TCEAL7, a putative tumor suppressor gene, negatively regulates NF-κB pathway

Rattan, Ramandeep; Narita, Keishi; Chien, Jeremy; Maguire, Jacie; Shridhar, Ravi; Giri, Shailendra; Shridhar, Viji

doi:10.1038/onc.2009.431

Cited by 49 publications

(48 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We showed that overexpression of TCEAL7 decreased cell proliferation and colony formation ability, and downregulated the expression of c-Myc and cyclin D1, suggesting that the loss of TCEAL7 in EC may specifically favor the survival of cancer cells. Furthermore, exogenous expression of TCEAL7 significantly decreased the levels of the NFκB p65 subunit, which is in agreement with prior results showing that TCEAL7 negatively regulates NFκB transcriptional activity in ovarian cancer [18]. These effects of TCEAL7 were mimicked by miR-182 inhibition, and miR-182 is significantly upregulated in EC.…”

Section: Discussionsupporting

confidence: 79%

“…TCEAL7 is also downregulated in gastric cancer, and low TCEAL7 expression is associated with large tumors, high histological grade, poor nodal status and poor prognosis of gastric adenocarcinoma patients [15]. Furthermore, the downregulation of TCEAL7 in breast, brain and prostate cancers indicates that it may play an important role in carcinogenesis, possibly through its effect on the NFκB pathway and the pro-proliferative genes cyclin D1 and c-Myc [16,17,18]. …”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

MicroRNA-182 Promotes Tumor Cell Growth by Targeting Transcription Elongation Factor A-like 7 in Endometrial Carcinoma

Guo

Liao

Jia

et al. 2013

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Endometrial carcinoma (EC) is the most common gynecological malignancy among women worldwide. Despite its prevalence, the molecular mechanisms underlying endometrial carcinogenesis are poorly understood. The purpose of this study was to examine the role of microRNA-182 and its target gene transcription elongation factor A-like 7 (TCEAL7) in EC. Methods: The expression of miR-182 in human normal endometrial epithelial cells (NEEC) and in three human endometrial carcinoma cell lines (HEC-1B, RL95-2 and AN3CA) was measured by qRT-PCR, and the mRNA and protein expression of TCEAL7 were assessed in the same three endometrial carcinoma cell lines and NEEC by qRT-PCR and western blotting, respectively. Subsequently, the target of miR-182 was predicted by bioinformatics and confirmed using a luciferase assay. Cell proliferation and colony formation of RL95-2 cells were examined by MTT assay and crystal violet staining, respectively. The expression of NFκB-p65, c-Myc and cyclin D1 proteins was determined by Western blot analysis. Results: MiR-182 was significantly upregulated and TCEAL7 was downregulated in EC cell lines compared to NEEC. We showed that MiR-182 binds directly to a conserved 8 bp sequence in the 3'-UTR of TCEAL7, and inhibition of miR-182 upregulated TCEAL7 mRNA and protein expression to levels comparable to those induced by lentiviral-mediated overexpression of TCEAL7. MiR-182 inhibition decreased cell proliferation and colony formation ability, downregulated the expression of the pro-proliferative genes c-Myc and cyclin D1, and inhibited NFκB activation, and these effects were mimicked by TCEAL7 overexpression. Conclusions: miR-182 acts as an oncogenic miRNA in EC, promoting cell proliferation by targeting the tumor suppressor gene TCEAL7 and modulating the activity of its downstream effectors c-Myc, cyclin D1 and NFκB.

show abstract

Section: Discussionsupporting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

MicroRNA-182 Promotes Tumor Cell Growth by Targeting Transcription Elongation Factor A-like 7 in Endometrial Carcinoma

Guo

Liao

Jia

et al. 2013

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…The function of this domain is still largely unknown. However, recent studies suggest that BEX domain-containing proteins are involved in the control of cellular growth [6][7][8]. All BEX genes cluster close to each other and human BEX genes were mapped to the Xq22 chromosome.…”

Section: Bex Genes and Proteinsmentioning

confidence: 99%

Brain-Expressed X-linked (BEX) proteins in human cancers

Kazi

Kabir

2015

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

View full text Add to dashboard Cite

The Brain-Expressed X-linked (BEX) family proteins are comprised of five human proteins including BEX1, BEX2, BEX3, BEX4 and BEX5. BEX family proteins are expressed in a wide range of tissues and are known to play a role in neuronal development. Recent studies suggest a role of BEX family proteins in cancers. BEX1 expression is lost in a subgroup of patients with acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). Expression of BEX1 controls cell surface receptor signaling and restores imatinib response in resistant cells. BEX2 is overexpressed in a group of breast cancer patients and also in gliomas. Increased BEX2 expression led to enhanced NF-κB signaling as well as cell proliferation. Although BEX2 acts as tumor promoter in a subset of breast cancer, BEX3 expression displayed an opposite role. Overexpression of BEX3 resulted in inhibition of tumor formation in breast cancer mouse xenograft models. The role of BEX4 and BEX5 in cancer has not yet been defined. Collectively this suggests that BEX family members have distinct roles in cancers.While BEX1 and BEX3 act as a tumor suppressors, BEX2 seems to act as an oncogene.

show abstract

“…A number of different human cancers like that of breast and prostate show high levels of NF-κB activation and thus is a popular therapeutic target for novel cancer therapies (Hoshiya et al 2003). However, the current understanding about the role of NF-κB in ovarian cancer is incomplete (Rattan et al 2010). Another important cell cycle participant and an oncogene, c-Myc, is aberrantly expressed in several cancers including ovarian carcinoma.…”

Section: Discussionmentioning

confidence: 97%

BRCA1-mediated signaling pathways in ovarian carcinogenesis

Karve

Saha

2011

Funct Integr Genomics

View full text Add to dashboard Cite

The link between loss or defect in functional BRCA1 and predisposition for development of ovarian and breast cancer is well established. Germ-line mutations in BRCA1 are responsible for both hereditary breast and ovarian cancer, which is around 5-10% for all breast and 10-15% of all ovarian cancer cases. However, majority of cases of ovarian cancer are sporadic in nature. The inactivation of cellular BRCA1 due to mutations or loss of heterozygosity is one of the most commonly observed events in such cases. Complement-resistant retroviral BRCA1 vector, MFG-BRCA1, is the only approved gene therapy for ovarian cancer patients by the Federal and Drug Administration. Given the limited available information, there is a need to evaluate the effects of BRCA1 on the global gene expression pattern for better understanding the etiology of the disease. Here, we use Ingenuity Pathway Knowledge Base to examine the differential pattern of global gene expression due to stable expression of BRCA1 in the ovarian cancer cell line, SKOV3. The functional analysis detected at least five major pathways that were significantly (p < 0.05) altered. These include: cell to cell signaling and interaction, cellular function and maintenance, cellular growth and proliferation, cell cycle and DNA replication, and recombination repair. In addition, we were able to detect several biologically relevant genes that are central for various signaling networks involved in cellular homeostasis; TGF-β1, TP53, c-MYC, NF-κB and TNF-α. This report provides a comprehensive rationale for tumor suppressor function(s) of BRCA1 in ovarian carcinogenesis.

show abstract

TCEAL7, a putative tumor suppressor gene, negatively regulates NF-κB pathway

Cited by 49 publications

References 30 publications

MicroRNA-182 Promotes Tumor Cell Growth by Targeting Transcription Elongation Factor A-like 7 in Endometrial Carcinoma

MicroRNA-182 Promotes Tumor Cell Growth by Targeting Transcription Elongation Factor A-like 7 in Endometrial Carcinoma

Brain-Expressed X-linked (BEX) proteins in human cancers

BRCA1-mediated signaling pathways in ovarian carcinogenesis

Contact Info

Product

Resources

About