Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Current glioma therapies allow in situ delivery of cytotoxic drugs to the tumour; however, gliomas show early recurrence due to their highly proliferative character. Long non-coding (lnc)RNAs play critical roles in tumorigenesis by controlling cell proliferation and cycling. However, the mechanism of action of lncRNAs in glioma development remains unclear. Here, we report that the lncRNA PLAC2 induces cell cycle arrest by targeting ribosomal protein (RP)L36 in glioma. RPL36 promoted cell proliferation and G1/S cell cycle progression. Mass spectrometry analysis revealed that signal transducer and activator of transcription (STAT)1 interacted with both lncRNA PLAC2 and the RPL36 promoter. We also found that the nucleus PLAC2 bind with STAT1 and interact with RPL36 promoters but the cytoplasmic lncRNA PLAC2 inhibited STAT1 nuclear transfer, thereby decreasing RP36 expression, inhibiting cell proliferation and inducing cell cycle arrest. These results provide evidence for a novel cell cycle regulatory network in glioma comprising the lncRNA PLAC2 along with STAT1 and RPL36 that can serve as a therapeutic target for glioma treatment.
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PMID:LncRNA PLAC2 down-regulates RPL36 expression and blocks cell cycle progression in glioma through a mechanism involving STAT1. 2892 48

It is known that lncRNA PLAC2 can inhibit glioma. This study explored the function of PLAC2 in hepatocellular carcinoma (HCC). Our data showed that PLAC2 expression in HCC was not affect by HCV and HBV infection, while PLAC2 levels were significantly lower in HCC tissues comparing to non-cancer tissues. Low PLAC2 levels in HCC tissues were associated with low overall 5-year survival rate. P53 mRNA was also downregulated in HCC and positively correlated with PLAC2. PLAC2 overexpression caused upregulated p53 and increase cancer cell apoptosis. P53 overexpression failed to affect PLAC2. In addition, p53 silencing reduced the effects of PLAC2 overexpression. Therefore, PLAC2 upregulated p53 to mediate cancer cell apoptosis.
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PMID:LncRNA PLAC2 upregulates p53 to induce hepatocellular carcinoma cell apoptosis. 3123 63

Long noncoding RNA placenta-specific 2 (PLAC2) blocks the cancer cell cycle in glioma, suggesting its tumor-suppressive role. The present study aimed to investigate the role of PLAC2 in retinoblastoma (Rb). It was found that PLAC2 was downregulated in Rb tissues and was not affected by the development of Rb. PTEN was also downregulated in Rb and positively correlated with PLAC2. In Rb cells, PLAC2 over-expression resulted in the upregulated expression of PTEN, while PTEN over-expression did not affect PLAC2 expression. PLAC2 and PTEN over-expression caused an increased apoptotic rate of Rb cells. PTEN small interfering RNA silencing led to a decreased apoptotic rate and attenuated the effects of PLAC2 over-expression. Therefore, PLAC2 regulates PTEN in Rb and participates in the regulation of cancer cell apoptosis.
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PMID:Long noncoding RNA PLAC2 regulates PTEN in retinoblastoma and participates in the regulation of cancer cell apoptosis. 3219 49