Regulation of SOX11 expression through CCND1 and STAT3 in mantle cell lymphoma

Mohanty, Atish; Sandoval, Natalie; Phan, An T.; Nguyen, Thang Van; Chen, Robert W.; Budde, Elizabeth; Mei, Matthew; Popplewell, Leslie; Pham, Lan V.; Kwak, Larry W.; Weisenburger, Dennis D.; Rosen, Steven T.; Chan, Wing C.; Müschen, Markus; Ngo, Vu N.

doi:10.1182/blood-2018-05-851667

Cited by 31 publications

(19 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SOCS3, a negatively regulator of the JAK-STAT signaling pathway, loses its expression in~50% of MCL due to DNA methylation [90]. A recent study has revealed a unique role of STAT3 in MCL, which demonstrates that STAT3 represses expression of SOX11, a critical transcription factor that promotes lymphomagenesis in MCL [91]. This finding indicates that STAT3 may not be an ideal target in MCL given its negative role in SOX11 regulation.…”

Section: Mantle Cell Lymphomamentioning

confidence: 99%

STAT3 Activation and Oncogenesis in Lymphoma

Zhu

Wang²,

2019

Cancers

View full text Add to dashboard Cite

Signal transducer and activator of transcription 3 (STAT3) is an important and the most studied transcription factor in the Janus kinase (JAK)/STAT signaling pathway. STAT3 mediates the expression of various genes that play a critical role in many cellular and biological processes, such as cell proliferation, survival, differentiation, migration, angiogenesis, and inflammation. STAT3 and associated JAKs are activated and tightly regulated by a variety of cytokines and growth factors and their receptors in normal immune responses. However, abnormal expression of STAT3 leads to its constitutive activation, which promotes malignant transformation and tumor progression through oncogenic gene expression in numerous human cancers. Human lymphoma is a heterogeneous malignancy of T and B lymphocytes. Constitutive signaling by STAT3 is an oncogenic driver in several types of B-cell lymphoma and most of T-cell lymphomas. Aberrant STAT3 activation can also induce inappropriate expression of genes involved in tumor immune evasion such as PD-L1. In this review, we focus on the oncogenic role of STAT3 in human lymphoma and highlight potential therapeutic intervention by targeting JAK/STAT3 signaling.

show abstract

Section: Mantle Cell Lymphomamentioning

confidence: 99%

STAT3 Activation and Oncogenesis in Lymphoma

Zhu

Wang²,

2019

Cancers

View full text Add to dashboard Cite

show abstract

“…Sex determining region Y-related HMG-box 11 (SOX11) is a type of structurally-related transcription factor and belongs to group C of SOX family (17,18). SOX11 is critical for regulating organ development, particularly in the nervous system (19,20).…”

Section: Introductionmentioning

confidence: 99%

lncRNA MEG3 inhibits the growth of hepatocellular carcinoma cells by sponging miR-9-5p to upregulate SOX11

Liu

Chen

et al. 2019

Braz J Med Biol Res

View full text Add to dashboard Cite

The long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3), a tumor suppressor, is critical for the carcinogenesis and progression of different cancers, including hepatocellular carcinoma (HCC). To date, the roles of lncRNA MEG3 in HCC are not well illustrated. Therefore, this study used western blot and qRT-PCR to evaluate the expression of MEG3, miR-9-5p, and Sex determining Region Y-related HMG-box 11 (SOX11) in HCC tissues and cell lines. RNA pull-down and luciferase reporter assay were used to evaluate these molecular interactions. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry detected the viability and apoptosis of HCC cells, respectively. The results showed that MEG3 and SOX11 were poorly expressed but miR-9-5p was highly expressed in HCC. The expression levels of these molecules suggested a negative correlation between MEG3 and miR-9-5p and a positive correlation with SOX11, confirmed by Pearson's correlation analysis and biology experiments. Furthermore, MEG3 could combine with miR-9-5p, and SOX11 was a direct target of miR-9-5p. Moreover, MEG3 over-expression promoted cell apoptosis and growth inhibition in HCC cells through sponging miR-9-5p to up-regulate SOX11. Therefore, the interactions among MEG3, miR-9-5p, and SOX11 might offer a novel insight for understanding HCC pathogeny and provide potential diagnostic markers and therapeutic targets for HCC.

show abstract

“…However, the mechanism of low expression of SOX11 in HCC remains unclear. STAT3 is an oncogene, which can negatively regulate SOX11 expression [24]. After the use of STAT3 inhibitor, SOX11 expression levels were upregulated in mantle cell lymphoma [24].…”

Section: Discussionmentioning

confidence: 99%

ZNF382 inhibits hepatocellular carcinoma (HCC) cell proliferation and motility and induces apoptosis by up-regulating SOX11

2021

JOMH

View full text Add to dashboard Cite

Background and Objective: To detect the mRNA and protein levels of Zinc-finger protein382 (ZNF382) in human hepatocellular carcinoma (HCC) tissues and cell lines and investigate its effects on the cellular processes of HCC cells in vitro.Methods: Quantitative PCR and Immunoblot assays were respectively conducted to detect the alteration of ZNF382 mRNA and protein levels in HCC human tissues and cell lines. MTT, FCM, wound closure, and transwell assays were performed to detect the effects of ZNF382 on HCC cell proliferation, apoptosis, and motility of HCC cells in vitro. Immunoblot assays were then performed to detect the effects of ZNF382 on the expression of Signal Transducer and Activator of Transcription 3 (STAT3) and SOX11 in HCC cells, and the rescue assays were conducted to confirm the conclusion. Results:We found ZNF382 was low expression in human HCC tissues and cell lines. ZNF382 suppressed the proliferation and stimulated the apoptosis of HCC cells. Additionally, ZNF382 inhibited the motility of HCC cells in vitro. Mechanically, ZNF382 mediated STAT3/SOX11, and therefore affected the proliferation, apoptosis, and motility of HCC cells. Conclusion:We showed the abnormal low expression of ZNF382 in human HCC tissues and cell lines, and confirmed the effects of ZNF382 on HCC cellular processes. We thought ZNF382 was a tumor suppressor in HCC.

show abstract

Regulation of SOX11 expression through CCND1 and STAT3 in mantle cell lymphoma

Cited by 31 publications

References 67 publications

STAT3 Activation and Oncogenesis in Lymphoma

STAT3 Activation and Oncogenesis in Lymphoma

lncRNA MEG3 inhibits the growth of hepatocellular carcinoma cells by sponging miR-9-5p to upregulate SOX11

ZNF382 inhibits hepatocellular carcinoma (HCC) cell proliferation and motility and induces apoptosis by up-regulating SOX11

Contact Info

Product

Resources

About