound healing and Transwell assays were applied to detect the effects of miR-454 and MECP2 in RCC. The interaction between miR-454 and MECP2 was assessed by western blot and luciferase reporter assays. MiR-454 was upregulated in RCC tissues and cell lines compared with matched adjacent normal tissues and the normal kidney tubular epithelial cell line HK-2. MiR-454 inhibition and methyl-CpG binding protein 2 (MECP2) overexpression could both decrease the proliferative, migrative and invasive abilities of RCC cells. Higher expression of miR-454 predicted a poor overall survival (OS) (HR: 1.8; P < 0.05), while MECP2 level was positively related with RCC OS (HR: 0.55; P < 0.05) and disease-free survival (HR: 0.56; P < 0.05). Mechanistically, we showed that miR-454 could directly target the downstream gene MECP2. Our findings indicated that miR-454 accelerates RCC progression via suppressing MECP2 expression, which may provide a novel potential target of RCC treatment in the future.
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PMID:Silencing miR-454 suppresses cell proliferation, migration and invasion via directly targeting MECP2 in renal cell carcinoma. 3291 4

Immune checkpoint blockade leads to unprecedented responses in many cancers. Although currently available agents mostly target the PD-1 and CTLA-4 pathways, agents targeting the immune checkpoint protein LAG-3 are under active clinical development, and early clinical data show that LAG-3 expression is a biomarker of response to LAG-3 blockade. To determine which cancers may benefit most from LAG-3 blockade, we performed a pan-cancer analysis of The Cancer Genome Atlas dataset to identify genomic and immunologic correlates of LAG-3 expression. High mutation burden, and expression of exogenous virus (EBV, HPV) or endogenous retrovirus (ERV3-2), were associated with overexpression of LAG-3 in multiple cancers. Although CD8+ T-cell marker (CD8A) and LAG-3 were strongly co-expressed with each other and with PD-L1 in most cancers, there were three notable exceptions: HPV+ head-neck squamous cell cancer, renal cell cancer, and glioblastoma. These results may have important implications for guiding development clinical trials of LAG-3 blockade.
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PMID:Genomic and immunologic correlates of LAG-3 expression in cancer. 3292 11

Overexpression of HECT-type E3 ubiquitin ligase SMURF1 is correlated with poor prognosis in patients with various cancers, such as glioblastoma, colon cancer, and clear cell renal cell carcinoma. SMURF1 acts as a tumor promoter by ubiquitination modification and/or degradation of tumor-suppressing proteins. Combined treatment of Smurf1 knockdown with rapamycin showed collaborative antitumor effects in mice. This review described the role of HECT, WW, and C2 domains in regulating SMURF1 substrate selection. We summarized up to date SMURF1 substrates regulating different type cell signaling, thus, accelerating tumor progression, invasion, and metastasis. Furthermore, the downregulation of SMURF1 expression, inhibition of its E3 activity and regulation of its specificity to substrates prevent tumor progression. The potential application of SMURF1 regulators, specifically, wisely choose certain drugs by blocking SMURF1 selectivity in tumor suppressors, to develop novel anticancer treatments.
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PMID:SMURF1, a promoter of tumor cell progression? 3320 2


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