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