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A Multiomics and Bioinformatics Analysis of the Role and Mechanism of CNKSR1 in Ovarian Cancer Progression
Weili Zhu1, Yimin Huang1, Jiayue Huang1
1Jiaxing Maternity and Child Health Care Hospital, Jiaxing, Zhejiang, 314001, China, jxfby.com.
Abstract:
This study aims to utilize multiomics and bioinformatics techniques to investigate the expression of the connection enzyme inhibitor Ras1 1 (CNKSR1) in ovarian cancer (OC) and its mechanism of action in the processes of tumor proliferation, invasion, and metastasis. Transcriptome sequencing was performed on paired cancerous and normal ovarian tissues from three OC patients. Differentially expressed genes (DEGs) mRNAs were analyzed using "limma", and key DEGs were identified through LASSO and random forest (RF) methods. CNKSR1 expression in OC tissues was assessed via quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blot, and immunohistochemistry. Gene Ontology (GO) enrichment analysis was conducted utilizing the Database for Annotation, Visualization, and Integrated Discovery (DAVID), and CancerSEA was employed to assess the functional status of CNKSR1 in OC. Also, the proliferation of cells, their invasion, and migration were evaluated. ChEA3 and hTFtarget were used to identify potential transcription factors targeting CNKSR1. The predicted factors were validated by Western blot analysis in OC cells overexpressing CNKSR1 or in OC cells with the CNKSR1 knockdown. Compared to normal tissues, 78 genes were downregulated, and 101 were upregulated in OC. LASSO and RF analyses identified CNKSR1 as a vital gene positively correlated with the progression of OC, which was then experimentally validated. CNKSR1 upregulation promoted the OC cells' proliferation, their invasion, and migration, while its silencing inhibited these processes. Analysis of the ChEA3 and hTFtarget databases, as well as Western blot analysis, suggested that CNKSR1 may drive epithelial-mesenchymal transition (EMT) by upregulating snail and ZEB1 expression. CNKSR1 serves a significant role in promoting the growth and progression of OC. It enhances OC cells' metastatic and invasive abilities by regulating the EMT mediated by the transcription factors Snail and ZEB1.
Insights
The connection enzyme inhibitor Ras1 1 (CNKSR1) promotes ovarian cancer (OC) progression by enhancing tumor cell proliferation, invasion, and metastasis. CNKSR1 upregulates Snail and ZEB1, driving epithelial-mesenchymal transition (EMT) in OC.
Area of Science:
- Oncology
- Bioinformatics
- Molecular Biology
Background:
- Ovarian cancer (OC) remains a significant health challenge with complex molecular underpinnings.
- Understanding the role of specific genes in OC progression is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the expression of CNKSR1 in OC.
- To elucidate the mechanism by which CNKSR1 influences OC proliferation, invasion, and metastasis.
Main Methods:
- Multiomics (transcriptome sequencing) and bioinformatics analyses (LASSO, random forest) were employed.
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blot, and immunohistochemistry were used to assess CNKSR1 expression.
- Functional assays evaluated cell proliferation, invasion, and migration; transcription factor analysis identified regulatory pathways.
Main Results:
- CNKSR1 was identified as a key gene upregulated in OC tissues and positively correlated with disease progression.
- CNKSR1 overexpression promoted OC cell proliferation, invasion, and migration.
- CNKSR1 silencing inhibited these aggressive phenotypes. Analysis suggested CNKSR1 upregulates Snail and ZEB1, driving epithelial-mesenchymal transition (EMT).
Conclusions:
- CNKSR1 plays a significant role in promoting OC growth and progression.
- CNKSR1 enhances OC cell metastatic and invasive abilities through EMT regulation via Snail and ZEB1.
- CNKSR1 represents a potential therapeutic target for ovarian cancer.
