Cyclin-Dependent Kinase 1 (CDK1) is Co-Expressed with CDCA5: Their Functions in Gastric Cancer Cell Line MGC-803

Huang, Zhigang; Zhang, Shizhuo; Du, Jinlin; Xing, Zhou; Zhang, Weijian; Huang, Zhaowei; Ouyang, Ping

doi:10.12659/msm.923664

Cited by 16 publications

(13 citation statements)

References 37 publications

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“…Moreover, CDCA5 cooperates with other key factor to play its functional roles has been identi ed in cancers. CDCA5 is demonstrated to coexpressed with cyclin-dependent kinase 1 (CDK1) enhances tumor cell proliferation, migration, and invasion abilities in gastric cancer [25]. Similar with this nding, by using a combinatory approach of LC-MS/MS analysis and Co-IP con rmation, we showed CDCA5 may cooperated with EEF1A1 to play its oncogenic role in ccRCC progression.…”

Section: Discussionsupporting

confidence: 71%

CDCA5 is a potent therapeutic target of clear cell renal cell carcinoma

Wang

Liu

et al. 2022

Preprint

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Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer in adult, and patients with advanced ccRCC are facing limited treatment options. Cell division cycle associated 5 (CDCA5), a key regulator for segregating sister chromatids in cell cycle, has been increasingly reported for a potential therapeutic target in multiple human cancers. However, the functional roles of CDCA5 in ccRCC remain uncertain. Here we identified that CDCA5 expression was frequently upregulated in ccRCC tumors and significantly associated with poor prognosis of ccRCC patients. To investigate the role of CDCA5 in ccRCC progression, loss function cell models were established. Knockdown of CDCA5 remarkably suppressed ccRCC cell proliferation and migration ability, and also induced cell apoptosis in vitro. In addition, the significance of CDCA5 in ccRCC was further demonstrated in a mouse xenograft model. Silencing of CDCA5 drastically inhibited in vivo tumorigenicity of ccRCC cells. Mechanically, we identified CDCA5 may cooperate with EEF1A1 to promote the tumorigenic phenotype of ccRCC. Overall, our results revealed the significant functional role of CDCA5 in ccRCC progression, which may pave a way for the development of new treatment strategies for ccRCC treatment.

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Section: Discussionsupporting

confidence: 71%

CDCA5 is a potent therapeutic target of clear cell renal cell carcinoma

Wang

Liu

et al. 2022

Preprint

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“…There is now growing evidence that CDCA5 is overexpressed as an oncogene in a variety of common malignancies and has been proven to play a crucial part in tumorigenesis and development, including NSCLC, 13 hepatocellular carcinoma, 14 , 15 prostate cancer, 16 , 17 gastric cancer, 18 , 19 ovarian cancer, 20 nasopharyngeal carcinoma, 21 bladder cancer, 22 esophageal squamous cell carcinoma, 23 colorectal cancer, 24 breast cancer, 25 oral squamous cell carcinoma. 26 So far, only Nguyen et al have discussed the relationship between CDCA5 and NSCLC in detail, and they reported that CDCA5, recognized as an independent prognostic factor of NSCLC, played an essential role in the growth of lung cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Silencing oncogene cell division cycle associated 5 induces apoptosis and G1 phase arrest of non‐small cell lung cancer cells via p53‐p21 signaling pathway

Shen¹,

Tong²,

Chen³

et al. 2022

Clinical Laboratory Analysis

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Backgrounds: As a regulator of cell cycle, cell division cycle-associated 5 (CDCA5) is involved in the progression of various malignant tumors. However, the potential relationship between CDCA5 and lung cancer has not been reported. Methods:In our study, we analyzed the expression of CDCA5 in a variety of malignant tumors, performed Kaplan-Meier survival analysis of lung adenocarcinoma (LUAD), explored the potential relationship between CDCA5 expression and clinicopathological characteristics, assessed the predictive capability of at different stages of clinicopathological characteristics, revealed the enriched functions and signaling pathways among LUAD paitents with high CDCA5 expression, and investigated the correlation between PD-1, PD-L1, and CDCA5 through bioinformatics analyses. Subsequently, we performed quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting (WB) to demonstrate that CDCA5 mediates the p53-p21 pathway and regulates the cell cycle. Result: CDCA5 is probably involved in the occurrence and development of NSCLC, and function as a reliable biomarker for predicting the survival outcomes of patients with early stage of patients with LUAD. Furthermore, CDCA5 may be a promising indicator of immunotherapy efficacy. In addition, silencing the expression of CDCA5 significantly increased the proportion of apoptotic NSCLC cells, and caused NSCLC cells to be arrested in the G1 phase. Conslusion: In conclusion, CDCA5 regulated the cell cycle of NSCLC cells by mediating the p53-p21 signaling pathway, participating in the development and progression of NSCLC patients.

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“…Aberrant expression of kinases has been reported in multiple cancers, including GC 4 . Some of the kinases activated/dysregulated in GC are mitogen‐activated protein kinase 3 (ERK1), mitogen‐activated protein kinase 1 (ERK2), GTPase KRas (K‐RAS), RAF proto‐oncogene serine/threonine‐protein kinase (RAF1), cyclin‐dependent kinase 5 (CDK5), and CAMKK 5–8 . CAMKK2, a 66‐ to 68‐kDa Serine/Threonine kinase, consists of unique N‐ and C‐terminal domains and a central Serine/Threonine‐directed kinase domain that is followed by a regulatory domain composed of overlapping autoinhibitory and CaM‐binding regions 9 .…”

Section: Introductionmentioning

confidence: 99%

Hyperactivation of MEK/ERK pathway by Ca²⁺/calmodulin‐dependent protein kinase kinase 2 promotes cellular proliferation by activating cyclin‐dependent kinases and minichromosome maintenance protein in gastric cancer cells

Najar

Aravind

Dagamajalu

et al. 2021

Molecular Carcinogenesis

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Although CAMKK2 is overexpressed in several cancers, its role and relevant downstream signaling pathways in gastric cancer (GC) are poorly understood. Treatment of AGS GC cells with a CAMKK2 inhibitor, STO‐609, resulted in decreased cell proliferation, cell migration, invasion, colony‐forming ability, and G1/S‐phase arrest. Quantitative phosphoproteomics in AGS cells with the CAMKK2 inhibitor led to the identification of 9603 unique phosphosites mapping to 3120 proteins. We observed decreased phosphorylation of 1101 phosphopeptides (1.5‐fold) corresponding to 752 proteins upon CAMKK2 inhibition. Bioinformatics analysis of hypo‐phosphorylated proteins revealed enrichment of MAPK1/MAPK3 signaling. Kinase enrichment analysis of hypo‐phosphorylated proteins using the X2K Web tool identified ERK1, cyclin‐dependant kinase 1 (CDK1), and CDK2 as downstream substrates of CAMKK2. Moreover, inhibition of CAMKK2 and MEK1 resulted in decreased phosphorylation of ERK1, CDK1, MCM2, and MCM3. Immunofluorescence results were in concordance with our mass spectroscopy data and Western blot analysis results. Taken together, our data reveal the essential role of CAMKK2 in the pathobiology of GC through the activation of the MEK/ERK1 signaling cascade.

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Cyclin-Dependent Kinase 1 (CDK1) is Co-Expressed with CDCA5: Their Functions in Gastric Cancer Cell Line MGC-803

Cited by 16 publications

References 37 publications

CDCA5 is a potent therapeutic target of clear cell renal cell carcinoma

CDCA5 is a potent therapeutic target of clear cell renal cell carcinoma

Silencing oncogene cell division cycle associated 5 induces apoptosis and G1 phase arrest of non‐small cell lung cancer cells via p53‐p21 signaling pathway

Hyperactivation of MEK/ERK pathway by Ca²⁺/calmodulin‐dependent protein kinase kinase 2 promotes cellular proliferation by activating cyclin‐dependent kinases and minichromosome maintenance protein in gastric cancer cells

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Cyclin-Dependent Kinase 1 (CDK1) is Co-Expressed with CDCA5: Their Functions in Gastric Cancer Cell Line MGC-803

Cited by 16 publications

References 37 publications

CDCA5 is a potent therapeutic target of clear cell renal cell carcinoma

CDCA5 is a potent therapeutic target of clear cell renal cell carcinoma

Silencing oncogene cell division cycle associated 5 induces apoptosis and G1 phase arrest of non‐small cell lung cancer cells via p53‐p21 signaling pathway

Hyperactivation of MEK/ERK pathway by Ca2+/calmodulin‐dependent protein kinase kinase 2 promotes cellular proliferation by activating cyclin‐dependent kinases and minichromosome maintenance protein in gastric cancer cells

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Hyperactivation of MEK/ERK pathway by Ca²⁺/calmodulin‐dependent protein kinase kinase 2 promotes cellular proliferation by activating cyclin‐dependent kinases and minichromosome maintenance protein in gastric cancer cells