Exploring Core Genes by Comparative Transcriptomics Analysis for Early Diagnosis, Prognosis, and Therapies of Colorectal Cancer

Islam, Md. Ariful; Hossen, Md. Bayazid; Horaira, Md. Abu; Hossen, Md. Alim; Kibria, Md. Kaderi; Reza, Md. Selim; Tuly, Khanis Farhana; Faruqe, Md. Omar; Kabir, Firoz; Mahumud, Rashidul Alam; Mollah, Md. Nurul Haque

doi:10.3390/cancers15051369

Cited by 8 publications

(10 citation statements)

References 108 publications

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“…27,28 TOP2A and CDNK3 have been screened to be involved in colorectal cancer progression. 29 Currently, TOP2 has been widely used in targeted therapy of cancers. By targeting TOP2 to disrupt the catalytic cycle of TOP2, it triggers the DNA damage response and promotes apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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Knockdown of TOP2A suppresses IL‐17 signaling pathway and alleviates the progression of ulcerative colitis

Li,

2024

Immunity Inflam & Disease

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BackgroundUlcerative colitis (UC) is a chronic inflammatory disease of the colonic mucosa, with a gradually increasing incidence. Therefore, it is necessary to actively seek targets for the treatment of UC.MethodsCommon differentially expressed genes (DEGs) were screened from two microarray data sets related to UC. Protein−protein interaction network was constructed to find the hub genes. The UC mouse model and cell model were induced by dextran sulfate sodium (DSS). The pathological changes of colon tissue were observed by hematoxylin‐eosin staining. Immunohistochemistry and immunofluorescence were performed to detect the expressions of Ki67 and Claudin‐1. The performance of mice was observed by disease activity index (DAI). The effect of TOP2A on proliferation, inflammation, oxidative stress, and interleukin‐17 (IL‐17) signaling pathway in UC model was measured by cell counting kit‐8, enzyme‐linked immunosorbent assay, and western blot.ResultsThrough bioinformatics analysis, 295 common DEGs were screened, and the hub gene TOP2A was selected. In UC model, there was obvious inflammatory cell infiltration in the colon and less goblet cells, while si‐TOP2A lessened it. More Ki67 positive cells and less Claudin‐1 positive cells were observed in UC model mice. Furthermore, knockdown of TOP2A increased the body weight and colon length of UC mice, while the DAI was decreased. Through in vivo and in vitro experiments, knockdown of TOP2A also inhibited inflammation and IL‐17 signaling pathway, and promoted proliferation in DSS‐induced NCM460 cells.ConclusionKnockdown of TOP2A alleviated the progression of UC by suppressing inflammation and inhibited IL‐17 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

“…ASPM has also been shown to promote cancer progression 27,28 . TOP2A and CDNK3 have been screened to be involved in colorectal cancer progression 29 …”

Section: Discussionmentioning

confidence: 99%

Knockdown of TOP2A suppresses IL‐17 signaling pathway and alleviates the progression of ulcerative colitis

Li,

2024

Immunity Inflam & Disease

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“…SLC2A1, the glucose transporter, could encourage the growth, invasion, resistance to chemotherapy, and metastasis of cancer cells by controlling aerobic glycolysis [29,30]. CDKN3, a cyclin-dependent kinase inhibitor, is usually high-expressed and regarded as a novel markers in several kinds of cancers [31][32][33]. CDKN3 promotes cancer growth via regulating cell cycle and DNA replication signaling [34], and inhibition of CDKN3 reduces cell proliferation, invasion and promotes apoptosis in cancer cells [35].…”

Section: Discussionmentioning

confidence: 99%

Identification of crucial anoikis-related genes as novel biomarkers and potential therapeutic targets for lung adenocarcinoma via bioinformatic analysis and experimental verification

Wu,

Zhang,

You

et al. 2024

Aging

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Lung adenocarcinoma (LUAD) is a malignant tumor of the respiratory system that has a poor 5-year survival rate. Anoikis, a type of programmed cell death, contributes to tumor development and metastasis. The aim of this study was to develop an anoikis-based stratified model, and a multivariable-based nomogram for guiding clinical therapy for LUAD. Through differentially expressed analysis, univariate Cox, LASSO Cox regression, and random forest algorithm analysis, we established a 4 anoikis-related genes-based stratified model, and a multivariable-based nomogram, which could accurately predict the prognosis of LUAD patients in the TCGA and GEO databases, respectively. The low and high-risk score LUAD patients stratified by the model showed different tumor mutation burden, tumor microenvironment, gemcitabine sensitivity and immune checkpoint expressions. Through immunohistochemical analysis of clinical LUAD samples, we found that the 4 anoikisrelated genes (PLK1, SLC2A1, ANGPTL4, CDKN3) were highly expressed in the tumor samples from clinical LUAD patients, and knockdown of these genes in LUAD cells by transfection with small interfering RNAs significantly inhibited LUAD cell proliferation and migration, and promoted anoikis. In conclusion, we developed an anoikisbased stratified model and a multivariable-based nomogram of LUAD, which could predict the survival of LUAD patients and guide clinical treatment.

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“…Therefore, using CDKN3 as a tumor treatment target will be very important. There have been studies using transcriptomics to determine that CDKN3 is a core gene for the prognosis of colorectal cancer [ 32 ]. We believe that CDKN3 will have broader research prospects in the future.…”

Section: Discussionmentioning

confidence: 99%

Human pan-cancer analysis of the predictive biomarker for the CDKN3

Chen,

Li,

Sha

et al. 2024

Eur J Med Res

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Background Cell cycle protein-dependent kinase inhibitor protein 3 (CDKN3), as a member of the protein kinase family, has been demonstrated to exhibit oncogenic properties in several tumors. However, there are no pan-carcinogenic analyses for CDKN3. Methods Using bioinformatics tools such as The Cancer Genome Atlas (TCGA) and the UCSC Xena database, a comprehensive pan-cancer analysis of CDKN3 was conducted. The inverstigation encompassed the examination of CDKN3 function actoss 33 different kinds of tumors, as well as the exploration of gene expressions, survival prognosis status, clinical significance, DNA methylation, immune infiltration, and associated signal pathways. Results CDKN3 was significantly upregulated in most of tumors and correlated with overall survival (OS) of patients. Methylation levels of CDKN3 differed significantly between tumors and normal tissues. In addition, infiltration of CD4 + T cells, cancer-associated fibroblasts, macrophages, and endothelial cells were associated with CDKN3 expression in various tumors. Mechanistically, CDKN3 was associated with P53, PI3K-AKT, cell cycle checkpoints, mitotic spindle checkpoint, and chromosome maintenance. Conclusion Our pan-cancer analysis conducted in the study provides a comprehensive understanding of the involvement of CDKN3 gene in tumorigenesis. The findings suggest that targeting CDKN3 may potentially lead to novel therapeutic strategies for the treatment of tumors.

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Exploring Core Genes by Comparative Transcriptomics Analysis for Early Diagnosis, Prognosis, and Therapies of Colorectal Cancer

Cited by 8 publications

References 108 publications

Knockdown of TOP2A suppresses IL‐17 signaling pathway and alleviates the progression of ulcerative colitis

Knockdown of TOP2A suppresses IL‐17 signaling pathway and alleviates the progression of ulcerative colitis

Identification of crucial anoikis-related genes as novel biomarkers and potential therapeutic targets for lung adenocarcinoma via bioinformatic analysis and experimental verification

Human pan-cancer analysis of the predictive biomarker for the CDKN3

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