High‑level SETD1B gene expression is associated with unfavorable prognosis in hepatocellular carcinoma

Chen, Dong; Li, Tieling; Wang, Cheng; Lei, Guanglin; Wang, Ruilan; Wang, Zhaohai; Yu, Lixin; Jin, Yan; Zhang, Peirui; Wang, Xiliang; Zhang, Shaogeng; Yang, Peng

doi:10.3892/mmr.2019.9832

Cited by 6 publications

(6 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…linc-POU3F3 [36,37] RUNX2, and SLP-2 [38] were found to enhance the invasion and migration of HCC cells. Regarding the prognosisrelated genes of HCC, some overexpressed genes, such as SETDB1 [39], SKA1 [40], and DSN1 [41], were reported to be associated with poor survival in HCC. In our study, we discovered that CELSR3 could promote the cell proliferation, invasion, and migration through our in vitro experiment.…”

Section: Discussionmentioning

confidence: 99%

Effect of CELSR3 on the Cell Cycle and Apoptosis of Hepatocellular Carcinoma Cells

Xie

Dang

et al. 2020

J. Cancer

View full text Add to dashboard Cite

Cadherin EGF LAG seven-pass G-type receptor 3 (CELSR3) has been reported in cancers but its role and potential molecular mechanism in hepatocellular carcinoma (HCC) is unclear. Therefore, we aimed to investigate the clinical value and molecular mechanism of CELSR3 in HCC using an in vitro experiment, a meta-analysis and bioinformatics. The in vitro experiment determined the promoting effect of CELSR3 in the proliferation, invasion, and migration of HCC cells. CELSR3 knockout causes S-phage arrest in HCC cells. CELSR3 can also inhibit the apoptosis of HCC cells. The expression of the CELSR3 gene and protein was significantly elevated in HCC. Elevated CELSR3 was correlated to the bigger tumor size, higher pathological stage, and the worse overall survival of HCC. Methylation analysis revealed that the hypomethylation of CELSR3 regulated by DNMT1, DNMT3A, and DNMT3B may be the underlying mechanism of upregulated CELSR3. Biological enrichment analysis uncovered that the cell cycle, DNA replication, and PI3K-Akt signaling pathways were important pathways regulated by CELSR3 and its co-expressed genes in HCC. Taken together, upregulated CELSR3 is an important regulator in the progression and prognosis of HCC. The hypomethylation of CELSR3 and its regulation in the cell cycle may be the potential molecular mechanism in HCC.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of CELSR3 on the Cell Cycle and Apoptosis of Hepatocellular Carcinoma Cells

Xie

Dang

et al. 2020

J. Cancer

View full text Add to dashboard Cite

show abstract

“…The third transcript was linked to USP6, which, when upregulated, is considered an oncogene causing bone neoplasms (Oliveira et al., 2004), and downregulation of this gene in older gulls suggests an anticancer mechanism. The fourth transcript was linked to SETD1B, which supports mitotic processes (Tajima et al., 2019) and is overexpressed in several cancer types (e.g., Yang & Ernst, 2017; Chen et al., 2019). A lower expression of SETD1B in older gulls thus suggests a method for suppressing uncontrolled cell growth and thus neoplasia.…”

Section: Discussionmentioning

confidence: 99%

Age‐dependent expression of cancer‐related genes in a long‐lived seabird

Meitern

Fort

Giraudeau

et al. 2020

Evolutionary Applications

View full text Add to dashboard Cite

Studies of model animals like mice and rats have led to great advances in our understanding of the process of tumorigenesis, but this line of study has less to offer for understanding the mechanisms of cancer resistance. Increasing the diversity of nonmodel species from the perspective of molecular mechanisms of natural cancer resistance can lead to new insights into the evolution of protective mechanisms against neoplastic processes and to a wider understanding of natural cancer defense mechanisms. Such knowledge could then eventually be harnessed for the development of human cancer therapies. We suggest here that seabirds are promising, albeit currently completely ignored candidates for studying cancer defense mechanisms, as they have a longer maximum life span than expected from their body size and rates of energy metabolism and may have thus evolved mechanisms to limit neoplasia progression, especially at older ages. We here apply a novel, intraspecific approach of comparing old and young seabirds for improving our understanding of aging and neoplastic processes in natural settings. We used the long‐lived common gulls (Larus canus) for studying the age‐related pattern of expression of cancer‐related genes, based on transcriptome analysis and databases of orthologues of human cancer genes. The analysis of differently expressed cancer‐related genes between young and old gulls indicated that similarly to humans, age is potentially affecting cancer risk in this species. Out of eleven differentially expressed cancer‐related genes between the groups, three were likely artifactually linked to cancer. The remaining eight were downregulated in old gulls compared to young ones. The downregulation of five of them could be interpreted as a mechanism suppressing neoplasia risk and three as increasing the risk. Based on these results, we suggest that old gulls differ from young ones both from the aspect of cancer susceptibility and tumor suppression at the genetic level.

show abstract

“…Signi cantly mutated gene (SMG) analysis identi ed several genes including SETD1B, RNF43, MBD6 and so on, whose mutation states were profoundly in uenced by NEB mutation. SETD1B mutation was associated with intellectual disability, epilepsy and autism (21), and was also found to be mutated in primary hepatic neuroendocrine (22), hepatocellular (23), gastric and colorectal tumors (24). RNF43 is a tumour suppressor gene that frequently mutated in colorectal and endometrial cancers (25,26).…”

Section: Discussionmentioning

confidence: 99%

NEB mutation is associated with high mutational burden and worse colorectal-cancer survival

Yuan

Yan

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Nebulin (NEB) as a protein-coding gene have been well demonstrated its vital roles in skeletal muscles but no study for association between NEB mutation and cancer.Methods: Here, we systematically analyzed mutation spectrum of colorectal cancer (CRC) samples and associations between NEB somatic mutation and CRC patients' tumor mutation burden (TMB) and prognosis by using TCGA-COAD project mutation dataset.Results: Mutational signatures detected from CRC samples indicated pivotal roles of defective DNA damage repair process and polymerase activity in CRC initiation. NEB somatic mutation was found in about 16% CRC patients. Besides, NEB mutation was identified as an independent factor for high CRC TMB and inferior prognosis. Significantly mutated gene (SMG) analysis identified several genes including RNF43, SETD1B, MBD6 and so on, whose mutation states were profoundly influenced by NEB mutation and might be tumor driver genes in CRC initiation and progression.Conclusions: In conclusion, NEB might be a novel CRC-related genes that could affect patients' prognosis by perturbing genome instability.

show abstract

High‑level SETD1B gene expression is associated with unfavorable prognosis in hepatocellular carcinoma

Cited by 6 publications

References 21 publications

Effect of CELSR3 on the Cell Cycle and Apoptosis of Hepatocellular Carcinoma Cells

Effect of CELSR3 on the Cell Cycle and Apoptosis of Hepatocellular Carcinoma Cells

Age‐dependent expression of cancer‐related genes in a long‐lived seabird

NEB mutation is associated with high mutational burden and worse colorectal-cancer survival

Contact Info

Product

Resources

About