Knockdown of BRCC3 exerts an anti‑tumor effect on cervical cancer in�vitro

Zhang, Feifang; Zhou, Qun

doi:10.3892/mmr.2018.9511

Cited by 13 publications

(16 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have shown that silencing DEPDC1B in NSCLC suppressed cell migration and invasion in both NSCLC and cervical cancer cells. 10,13 Consistent with previous reports, DEPDC1B knockdown in PANC-1 and CFPAC-1 cells significantly inhibited cell migration and invasion. Yang et al demonstrated that ectopic expression of DEPDC1B in NSCLC enhanced cell migration and invasion.…”

Section: Discussionsupporting

confidence: 90%

“…15 Previous results have proven that DEPDC1B plays a crucial role in cell growth, movement, differentiation, cell cycle progression and cytoskeleton reorganization. 15 Subsequent studies demonstrated that it is also overexpressed in other types of cancer, [8][9][10][11][12][13][14] and it is used as a prognostic factor that predicts outcomes in patients with non-small cell lung cancer 10 and prostate cancer. 11 In our present study, we show that the expression of DEPDC1B was obviously higher in PC cell lines than in normal human pancreatic ductal cell lines, which is similar to the results in non-small cell lung cancer 10 and cervical cancer 13 cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…7 DEP domain-containing protein 1B (DEPDC1B) was initially discovered by mRNA expression profiling in MDA-MB 231 human breast cancer cells. 8 DEPDC1B has also been reported to be overexpressed in oral cancer, 9 nonsmall cell lung cancer, 10 prostate cancer, 11 soft tissue sarcoma, 12 cervical cancer 13 and malignant melanoma. 14 The DEPDC1B gene contains two important domains: the DEP domain and the Rho-GAP domain, which are correlated with cell proliferation, migration, invasion, cell cycle progression and cytoskeleton reorganization.…”

Section: Introductionmentioning

confidence: 99%

“…10 Moreover, DEPDC1B knockdown suppresses the viability, migration and invasion abilities of HeLa and SiHa cells through regulating EMT progression and Snai family member expression levels. 13 However, the role of DEPDC1B in PC remains unknown. Our present study aimed to investigate the biological function of DEPDC1B and the associated molecular mechanisms in PC.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

<p>DEP Domain-Containing Protein 1B (DEPDC1B) Promotes Migration and Invasion in Pancreatic Cancer Through the Rac1/PAK1-LIMK1-Cofilin1 Signaling Pathway</p>

Zhang¹,

Shi²,

Hu³

et al. 2020

OTT

View full text Add to dashboard Cite

Background: With increasing incidence, pancreatic cancer (PC) is one of the most common digestive tract tumors. However, the prognosis of PC is particularly dismal due to the highly invasive and metastatic behavior of this deadly disease. DEP domain-containing protein 1B (DEPDC1B), which is overexpressed in multiple tumors, such as breast cancer, oral cancer and non-small cell lung cancer, plays a significant role in cell movement, cell cycle and cytoskeleton reorganization. However, the function of DEPDC1B in PC remains poorly understood. Methods: The function of DEPDC1B in the migration and invasion of PC was evaluated by wound healing and Transwell assays in vitro and PC-derived liver metastasis models in vivo. The molecular mechanisms of DEPDC1B were investigated through cell line establishment, Western blotting, qRT-PCR, immunoprecipitation, histological examination and immunohistochemistry analysis. Results: DEPDC1B was overexpressed in PC cell lines. DEPDC1B regulated cell migration and invasion. DEPDC1B regulated the Rac1/PAK1-LIMK1-cofilin1 signaling pathway by interacting with Rac1. Rac1 inhibition suppressed DEPDC1B-induced migration and invasion in PC in vitro and DEPDC1B-induced liver metastasis in vivo. Conclusion: DEPDC1B promoted cell migration and invasion by activating the Rac1/ PAK1-LIMK1-cofilin1 signaling pathway, thus providing a potential therapeutic target against PC.

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

<p>DEP Domain-Containing Protein 1B (DEPDC1B) Promotes Migration and Invasion in Pancreatic Cancer Through the Rac1/PAK1-LIMK1-Cofilin1 Signaling Pathway</p>

Zhang¹,

Shi²,

Hu³

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…Within several of the conserved MIGs identified herein, mutations have been linked to abnormal cell proliferation or cancer in humans. For example, mutations in BRCC3, which encodes a cell cycle regulator involved in G2/M phase transition, has been linked to myelodysplastic syndrome (MDS), as well as breast and cervical cancers (Boudreau et al 2007;Huang et al 2015;Zhang, Zhou 2018). Mutations in E2F3 have been associated with retinoblastoma, bladder and lung cancer (Ziebold et al 2001;Wang et al 2017a;Liu et al 2018).…”

Section: Discussionmentioning

confidence: 99%

Genetic Analysis of Human RNA Binding Motif Protein 48 (RBM48) Reveals an Essential Role in U12-Type Intron Splicing

Siebert

Corll

Gronevelt

et al. 2020

Preprint

View full text Add to dashboard Cite

U12-type (minor) introns are found in most multicellular eukaryotes, and constitute ~0.5% of all introns in species with a minor spliceosome required for their splicing. However, the biological relevance of U12-type introns is not well understood. It is known that mutations resulting in aberrant U12-type intron splicing cause developmental defects in both plants and animals. We recently reported that maize RNA Binding Motif Protein 48 (RBM48) is an essential splicing factor for U12-type introns. Maize rbm48 mutants display aberrant genome-wide U12-type intron splicing. This leads to severe defects in endosperm development, resulting in non-viable seeds. In this report, we use CRISPR/Cas9-mediated ablation of RBM48 in human K-562 cells to establish the evolutionary conservation of RBM48 dependent U12-type intron splicing between maize and humans. Comparative RNA-seq analysis performed on RBM48 deficient human cell lines and maize endosperm defined a subset of orthologous minor U12-type containing genes (MIGs) displaying aberrant splicing of U12-type introns in both species. Mutations in the majority of these MIGs have been reported to cause developmental defects in both plants and animals. Thus, a comparison of RNA-seq data between distantly related species containing mutations in RBM48 identifies candidate genes likely to mediate mutant phenotypes of U12-type splicing defects. Our results elucidate deeply conserved post-transcriptional processing mechanisms that are required for normal growth and development of eukaryotes with a minor spliceosome.

show abstract

ABRO1 stabilizes the deubiquitinase BRCC3 through inhibiting its degradation mediated by the E3 ubiquitin ligase WWP2

et al. 2020

View full text Add to dashboard Cite

BRCA1/BRCA2‐containing complex subunit 3 (BRCC3) is a lysine 63‐specific deubiquitinase involved in multiple biological processes, such as DNA repair and immune responses. However, the regulation mechanism for BRCC3 protein stability is still unknown. Here, we demonstrate that BRCC3 is mainly degraded through the ubiquitin‐proteasome pathway. The HECT‐type E3 ubiquitin ligase WWP2 modulates BRCC3 ubiquitination and degradation. ABRO1, a subunit of the BRCC36 isopeptidase complex (BRISC), competes with WWP2 to bind to BRCC3, thereby preventing WWP2‐mediated BRCC3 ubiquitination and enhancing BRCC3 stability. Functionally, we show that lentivirus‐mediated overexpression of WWP2 in murine macrophages inhibits NLRP3 inflammasome activation by decreasing BRCC3 protein level. This study provides the first insights into the regulation of BRCC3 stability and expands our knowledge about the physiological function of WWP2.

show abstract

Knockdown of BRCC3 exerts an anti‑tumor effect on cervical cancer in�vitro

Cited by 13 publications

References 44 publications

<p>DEP Domain-Containing Protein 1B (DEPDC1B) Promotes Migration and Invasion in Pancreatic Cancer Through the Rac1/PAK1-LIMK1-Cofilin1 Signaling Pathway</p>

<p>DEP Domain-Containing Protein 1B (DEPDC1B) Promotes Migration and Invasion in Pancreatic Cancer Through the Rac1/PAK1-LIMK1-Cofilin1 Signaling Pathway</p>

Genetic Analysis of Human RNA Binding Motif Protein 48 (RBM48) Reveals an Essential Role in U12-Type Intron Splicing

ABRO1 stabilizes the deubiquitinase BRCC3 through inhibiting its degradation mediated by the E3 ubiquitin ligase WWP2

Contact Info

Product

Resources

About