SKA1/2/3 serves as a biomarker for poor prognosis in human lung adenocarcinoma

Chen, Cheng; Guo, Qiang; Song, Yimin; Xu, Gang; Liu, Lunxu

doi:10.21037/tlcr.2020.01.20

Cited by 28 publications

(21 citation statements)

References 31 publications

(36 reference statements)

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“…26 In patients with lung adenocarcinoma, the SKA1 expression was upregulated and could act as a promising prognostic biomarker and target. 22 Furthermore, SKA1…”

Section: Discussionmentioning

confidence: 98%

“…18,19 SKA1 is upregulated in a variety of cancers, and its carcinogenic effects, including its participation in the cell cycle, proliferation, and metastasis, have been confirmed. [20][21][22] Therefore, interference with SKA1 expression may inhibit cancer progression. Some studies have shown that the expression of miR-10a-5p in HCC tissues is lower than that in paracancerous tissues, but the specific mechanism has not been studied.…”

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confidence: 99%

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miRNA‐10a‐5p inhibits cell metastasis in hepatocellular carcinoma via targeting SKA1

Shen

Zhao

et al. 2021

The Kaohsiung J of Med Scie

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A variety of microRNAs (miRNAs) are involved in the occurrence and development of hepatocellular carcinoma (HCC). However, the role of miR-10a-5p in the progression of HCC remains unclear. Therefore, the purpose of this study was to determine the role of miR-10a-5p in the development of HCC and the possible molecular mechanism. miR-10a-5p expression in HCC tissues and plasma from patients was detected by quantitative real-time polymerase chain reaction. Migratory changes in HCC cells were detected after the overexpression of miR-10a-5p. Epithelial-mesenchymal transition (EMT)related proteins were detected by Western blot. Finally, through luciferase assay and rescue experiments, the mechanism by which miR-10a-5p regulates its downstream gene, human spindle and kinetochore-associated complex subunit 1, SKA1 and the interaction between these molecules in the development of HCC were determined. The expression of miR-10a-5p was markedly downregulated in HCC tissues, cell lines, and plasma. The overexpression of miR-10a-5p significantly inhibited the migration, invasion, and EMT of HCC cells. Furthermore, SKA1 was shown to be a downstream gene of miR-10a-5p. SKA1 silencing had the same effect as miR-10a-5p overexpression in HCC.In particular, the overexpression of SKA1 reversed the inhibitory effects of miR-10a-5p in HCC. Taken together, low miR-10a-5p expression is associated with HCC progression. miR-10a-5p inhibits the malignant development of HCC by negatively regulating SKA1.

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“…26 In patients with lung adenocarcinoma, the SKA1 expression was upregulated and could act as a promising prognostic biomarker and target. 22 Furthermore, SKA1…”

Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 99%

miRNA‐10a‐5p inhibits cell metastasis in hepatocellular carcinoma via targeting SKA1

Shen

Zhao

et al. 2021

The Kaohsiung J of Med Scie

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“…GSEA analysis was performed between normal tissues and tumor tissues, or normal and cancer organoids of LUAD and LUSC. The GO terms of the P53 signaling pathway, cell cycle, and DNA replication were upregulated in both LUAD and LUSC, which played crucial roles in lung cancer carcinogenesis and progression [ 18 – 20 ]. Further screening by establishing gene co-expression networks and preforming prognostic analysis identified CDK1, CCNB2, and CDC25A as the hub genes involved in lung cancer carcinogenesis and development.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic analysis of tumor tissues and organoids reveals the crucial genes regulating the proliferation of lung adenocarcinoma

Yang

Jiang

et al. 2021

J Transl Med

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Background Accumulative evidence shows that an organoid is a more practical and reliable tool in cancer biology research. This study aimed to identify and validate crucial genes involved in non-small cell lung cancer carcinogenesis and development using the transcriptomic analysis of tumor tissues and organoids. Methods Gene set enrichment analysis (GSEA) of tumor tissues, tumor organoids, and normal tissues was performed to reveal the similar and different mechanisms involved in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) carcinogenesis and progression. Differentially expressed gene analysis, prognostic analysis, and gene co-expression network analysis were further used to identify hub genes involved in LUAD and LUSC carcinogenesis and development. Finally, LUAD cell lines and organoids were used to validate these findings. Results GSEA analysis was performed to reveal the similar mechanisms involved in LUAD and LUSC carcinogenesis and development, such as P53 signaling pathway, base mismatch repair, DNA replication, cAMP signaling pathway and PPAR pathway. However, comparing with LUSC organoids, LUAD organoids showed downregulation of immune-related pathways, inflammation-related pathways, MAPK signaling pathways, and Rap1 signaling pathways, although these pathways were downregulated in LUAD and LUSC tissues by comparing with normal lung tissues. Further gene co-expression network analysis and prognostic analysis indicated CDK1, CCNB2, and CDC25A as the hub tumor-promoting genes in LUAD but not in LUSC, which were further validated in other datasets. Using LUAD cell lines and organoid models, CDK1 and CCNB2 knockdown were found to suppress LUAD proliferation. However, CDC25A knockdown did not inhibit LUAD cell line proliferation but could effectively suppress LUAD organoid growth, indicating that an organoid could be used as an effective tool to study cancer biology in LUAD. Conclusions The results revealed CDK1, CCNB2, and CDC25A as the hub genes involved in LUAD carcinogenesis and development, which could be used as the potential biomarkers and targets for LUAD.

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“…BIRC5, which is overexpressed in our data, performed a role in apoptosis and cell proliferation (Zhang et al 2020). CCNB2 which was essential for the regulation of the cell cycle at the G2/M (mitosis) transition, played a significant role in LUAD development (Chen et al 2020; Zhang et al 2020). A current study by He et al reported SPAG5 as “As emerging oncogene” for its overexpression in cancer types (He et al 2020).…”

Section: Discussionmentioning

confidence: 99%

Integrated Bioinformatics Analysis Deciphering the microRNA Regulation in Protein-Protein Interaction Network in Lung Adenocarcinoma

Sengupta¹,

Saha²,

Maji³

et al. 2020

Preprint

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Background: The architecture of the protein-protein interaction (PPI) network in any organism relies on their gene expression signature. microRNAs (miRNAs) have recently emerged as major post transcriptional regulators that control PPI by targeting mainly untranslated regions of the gene encoding proteins. Here, we aimed to unveil the role of miRNAs in the PPI network for identifying potential molecular targets for lung adenocarcinoma (LUAD). Materials and methods: The expression profiles of miRNAs and mRNAs were collected from the NCBI Gene Expression Omnibus (GEO) database (GSE74190 and GSE116959). Abnormally expressed mRNAs from the data were appointed to construct a PPI network and hence incorporated with the miRNA−mRNA regulatory network. The miRNAs and mRNAs in this network were subjected to functional enrichment. Through the network analysis, hubs were identified and their mutation rate and probability of cooccurrence were calculated. Results: We identified 17 miRNAs and 429 mRNAs signature for differentially altered transcriptome in LUAD. The combined miRNA−mRNA regulatory network exhibited scale−free characteristics. Network analysis showed 5 miRNA (including hsa−miR−486−5p, hsa−miR−200b−5p, and hsa−miR−130b−5p) and 10 mRNA (including ASPM, CCNB1, TTN, TPX2, and BIRC5) which expressively contribute in the LUAD. We further investigated the hub genes and noticed that ASPM and TTN had the maximum rate of mutation and possessed a high tendency of cooccurrence in LUAD. Conclusion: This study provides a unique network approach to the exploration of the underlying molecular mechanism in LUAD. Identified mRNAs and miRNAs may therefore, serve as significant prognostic predictors and therapeutic targets.

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SKA1/2/3 serves as a biomarker for poor prognosis in human lung adenocarcinoma

Cited by 28 publications

References 31 publications

miRNA‐10a‐5p inhibits cell metastasis in hepatocellular carcinoma via targeting SKA1

miRNA‐10a‐5p inhibits cell metastasis in hepatocellular carcinoma via targeting SKA1

Transcriptomic analysis of tumor tissues and organoids reveals the crucial genes regulating the proliferation of lung adenocarcinoma

Integrated Bioinformatics Analysis Deciphering the microRNA Regulation in Protein-Protein Interaction Network in Lung Adenocarcinoma

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