Functional analysis of the DEPDC1 oncoantigen in malignant glioma and brain tumor initiating cells

Kikuchi, Ryogo; Sampetrean, Oltea; Saya, Hideyuki; Yoshida, Kazunari; Toda, Masahiro

doi:10.1007/s11060-017-2457-1

Cited by 18 publications

(15 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have indicated that DEPDC1 is elevated in several types of cancer and is implicated in tumorigenesis (6)(7)(8)(9)(10). It has also been revealed that DEPDC1 is upregulated in HCC tissue and may therefore be an independent predictor of HCC (11).…”

Section: Discussionmentioning

confidence: 99%

“…It is primarily expressed in the testis and is not detected in other normal human tissues (6). Recently, several studies revealed that DEPDC1 was upregulated in many tumor types, indicating its important role in tumorigenesis (7)(8)(9)(10). For example, DEPDC1 was upregulated in bladder carcinogenesis and the inhibition of DEPDC1 via small-interfering RNA (siRNA) significantly suppressed the growth of bladder cancer cells (7).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

DEPDC1 drives hepatocellular carcinoma cell proliferation, invasion and angiogenesis by regulating the CCL20/CCR6 signaling pathway

Guo

Liu

et al. 2019

Oncol Rep

View full text Add to dashboard Cite

DEP domain containing 1 (DEPDC1) functions as an oncogene in hepatocellular carcinoma (HCC). However, the underlying mechanism of DEPDC1 remains largely unknown. The present study revealed that DEPDC1 knockdown inhibited HCC cell proliferation, colony formation and invasion in vitro and suppressed the growth of HCC xenografts in vivo. Furthermore, DEPDC1 overexpression promoted HCC cell proliferation, colony formation and invasion. DNA microarray, reverse transcription-quantitative-PCR and western blotting results demonstrated that DEPDC1 knockdown in Huh-7 significantly inhibited the expression of chemokine (C-C motif) ligand 20 (CCL20) and chemokine (C-C motif) receptor 6 (CCR6). In addition, the expression of CCL20 and CCR6 were upregulated in HCC tissues and cell lines, and were positively correlated with DEPDC1 expression. CCL20 or CCR6 knockdown via small interfering RNA reversed the effects of DEPDC1 overexpression in HCC cells. Furthermore, it was revealed that conditioned medium from DEPDC1 upregulated Li-7 and Hep3B cells led to angiogenesis in vitro, whereas CCL20 knockdown in Li-7 and Hep3B cells or CCR6 knockdown in human umbilical vein endothelial cells reversed the angiogenic effect of DEPDC1 overexpression. In conclusion, DEPDC1 facilitated cell proliferation, invasion and angiogenesis via the CCL20/CCR6 pathway in HCC.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

DEPDC1 drives hepatocellular carcinoma cell proliferation, invasion and angiogenesis by regulating the CCL20/CCR6 signaling pathway

Guo

Liu

et al. 2019

Oncol Rep

View full text Add to dashboard Cite

show abstract

“…The role of DEPDC1B in prostate cancer was reported by Huang et al DEPDC1B expression significantly upregulated the level of cancer tissue and its mRNA in prostate gland could be used as an independent prognostic indicator for survival rate of prostate cancer patients [25]. In addition, Kikuchi et al found that inhibition of endogenous DEPDC1 expression by small interfering RNA (siRNA) inhibits GBM cell viability and induces apoptosis through NF-κB signaling [26]. Therefore, we set out to explore the effects of DEPDC1B in GBM.…”

Section: Discussionmentioning

confidence: 93%

Knockdown of DEPDC1B inhibits the development of glioblastoma

Guo

Cao

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

Background: Glioblastoma (GBM) is the most common primary malignant brain tumor in adults with a poor prognosis. DEPDC1B (DEP domain-containing protein 1B) has been shown to be associated with some types of malignancies. However, the role and underlying regulatory mechanisms of DEPDC1B in GBM remain elusive. Methods: In this research, the expression level of DEPDC1B in GBM tissues was detected by IHC. The DEPDC1B knockdown cell line was constructed, identified by qRT-PCR and western blot and used to construct the xenotransplantation mice model and intracranial xenograft model. MTT assay, colony formation assay, flow cytometry, and Transwell assay were used to detected cell proliferation, apoptosis and migration. Results: The results proved that DEPDC1B was significantly upregulated in tumor tissues, and silencing DEPDC1B could inhibit proliferation, migration and promote apoptosis of GBM cell. In addition, human apoptosis antibody array detection showed that after DEPDC1B knockdown, the expression of apoptosis-related proteins was downregulated, such as IGFBP-2, Survivin, N-cadherin, Vimentin and Snail. Finally, we indicated that knockdown of DEPDC1B significantly inhibited tumor growth in vivo. Conclusions: In summary, DEPDC1B was involved in the development and progression of GBM, which may be a potential therapeutic target and bring a breakthrough in the treatment.

show abstract

“…EP300, an apoptosis-associated transcription factor, has been shown to be downregulated in meningioma when compared to normal arachnoid 27 though it's role in meningioma prognostication is not well understood. While DEPDC1 has not been studied in meningioma, it is a known regulator of NFkB signaling and is overexpressed in multiple cancers such as glioma, breast cancer, and nasopharyngeal cancer, having been proposed as a potential therapeutic target in each [28][29][30] . Similarly, the roles of RUNX1, STAT5, and TWIST1 in meningioma remain poorly understood, and could represent novel therapeutic targets.…”

Section: Discussionmentioning

confidence: 99%

Meta-gene markers predict meningioma recurrence with high accuracy

Zádor

Landry

Haibe‐Kains

et al. 2020

Sci Rep

View full text Add to dashboard Cite

Meningiomas, the most common adult brain tumors, recur in up to half of cases. This requires timely intervention and therefore accurate risk assessment of recurrence is essential. Our current practice relies heavily on histological grade and extent of surgical excision to predict meningioma recurrence. However, prediction accuracy can be as poor as 50% for low or intermediate grade tumors which constitute the majority of cases. Moreover, attempts to find molecular markers to predict their recurrence have been impeded by low or heterogenous genetic signal. We therefore sought to apply systems-biology approaches to transcriptomic data to better predict meningioma recurrence. We apply gene co-expression networks to a cohort of 252 adult patients from the publicly available genetic repository Gene Expression Omnibus. Resultant gene clusters (“modules”) were represented by the first principle component of their expression, and their ability to predict recurrence assessed with a logistic regression model. External validation was done using two independent samples: one merged microarray-based cohort with a total of 108 patients and one RNA-seq-based cohort with 145 patients, using the same modules. We used the bioinformatics database Enrichr to examine the gene ontology associations and driver transcription factors of each module. Using gene co-expression analysis, we were able predict tumor recurrence with high accuracy using a single module which mapped to cell cycle-related processes (AUC of 0.81 ± 0.09 and 0.77 ± 0.10 in external validation using microarray and RNA-seq data, respectively). This module remained predictive when controlling for WHO grade in all cohorts, and was associated with several cancer-associated transcription factors which may serve as novel therapeutic targets for patients with this disease. With the easy accessibility of gene panels in healthcare diagnostics, our results offer a basis for routine molecular testing in meningioma management and propose potential therapeutic targets for future research.

show abstract

Functional analysis of the DEPDC1 oncoantigen in malignant glioma and brain tumor initiating cells

Cited by 18 publications

References 30 publications

DEPDC1 drives hepatocellular carcinoma cell proliferation, invasion and angiogenesis by regulating the CCL20/CCR6 signaling pathway

DEPDC1 drives hepatocellular carcinoma cell proliferation, invasion and angiogenesis by regulating the CCL20/CCR6 signaling pathway

Knockdown of DEPDC1B inhibits the development of glioblastoma

Meta-gene markers predict meningioma recurrence with high accuracy

Contact Info

Product

Resources

About