Low expression of Mda-7/IL-24 and high expression of C-myb in tumour tissues are predictors of poor prognosis for Burkitt lymphoma patients

Ma, Ming; Zhao, Riyang; Yang, Xingxiao; Zhao, Lianmei; Liu, Lihua; Zhang, Cong; Wang, Xuexiao; Shan, Baoen

doi:10.1080/10245332.2018.1435046

Cited by 12 publications

(12 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ma et al found that high expression of c‐Myb was associated with advanced clinical stage and worse OS/progression‐free survival in patients with diffuse large B‐cell lymphoma. They also proved its same prognostic value in patients with Burkitt lymphoma . Li et al found that a high mRNA level of c‐Myb indicated worse relapse‐free survival in patients with breast cancer, and that it can combine with interleukin (IL)‐1β to predict OS in patients who are estrogen receptor(−).…”

Section: Discussionmentioning

confidence: 95%

c‐Myb promotes growth and metastasis of colorectal cancer through c‐fos‐induced epithelial‐mesenchymal transition

Yan

Kong

et al. 2019

Cancer Science

View full text Add to dashboard Cite

c‐Myb is a crucial transcription factor that participates in various biological functions; however, its role in colorectal cancer (CRC) remains poorly investigated. We first analyzed the expression and clinical significance of c‐Myb in a retrospective cohort enrolling 132 CRC patients. Then, the CRISPR/Cas9 technique was used to establish c‐Myb gene KO CRC cell lines. Cellular functional assays in vitro and in vivo were used to evaluate the impact of c‐Myb KO in CRC cells. Finally, RNA sequencing was used to investigate the potential oncogenic mechanisms regulated by c‐Myb in CRC progression and related cellular validations were accordingly carried out. As a result, c‐Myb is significantly overexpressed in CRC tissues as compared with adjacent normal tissues. High expression of c‐Myb is positively correlated with lymph node metastasis and poor prognosis. Univariate analysis and multivariate analysis further identify c‐Myb as an independent unfavorable prognostic factor for CRC patients. c‐Myb KO inhibits the proliferation, apoptosis resistance, invasion, metastasis, colony formation and in vivo tumorigenesis of CRC cells. Also, the mechanism investigation indicates that c‐Myb may promote CRC progression by regulating c‐fos. c‐fos overexpression can rescue the inhibitory effect of c‐Myb KO on the malignant characteristics of CRC cells. Finally, we find that c‐Myb KO inhibits the epithelial‐mesenchymal transition (EMT) molecular phenotype in CRC cells, whereas c‐fos overexpression can rescue this inhibitory effect. This study suggests that c‐Myb promotes the malignant progression of CRC through c‐fos‐induced EMT and has the potential to be a promising prognostic biomarker and therapeutic target.

show abstract

Section: Discussionmentioning

confidence: 95%

c‐Myb promotes growth and metastasis of colorectal cancer through c‐fos‐induced epithelial‐mesenchymal transition

Yan

Kong

et al. 2019

Cancer Science

View full text Add to dashboard Cite

show abstract

“…The oncogenic roles of transcription factor MYB have been widely studied in different types of cancer including leukemia, colon and breast cancer and adenoid cystic carcinoma (55)(56)(57). Overexpression of MYB has been reported to be associated with poor prognosis in leukemogenesis (58), colorectal (59) and breast cancer (60) and Burkitt lymphoma (61). Therefore, DDX41 may function in tumorigenesis by regu-lating the expression levels of certain oncogenes and tumor suppressors.…”

Section: Discussionmentioning

confidence: 99%

DDX41 regulates the expression and alternative splicing of genes involved in tumorigenesis and immune response

Jian

Xue²,

Cheng

et al. 2021

Oncol Rep

View full text Add to dashboard Cite

DEAD-box helicase 41 (DDX41) is an RNA helicase and accumulating evidence has suggested that DDX41 is involved in pre-mRNA splicing during tumor development. However, the role of DDX41 in tumorigenesis remains unclear. In order to determine the function of DDX41, the human DDX41 gene was cloned and overexpressed in HeLa cells. The present study demonstrated that DDX41 overexpression inhibited proliferation and promoted apoptosis in HeLa cells. RNA-sequencing analysis of the transcriptomes in overexpressed and normal control samples. DDX41 regulated 959 differentially expressed genes compared with control cells. Expression levels of certain oncogenes were also regulated by DDX41. DDX41 selectively regulated the alternative splicing of genes in cancer-associated pathways including the EGFR and FGFR signaling pathways. DDX41 selectively upregulated the expression levels of five antigen processing and presentation genes ( HSPA1A, HSPA1B, HSPA6, HLA-DMB and HLA-G ) and downregulated other immune-response genes in HeLa cells. Additionally, DDX41-regulated oncogenes and antigen processing and presentation genes were associated with patient survival rates. Moreover, DDX41 expression was associated with immune infiltration in cervical and endocervical squamous cancer. The present findings showed that DDX41 regulated the cancer cell transcriptome at both the transcriptional and alternative splicing levels. The DDX41 regulatory network predicted the biological function of DDX41 in suppressing tumor cell growth and regulating cancer immunity, which may be important for developing anticancer therapeutics.

show abstract

“…It was well accepted that IL-24 mediated cancer cell-specific death and apoptosis via multiple signaling pathways (21)(22)(23). Significantly lower IL-24 expression predicted poorer prognosis in lung adenocarcinoma (24), breast cancer (25), head and neck squamous cell carcinoma (26), and lymphoma (27,28). IL-24 high adenocarcinoma patients showed a notably higher incidence of apoptotic tumor cell death, and displayed favorable post-therapy prognosis as compared with IL-24 low patients (24).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-24 Regulates T Cell Activity in Patients With Colorectal Adenocarcinoma

Zhang

Liu²,

2019

Front. Oncol.

View full text Add to dashboard Cite

Interleukin (IL)-24 plays a potential anti-tumor activity in colorectal cancer in a dose-dependent manner. However, the immunoregulatory role of IL-24 to peripheral and tumor-infiltrating T cell function in colorectal cancer was not fully elucidated. In this study, twenty-nine colorectal adenocarcinoma patients and fifteen healthy individuals were enrolled. IL-24 expression and IL-24 receptor (IL-20R1, IL-20R2, and IL-22R1) mRNA relative level was measured by ELISA and real-time PCR, respectively. CD4 + and CD8 + T cells were purified from peripheral bloods and cancer specimens, and were stimulated with low (10 ng/ml) and high (100 ng/ml) concentration of recombinant IL-24. CD4 + T cells activity was assessed by measurement of Th cell percentage, transcriptional factors, and cytokine production. CD8 + T cells activity was evaluated by investigation of cytotoxic molecules, target cell death, and interferon-γ (IFN-γ) secretion. IL-24 was decreasingly expressed in both peripheral bloods and cancer tissues in colorectal adenocarcinoma patients. However, IL-20R1 and IL-20R2 was comparable between healthy controls and colorectal adenocarcinoma patients. Low concentration of IL-24 suppressed CD4 + T cell proliferation. In contrast, high concentration of IL-24 not only promoted CD4 + T cell proliferation, but also enhanced CD4 + T cell activity, which mainly presented as up-regulation of Th1/Th17 frequency, T-bet/RORγt mRNA, and IFN-γ/IL-17 production but down-regulation of Treg percentage, FoxP3 mRNA, and IL-10/IL-35 secretion. Moreover, high concentration of IL-24 also increased perforin and granzyme B expression in CD8 + T cells, and elevated cytolytic and non-cytolytic activity of CD8 + T cells, which presented as induction of target cell death and elevation of IFN-γ expression. However, low concentration of IL-24 did not affect bioactivity of CD8 + T cells. The current data indicated that IL-24 might regulate T cell function in a dose-dependent manner. High-concentration of IL-24 might promote anti-tumor immune responses in development novel therapeutic approaches to colorectal adenocarcinoma.

show abstract

Low expression of Mda-7/IL-24 and high expression of C-myb in tumour tissues are predictors of poor prognosis for Burkitt lymphoma patients

Abstract: Mda-7/IL-24: melanoma differentiation associated gene7/interleukin 24; FCM: flow cytometry; Ecog: Eastern Cooperative Oncology Group; IPI: International lymphoma prognosis index.

Cited by 12 publications

References 25 publications

c‐Myb promotes growth and metastasis of colorectal cancer through c‐fos‐induced epithelial‐mesenchymal transition

c‐Myb promotes growth and metastasis of colorectal cancer through c‐fos‐induced epithelial‐mesenchymal transition

DDX41 regulates the expression and alternative splicing of genes involved in tumorigenesis and immune response

Interleukin-24 Regulates T Cell Activity in Patients With Colorectal Adenocarcinoma

Contact Info

Product

Resources

About