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

Shen, Wei; Tong, Dimin; Chen, Jie; Hu, Zeyang; Xu, Shuguang; He, Shan; Ge, Zhen; Zhang, Jianan; Mao, Qinan; Chen, Hang; Xu, Guodong

doi:10.1002/jcla.24396

Cited by 12 publications

(9 citation statements)

References 32 publications

(54 reference statements)

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“…This study indicated that CDCA5 expression could impact TMB, MSI and immune cell infiltration and thus impacting response to immunotherapy for the first time. Besides, positive relationship of CD274 (PD-L1) and CDCA5 was found in most tumors, which was in line with the finding of Shen et al 13 Therefore, there is potential for CDCA5 to serve as a new immunotherapeutic target. However, the potential mechanisms should be identified through in vitro and in vivo experiments.…”

supporting

confidence: 87%

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Prognostic and Immunological Roles of Cell Cycle Regulator CDCA5 in Human Solid Tumors

He¹,

Zhou²,

Wang³

et al. 2022

IJGM

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Background: There have been several studies evaluating the prognostic significance of cell division cycle associated 5 (CDCA5). However, few reports analyzed the correlation between CDCA5 and prognosis of diverse cancers based on large clinical data. We thus comprehensively analyzed CDCA5 expression and clinical significance using The Cancer Genome Atlas (TCGA) data from 31 types of solid tumors. Methods: The expression profiles of CDCA5 were investigated across pan-cancer samples from the TCGA. Cox regression and Kaplan-Meier analysis was performed to determine CDCA5's prognostic value. CDCA5 expression was further validated by quantitative real-time PCR (qRT-PCR) and immunohistochemistry (IHC) in lung adenocarcinoma (LUAD). Results: We found that CDCA5 was significantly overexpressed in 22 types of tumors. Up-regulated CDCA5 was significantly related to poor survival in 13 types of tumors. Furthermore, CDCA5 expression was significantly associated with immune cell infiltration. Tumor mutation burden (TMB), microsatellite instability (MSI), and immune checkpoint expression were significantly correlated with CDCA5 expression. Additional analysis of IMvigor 210 cohort validated that patients with high level of CDCA5 had superior response to anti-PD-L1 therapy. Conclusion: Our findings suggested that CDCA5 could provide prognostic information in most types of cancers and contributed to tumor immune microenvironment.

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supporting

confidence: 87%

“…12 A recent study demonstrated the positive relationship between CDCA5 and PD-1/PD-L1 in non-small-cell lung cancer (NSCLC). 13 However, there is still no systematic analysis on the relationship of CDCA5 in different human cancers based on large clinical data.…”

Section: Introductionmentioning

confidence: 99%

Prognostic and Immunological Roles of Cell Cycle Regulator CDCA5 in Human Solid Tumors

He¹,

Zhou²,

Wang³

et al. 2022

IJGM

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“…We performed DO/GO/KEGG functional enrichment analysis on these core genes and found that these genes were strongly associated with the progression of NSCLC. In particular, KEGG analysis results showed that these core genes were enriched in pathways such as platinum resistance [43], Cellular senescence [44] and P53 signaling pathway [45], This also suggests that the hub gene may affect NSCLC through those ways.…”

Section: Discussionmentioning

confidence: 94%

New perspectives on the potential of tetrandrine in the treatment of non-small cell lung cancer: bioinformatics, Mendelian randomization study and experimental investigation

Luo,

Mo,

et al. 2024

Aging

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Background: Although there are numerous treatment methods for NSCLC, long-term survival remains a challenge for patients. The objective of this study is to investigate the role and causal relationship between the target of tetrandrine and non-small cell lung cancer (NSCLC) through transcriptome and single-cell sequencing data, summary-data-based Mendelian Randomization (SMR) and basic experiments. The aim is to provide a new perspective for the treatment of NSCLC. Methods: We obtained the drug target gene of tetrandrine through the drug database, and then used the GSE19188 data set to obtain the NSCLC pathogenic gene, established a drug-disease gene interaction network, screened out the hub drug-disease gene, and performed bioinformatics and tumor cell immune infiltration analysis. Single-cell sequencing data (GSE148071) to determine gene location, SMR to clarify causality and drug experiment verification. Results: 10 drug-disease genes were obtained from 213 drug targets and 529 disease genes. DO/GO/KEGG analysis showed that the above genes were all related to the progression and invasion of NSCLC. Four drugdisease genes were identified from a drug-disease PPI network. These four genes were highly expressed in tumors and positively correlated with plasma cells, T cells, and macrophages. Subsequent single-cell sequencing data confirmed that these four genes were distributed in epithelial cells, and SMR analysis revealed the causal relationship between CCNA2 and CCNB1 and the development of NSCLC. The final molecular docking and drug experiments showed that CCNA2 and CCNB1 are key targets for tetrandrine in the treatment of NSCLC.

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“…CDCA5 can also promote cell proliferation and participate in apoptosis by regulating the function of cell cycle related proteins and transcription factors [10]. As reported, upregulated CDCA5 expression level was found in many types of cancers, including bladder cancer, lung cancer, liver cancer, colorectal cancer, indicating CDCA5 may participate in the development of these diseases [11][12][13][14]. However, the functional role of CDCA5 in ccRCC progression remains unclear.…”

Section: Introductionmentioning

confidence: 86%

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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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

Cited by 12 publications

References 32 publications

Prognostic and Immunological Roles of Cell Cycle Regulator CDCA5 in Human Solid Tumors

Prognostic and Immunological Roles of Cell Cycle Regulator CDCA5 in Human Solid Tumors

New perspectives on the potential of tetrandrine in the treatment of non-small cell lung cancer: bioinformatics, Mendelian randomization study and experimental investigation

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

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