Erratum: Whole genome and transcriptome sequencing of matched primary and peritoneal metastatic gastric carcinoma

Zhang, J.; Huang, J. Y.; Chen, Yixuan; Yuan, F.; Yan, F. H.; Wang, M. J.; Wang, G.; Su, M.; Lu, G; Huang, Y.; Dai, H.; Ji, J.; Zhang, J.; Zhang, J. N.; Jiang, Yongjie; Chen, Shanghua; Zhu, Zhiqiang; Yu, Y. Y.

doi:10.1038/srep15309

Cited by 10 publications

(5 citation statements)

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“…These processes provide intermediates for several metabolic pathways to enhance cell growth, including cancer proliferation. The coiled-coil domain-containing protein 178 (CCDC178) is an 867 amino acid polypeptide that is mutated in several human cancers including gastric cancer (168) and HCC (169). CCDC178 was reported to be overexpressed in HCC and promoted metastasis by mediating anoikis resistance via activation of the ERK/MAPK signaling pathway (24).…”

Section: Protein Metabolismmentioning

confidence: 99%

Mechanisms for Modulating Anoikis Resistance in Cancer and the Relevance of Metabolic Reprogramming

et al. 2021

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The attachment of cells to the extracellular matrix (ECM) is the hallmark of structure–function stability and well-being. ECM detachment in localized tumors precedes abnormal dissemination of tumor cells culminating in metastasis. Programmed cell death (PCD) is activated during tumorigenesis to clear off ECM-detached cells through “anoikis.” However, cancer cells develop several mechanisms for abrogating anoikis, thus promoting their invasiveness and metastasis. Specific factors, such as growth proteins, pH, transcriptional signaling pathways, and oxidative stress, have been reported as drivers of anoikis resistance, thus enhancing cancer proliferation and metastasis. Recent studies highlighted the key contributions of metabolic pathways, enabling the cells to bypass anoikis. Therefore, understanding the mechanisms driving anoikis resistance could help to counteract tumor progression and prevent metastasis. This review elucidates the dynamics employed by cancer cells to impede anoikis, thus promoting proliferation, invasion, and metastasis. In addition, the authors have discussed other metabolic intermediates (especially amino acids and nucleotides) that are less explored, which could be crucial for anoikis resistance and metastasis.

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Section: Protein Metabolismmentioning

confidence: 99%

Mechanisms for Modulating Anoikis Resistance in Cancer and the Relevance of Metabolic Reprogramming

et al. 2021

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“…PMPCB is the mediator for the majority of mitochondrial proteins [32]. ARMC4 is a new gene that has been found in peritoneal metastatic gastric carcinoma [33]. PDE9A is expressed highly in the brain, and it is a cGMP-specific phosphodiesterase [34].…”

Section: Discussionmentioning

confidence: 99%

Phytanoyl-CoA 2-Hydroxylase-Interacting Protein-Like Gene Is a Therapeutic Target Gene for Glioblastoma Multiforme

Chen

et al. 2019

Med Sci Monit

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Glioblastoma multiforme (GBM) is the most common primary CNS cancer and has a poor prognosis. This study searched for significant genes and the mechanisms involved in GBM. We used the Gene Expression Omnibus (GEO) to test the WHO normal and IV glioma database, used R tool to identify the significant gene, and finally, combined these with The Cancer Genome Atlas (TCGA) to verify the significant genes. Subsequently, we explored the biological mechanisms involved. Phytanoyl-CoA 2-hydroxylase-interacting protein-like gene (PHYHIPL) is downregulated in grade IV glioma (GBM). The downregulation of PHYHIPL in GBM is accompanied by poor overall survival in the TCGA database, which indicates that PHYHIPL is a protection gene in GBM development. Bioinformatics analysis shows that the poor prognosis with downregulated PHYHIPL may be the result of the TNF signaling pathway and the IL-17 signaling pathway, but good prognosis accompanied by upregulated PHYHIPL may be the result of retrograde endocannabinoid signaling and the cAMP signaling pathway. Protein-protein interactions (PPI) net indicated that PHYHIPL may play a vital role in cell metabolism, and we hypothesize that the downregulation mechanism may be the result of mutations of the β-catenin gene and the endogenous siRNA, as shown in previous studies. PHYHIPL may be a target gene for the treatment and prognosis of GBM.

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“…Recently, whole-genome sequencing techniques that allowed to identify molecular subtypes in primitive gastric cancer cohorts have been applied to study the molecular signature of GC metastasis from different sites [31]. Recent evidences showed that CCNE1 amplification was found associated with liver metastasis in GC of the TP53 subtype [32] while mutations activating or inactivating specific genes were identified in peritoneal metastasis [33]. Circulating tumor DNA (ctDNA) detection is another innovative approach to analyze GC disease.…”

Section: Molecular Insight For Metastatic Lesionsmentioning

confidence: 99%

Update on gastric cancer treatments and gene therapies

Biagioni

Skalamera

Peri

et al. 2019

Cancer Metastasis Rev

146

100

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Gastric cancer is an active topic of clinical and basic research due to high morbidity and mortality. To date, gastrectomy and chemotherapy are the only therapeutic options for gastric cancer patients, but drug resistance, either acquired or primary, is the main cause for treatment failure. Differences in development and response to cancer treatments have been observed among ethnically diverse GC patient populations. In spite of major incidence, GC Asian patients have a significantly better prognosis and response to treatments than Caucasian ones due to genetic discordances between the two populations. Gene therapy could be an alternative strategy to overcome such issues and especially CRISPR/Cas9 represents one of the most intriguing gene-editing system. Thus, in this review article, we want to provide an update on the currently used therapies for the treatment of advanced GC.

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Erratum: Whole genome and transcriptome sequencing of matched primary and peritoneal metastatic gastric carcinoma

Cited by 10 publications

References 0 publications

Mechanisms for Modulating Anoikis Resistance in Cancer and the Relevance of Metabolic Reprogramming

Mechanisms for Modulating Anoikis Resistance in Cancer and the Relevance of Metabolic Reprogramming

Phytanoyl-CoA 2-Hydroxylase-Interacting Protein-Like Gene Is a Therapeutic Target Gene for Glioblastoma Multiforme

Update on gastric cancer treatments and gene therapies

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