CCNA2 acts as a novel biomarker in regulating the growth and apoptosis of colorectal cancer

Gan, Yaqi; Li, Yimin; Li, Tong; Shu, Guang; Yin, Gang

doi:10.2147/cmar.s176833

Cited by 88 publications

(73 citation statements)

References 57 publications

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“…37 CCNA2 was shown to act as a oncogene and played a crucial role in regulating cancer cell growth and apoptosis, serving as a new biomarker for the diagnosis and therapy of CRC. 38,39 These findings support the potential of URB1 and CCNA2 as a linkage of crosstalk between mTORC1 and p53/ p21 signaling. Thus, it is reasonable to propose that the essential mTORC1/RAPTOR-URB1-CCNA2 axis plays a role in tumorigenesis.…”

Section: F I G U R Esupporting

confidence: 58%

RAPTOR promotes colorectal cancer proliferation by inducing mTORC1 and upregulating ribosome assembly factor URB1

et al. 2019

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Mammalian target of rapamycin complex 1 (mTORC1) is evolutionally conserved and frequently activated in various tumors, including colorectal cancer (CRC). It has been reported that the ribosome assembly factor Urb1 acts downstream of mTORC1/raptor signaling and contributes to digestive organ development in zebrafish. Previously, we highlighted that URB1 was overexpressed in CRC. Here, we assessed the mTORC1/regulatory associated protein with mTOR (RAPTOR)‐URB1 axis in CRC tumorigenesis. We found that RAPTOR was overexpressed in CRC tissues and cell lines, was a favorable predictor in patients with CRC, and positively correlated with URB1. Silencing of RAPTOR suppressed CRC cell proliferation and migration and induced cell cycle arrest and apoptosis in vitro and inhibited xenograft growth in vivo. Moreover, ectopic overexpression of RAPTOR exerted an inverse biological phenotype. Knockdown of RAPTOR quenched mTORC1 activity and reduced the expression of URB1 and cyclinA2 (CCNA2). In contrast, overexpression of RAPTOR activated mTORC1 and upregulated URB1 and CCNA2. Furthermore, URB1 and CCNA2 expression were also impeded by rapamycin, which is a specific inhibitor of mTORC1. Thus, RAPTOR promoted CRC proliferation, migration, and cell cycle progression by inducing mTORC1 signaling and transcriptional activation of both URB1 and CCNA2. Taken together, we concluded that RAPTOR has the potential to serve as a novel biomarker and therapeutic target for CRC.

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Section: F I G U R Esupporting

confidence: 58%

RAPTOR promotes colorectal cancer proliferation by inducing mTORC1 and upregulating ribosome assembly factor URB1

et al. 2019

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“…We searched the literature in PubMed for associations among the twenty hub genes in CRC. In Yanqi Gan et al's study, they revealed that expression of CCNA2 in CRC tissues is higher than that in normal tissues and that CCNA2 knockdown could significantly suppress CRC cell growth by impairing cell cycle progression and inducing cell apoptosis (Gan et al, 2018). TOP2A is a gene that involves copy number variations and chromosomal instability in many cancers (Simon et al, 2002;Bofin et al, 2003;Chen et al, 2015;Sonderstrup et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Identification of Core Gene Expression Signature and Key Pathways in Colorectal Cancer

2020

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Objective: Colorectal cancer (CRC) is considered the most prevalent malignant tumor that contributes to high cancer-related mortality. However, the signaling pathways involved in CRC and CRC-driven genes are largely unknown. We sought to discover a novel biomarker in CRC. Materials and Methods:All clinical CRC samples (n = 20) were from Renmin Hospital of Wuhan University. We first selected MAD2L1 by integrated bioinformatics analysis of a GSE dataset. Next, the expression of MAD2L1 in tissues and cell lines was verified by quantitative real-time PCR. The effects of MAD2L1 on cell growth, proliferation, the cell cycle, and apoptosis were examined by in vitro assays. Results:We identified 683 shared DEGs (420 upregulated and 263 downregulated), and the top twenty genes (CDK1, CCNA2, TOP2A, PLK1, MAD2L1, AURKA, BUB1B, UBE2C, TPX2, RRM2, KIF11, NCAPG, MELK, NUSAP1, MCM4, RFC4, PTTG1, CHEK1, CEP55, DTL) were selected by integrated analysis. These hub genes were significantly overexpressed in CRC samples and were positively correlated. Our data revealed that the expression of MAD2L1 in CRC tissues is higher than that in normal tissues. MAD2L1 knockdown significantly suppressed CRC cell growth by impairing cell cycle progression and inducing cell apoptosis.Conclusion: MAD2L1,asanoveloncogenicgene,playsaroleinregulatingcancercellgrowth and apoptosis and could be used as a new biomarker for diagnosis and therapy in CRC.

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“…In a study of liver cancer, researchers found that ZHX2 can repress CCNA2 transcription by binding the promoter regions of CCNA2, thereby inhibiting the proliferation of hepatoma cells [25]. Ya qi Gan et al found the expression of CCNA2 was higher in colorectal cancer than the normal colorectum, and reducing the expression of CCNA2 could influence cell cycle, inhibit the proliferation of tumor cells and increase apoptosis [26]. Francesca et al showed that miR-10b may affect tumor cell proliferation and invasion by acting on CCNA2 in breast cancer [27].…”

Section: Discussionmentioning

confidence: 99%

Weighted gene co-expression network analysis identifies CCNA2 as a treatment target of prostate cancer through inhibiting cell cycle

Yang

Wang

et al. 2020

J. Cancer

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Prostate cancer is a malignant tumor disease that seriously harms the lives of middle-aged and elderly men. Weighted gene co-expression analysis can be used to construct gene co-expression networks to explore gene sets and genes that are significantly correlated with clinical features. In this study, the transcriptome data of prostate cancer on TCGA was analyzed by weighted gene co-expression network, and the gene with a significant correlation with disease Gleason stage and tumor T stage was identified: CCNA2. CCNA2 was significantly associated with biochemical recurrence, disease-free survival and overall survival rate of prostate cancer. The ability of cancer cell proliferation, invasion and metastasis was decreased after down-regulated expression of CCNA2 in prostate cancer cell lines. Flow cytometry revealed that tumor cells were arrested in the S phase after down-regulated the expression of CCNA2. Taken together, we used WGCNA and obtain a gene CCNA2 which is significantly associated with the prognosis of prostate cancer, which may be an indicator of the prognosis of prostate cancer and a new therapeutic target.

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CCNA2 acts as a novel biomarker in regulating the growth and apoptosis of colorectal cancer

Cited by 88 publications

References 57 publications

RAPTOR promotes colorectal cancer proliferation by inducing mTORC1 and upregulating ribosome assembly factor URB1

RAPTOR promotes colorectal cancer proliferation by inducing mTORC1 and upregulating ribosome assembly factor URB1

Identification of Core Gene Expression Signature and Key Pathways in Colorectal Cancer

Weighted gene co-expression network analysis identifies CCNA2 as a treatment target of prostate cancer through inhibiting cell cycle

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