Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previously, we identified noscapine as a small molecule inhibitor of the hypoxia-inducible factor-1 pathway in hypoxic human glioma cells and human umbilical vein endothelial cells. Noscapine is a nontoxic ingredient in cough medicine currently used in clinical trials for patients with non-Hodgkin's lymphoma or chronic lymphocytic leukemia to assess antitumor efficacy. Here, we have evaluated the sensitivity of four human glioma cell lines to noscapine-induced apoptosis. Noscapine was a potent inhibitor of proliferation and inducer of apoptosis. Induction of apoptosis was associated with activation of the c-jun N-terminal kinase signaling pathway concomitant with inactivation of the extracellular signal regulated kinase signaling pathway and phosphorylation of the antiapoptotic protein Bcl-2. Noscapine-induced apoptosis was associated with the release of mitochondrial proteins apoptosis-inducing factor (AIF) and/or cytochrome c. In some glioma cell lines, only AIF release occurred without cytochrome c release or poly (ADP-ribose) polymerase cleavage. Knock-down of AIF decreased noscapine-induced apoptosis. Our results suggest the potential importance of noscapine as a novel agent for use in patients with glioblastoma owing to its low toxicity profile and its potent anticancer activity.
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PMID:Noscapine induces apoptosis in human glioma cells by an apoptosis-inducing factor-dependent pathway. 1852 14

Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of adult non-Hodgkin's lymphoma (NHL). While DLBCL is sensitive to chemotherapy, a certain percentage of patients with DLBCL experience relapse. Previous studies have indicated that Yiqichutan treatment, which was developed to treat NHL, can inhibit DLBCL cell growth, but the mechanism is not fully understood. The present study identified 991 differentially expressed mRNAs, with 498 upregulated and 493 downregulated (P<0.05), in SUDHL-6 cells exposed to Yiqichutan. The underlying pathways included the Jak/Stat and PI3K signaling pathways. In total, six representative mRNAs were selected for validation with reverse transcription-quantitative PCR (RT-qPCR), and a strong correlation was identified between the RT-qPCR results and microarray data. Since the transcription factor C-MYC is involved in both the Jak/Stat and PI3K signaling pathways, C-MYC and its associated microRNA (miR) were selected for further analysis. It was found that knockdown of C-MYC increased miR-34a expression levels, inhibited forkhead box P1 (Foxp1) expression levels and promoted DLBCL cell apoptosis. In addition, the miR-34a mimics further enhanced the role of C-MYC knockdown. It was demonstrated that, the expression levels of apoptotic factors Bax and poly (ADP-ribose) polymerase were significantly upregulated with C-MYC knockdown and miR-34a mimics in SUDHL-6 cells, while the Bcl2 expression level was significantly reduced. Moreover, Yiqichutan treatment increased miR-34a expression levels and induced apoptosis, as well as reducing Foxp1 expression level in SUDHL-6 cells. Therefore, the present results suggested that Yiqichutan treatment affected DLBCL cells via several signaling pathways. Furthermore, Yiqichutan may inhibit the proliferation of DLBCL cells by blocking the C-MYC/miR-34a signaling pathway.
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PMID:mRNA expression profile analysis reveals a C-MYC/miR-34a pathway involved in the apoptosis of diffuse large B-cell lymphoma cells induced by Yiqichutan treatment. 3276 91