RETRACTED: ASPM predicts poor prognosis and regulates cell proliferation in bladder cancer

Clinical Laboratory Analysis

Chen

et al. 2021

Background Abnormal spindle‐like microcephaly (ASPM) has been proved to participate in tumor progression. However, the underlying mechanism of ASPM in liver hepatocellular carcinoma (LIHC) remains elusive. Methods The mRNA and protein expression were determined using Western blot and qRT‐PCR, and the capacities of cells proliferation, migration, and invasion were evaluated by CCK‐8, colony formation, wound healing, and transwell. MeRIP was performed to validate the interaction between ASPM and methyltransferase‐like 3 (METTL3). Results Herein, we found that ASPM was significantly upregulated in LIHC, and the high expression of ASPM was associated with poor LIHC prognosis. Furthermore, ASPM knockdown could suppress LIHC cells proliferation, migration, and invasion, while ASPM overexpression exerted reverse effect. Mechanistically, we revealed that the N6‐methyladenosine (m6A) modification of ASPM mRNA mediated by METTL3 promoted its expression in LIHC. More importantly, silencing METTL3 suppressed LIHC cells proliferation, migration, and invasion, which could be retained by ASPM overexpression. Conclusion Collectively, our findings suggested that METTL3/ASPM axis could serve as a novel promising therapeutic candidate for LIHC.

Section: Discussionmentioning

confidence: 99%

METTL3‐mediated m6A methylation of ASPM drives hepatocellular carcinoma cells growth and metastasis

Clinical Laboratory Analysis

Chen

et al. 2021

“…These characteristics have been considered to be responsible for at least 90% of colon cancer‐associated mortality 16 . Overexpression of ASPM has been reported in breast, prostate, bladder, and colon cancers 9–11,17 and several studies have shown that knockdown of ASPM inhibits cancer cell proliferation, migration, and invasion in vitro and reduces the size of some solid tumors in vivo 18–20 . ASPM expression is more intense in stage III and IV than II and I stage CRC patients, and positively correlated with lymph node metastasis 11 .…”

Section: Discussionmentioning

confidence: 99%

“…In human glioblastoma, ASPM promotes glioblastoma cell growth by regulating G1 restriction point progression and Wnt/β‐catenin signaling 8 . High expression of ASPM is positively associated with poor prognosis in bladder cancer 9 . ASPM expression is incrementally upregulated in metastatic prostate cancer and promotes prostate cancer stemness by augmenting Wnt/Dvl‐3/β‐catenin signaling 10 .…”

Section: Introductionmentioning

confidence: 99%

ASPM facilitates colorectal cancer cells migration and invasion by enhancing β‐catenin expression and nuclear translocation

The Kaohsiung J of Med Scie

et al. 2021

Increased abnormal spindle‐like microcephaly (ASPM) expression has been linked to clinical stage and poor prognosis in cancers, but the molecular mechanisms by which ASPM promotes cell metastasis in colorectal cancer (CRC) has not been identified. This study showed that the abilities of cell migration, invasion, and epithelial–mesenchymal transition (EMT) were attenuated in ASPM‐deficient CRC cell lines. Furthermore, we reported that attenuation of ASPM expression inhibited CRC cell metastasis in vivo. Additionally, the expression of ASPM was positively correlated with β‐catenin level in CRC tissues. Mechanistically, ASPM can upregulate β‐catenin transcription by stimulating the β‐catenin promoter and enhancing the nuclear translocation of β‐catenin in CRC cells, which leads to the activation of the Wnt/β‐catenin pathway. Finally, we showed that ASPM effectively induced CRC cell migration and invasion in a β‐catenin‐dependent manner.

“…For instance, ASPM triggers prostate carcinoma stemness and progression through enhancing the Wnt-Dvl-3-beta-catenin pathway [ 20 ]. It is predictive of undesirable prognosis and modulates cellular proliferation in bladder carcinoma [ 21 ]. Its upregulation accelerates glioblastoma growth through modulating G1 restriction point progression as well as the Wnt-beta-catenin pathway [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Weighted Gene Correlation Network Analysis Identifies Specific Functional Modules and Genes in Esophageal Cancer

et al. 2021

Journal of Oncology

Objective. Esophageal cancer (ESCA) is one of the most aggressive malignancies globally with an undesirable five-year survival rate. Here, this study was conducted for determining specific functional genes linked with ESCA initiation and progression. Methods. Gene expression profiling of ESCA was curated from TCGA (containing 160 ESCA and 11 nontumor specimens) and GSE38129 (30 paired ESCA and nontumor tissues) datasets. Differential expression analysis was conducted between ESCA and nontumor tissues with adjusted p value <0.05 and |log2fold-change|>1. Weighted gene coexpression network analysis (WGCNA) was conducted for determining the ESCA-specific coexpression modules and genes. Thereafter, ESCA-specific differentially expressed genes (DEGs) were intersected. Functional enrichment analysis was then presented with clusterProfiler package. Protein-protein interaction was conducted, and hub genes were determined. Association of hub genes with pathological staging was evaluated, and survival analysis was presented among ESCA patients. Results. This study determined 91 ESCA-specific DEGs following intersection of DEGs and ESCA-specific genes in TCGA and GSE38129 datasets. They were remarkably linked to cell cycle progression and carcinogenic pathways like the p53 signaling pathway, cellular senescence, and apoptosis. Ten ESCA-specific hub genes were determined, containing ASPM, BUB1B, CCNA2, CDC20, CDK1, DLGAP5, KIF11, KIF20 A, TOP2A, and TPX2. They were prominently associated with pathological staging. Among them, KIF11 upregulation was in relation to undesirable prognosis of ESCA patients. Conclusion. Collectively, we determined ESCA-specific coexpression modules and hub genes, which offered the foundation for future research concerning the mechanistic basis of ESCA.