Overexpression of cell cycle regulator CDCA3 promotes oral cancer progression by enhancing cell proliferation with prevention of G1 phase arrest

Uchida, Fumihiko; Uzawa, Katsuhiro; Kasamatsu, Atsushi; Takatori, Hiroaki; Sakamoto, Yosuke; Ogawara, Katsunori; Shiiba, Masashi; Tanzawa, Hideki; Bukawa, Hiroki

doi:10.1186/1471-2407-12-321

Cited by 75 publications

(61 citation statements)

References 37 publications

(36 reference statements)

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“…Recent studies have demonstrated that the proliferation of cancer is closely correlated to the altered regulation of cell cycles, which might cause uncontrolled growth and contribute to the development and progression of tumor cells [27]. In the present study, our data illustrated that fewer ESCC cells transfected with BANCR siRNA were arrested in the S phage compared to that transfected with NC siRNA (Figure 3 and Figure 4).…”

Section: Bancr Expression Affects the Growth Of Escc Cellssupporting

confidence: 65%

BRAF-activated non-protein coding RNA (BANCR) advances the development of esophageal squamous cell carcinoma via cell cycle

Yang¹,

Wang²,

Chen

et al. 2017

Open Life Sciences

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Esophageal carcinoma is one of the important lethal tumors in the world, but the mechanism of esophageal cancer progression is still unclear. The long non-coding RNAs are known to regulate tumor progression. Here we report that BRAF-activated nonprotein coding RNA (BANCR) is associated with the development of esophageal squamous cell carcinoma (ESCC). The expression levels of BANCR in 132 ESCC tumor tissues detected by quantitative real-time PCR were significantly higher than that in the adjacent normal tissues. The expression level of BANCR was down-regulated by transfecting small interrupting RNA against BANCR (BANCR siRNA) in Eca109 cells. Eca109 and TE-1 cells transfected with BANCR siRNA led to the delayed cell cycles compared to the cells transfected with negative control siRNA. Moreover, MTT assays demonstrated that Eca109 cells transfected with BANCR siRNA resulted in the inhibition of cell proliferation. These results suggested that BANCR advances the development and progression of ESCC cells through regulating their cell cycles.

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Section: Bancr Expression Affects the Growth Of Escc Cellssupporting

confidence: 65%

BRAF-activated non-protein coding RNA (BANCR) advances the development of esophageal squamous cell carcinoma via cell cycle

Yang¹,

Wang²,

Chen

et al. 2017

Open Life Sciences

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“…To correlate increased expression of these genes with patient outcome, we associated CDC20 and CDCA3 expression levels with survival data and found that patients with higher CDC20 or CDCA3 expression had shorter event-free survival times (Fig-Figure 4 ure 6E and 6F). In support of this observation, CDCA3 over-expression has been associated with poor prognosis in oral cancers by preventing G1 phase arrest [44]. Thus, the identification of a core gene set with periodic regulation across various tissue-types in multiple studies revealed a common epigenetic state in these genes, and uncovered an unexpected association of their expression levels with SETD2 mutation status in kidney tumors that was not reported in previous TCGA analysis.…”

Section: The Core Periodic Genes Have Unique Chromatin Features Thatmentioning

confidence: 61%

A high-resolution transcriptome map of cell cycle reveals novel connections between periodic genes and cancer

et al. 2016

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Progression through the cell cycle is largely dependent on waves of periodic gene expression, and the regulatory networks for these transcriptome dynamics have emerged as critical points of vulnerability in various aspects of tumor biology. Through RNA-sequencing of human cells during two continuous cell cycles (>2.3 billion paired reads), we identified over 1 000 mRNAs, non-coding RNAs and pseudogenes with periodic expression. Periodic transcripts are enriched in functions related to DNA metabolism, mitosis, and DNA damage response, indicating these genes likely represent putative cell cycle regulators. Using our set of periodic genes, we developed a new approach termed "mitotic trait" that can classify primary tumors and normal tissues by their transcriptome similarity to different cell cycle stages. By analyzing >4 000 tumor samples in The Cancer Genome Atlas (TCGA) and other expression data sets, we found that mitotic trait significantly correlates with genetic alterations, tumor subtype and, notably, patient survival. We further defined a core set of 67 genes with robust periodic expression in multiple cell types. Proteins encoded by these genes function as major hubs of protein-protein interaction and are mostly required for cell cycle progression. The core genes also have unique chromatin features including increased levels of CTCF/RAD21 binding and H3K36me3. Loss of these features in uterine and kidney cancers is associated with altered expression of the core 67 genes. Our study suggests new chromatin-associated mechanisms for periodic gene regulation and offers a predictor of cancer patient outcomes.

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“…Because these genes are involved in DNA repair after damage [17], [18] and cell cycle arrest [2], [19], FCM was performed to investigate the effect of FN1BP1 expression on cell cycle in Hep3B cells after the synchronization of nocodazole and UV irradiation. The result of FCM analysis showed that, compared with the non-induced cells, the Dox-induced FN1BP1 over-expression arrested 134±17% of Hep3B cells in the G1 phase (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Some genes ( p21cip1 , ID2 , GMSF , ERCC5, and RPA1 ), which changed in the cDNA microarray analysis, were confirmed by semi-qRT-PCR, and similar changes in expression were observed. According to the Atlas microarray assay, most of these genes were involved in DNA repair after damage [17], [18] and cell-cycle arrest [2], [19]. We performed the cell-cycle analysis using FCM; our results indicated that FN1BP1 over-expression could result in G1 phase arrest.…”

Section: Discussionmentioning

confidence: 96%

Identification of FN1BP1 as a Novel Cell Cycle Regulator through Modulating G1 Checkpoint in Human Hepatocarcinoma Hep3B Cells

Liu

Feng

et al. 2013

PLoS ONE

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A novel human gene, FN1BP1 (fibronectin 1 binding protein 1), was identified using the human placenta cDNA library. Northern blotting showed a transcript of ∼2.8 kb in human placenta, liver, and skeletal muscle tissues. This mRNA transcript length was similar to the full FN1BP1 sequence obtained previously. We established a conditionally induced stable cell line of Hep3B-Tet-on-FN1BP1 to investigate the preliminary function and mechanism of the secretory FN1BP1 protein. Cell-proliferation and colony-conformation assays demonstrated that FN1BP1 protein suppressed Hep3B cell growth and colonization in vitro. Analysis of Atlas human cDNA expression indicated that after FN1BP1 Dox-inducing expression for 24 h, 19 genes were up-regulated and 22 genes were down-regulated more than two-fold. Most of these gene changes were related to cell-cycle-arrest proteins (p21cip1, p15, and cyclin E1), transcription factors (general transcription factors, zinc finger proteins, transcriptional enhancer factors), SWI/SNF (SWItch/Sucrose NonFermentable) complex units, early-response proteins, and nerve growth or neurotrophic factors. Down-regulated genes were subject to colony-stimulating factors (e.g., GMSFs), and many repair genes were involved in DNA damage (RAD, ERCC, DNA topoisomerase, polymerase, and ligase). Some interesting genes (p21cip1, ID2, GMSF, ERCC5, and RPA1), which changed in the cDNA microarray analysis, were confirmed by semi-qRT-PCR, and similar changes in expression were observed. FCM cell-cycle analysis indicated that FN1BP1 over-expression could result in G1 phase arrest. FN1BP1 might inhibit cell growth and/or colony conformation through G1 phase arrest of the Hep3B cell cycle. These results indicate the potential role of FN1BP1 as a treatment target for hepatocellular carcinoma.

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Overexpression of cell cycle regulator CDCA3 promotes oral cancer progression by enhancing cell proliferation with prevention of G1 phase arrest

Cited by 75 publications

References 37 publications

BRAF-activated non-protein coding RNA (BANCR) advances the development of esophageal squamous cell carcinoma via cell cycle

BRAF-activated non-protein coding RNA (BANCR) advances the development of esophageal squamous cell carcinoma via cell cycle

A high-resolution transcriptome map of cell cycle reveals novel connections between periodic genes and cancer

Identification of FN1BP1 as a Novel Cell Cycle Regulator through Modulating G1 Checkpoint in Human Hepatocarcinoma Hep3B Cells

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