Genetic variants and risk of prostate cancer using pathway analysis of a genome-wide association study

Kim, Yong Soo; Kim, Yonggyun; Jw, Choi; He, Oh; Lee, Ju Han

doi:10.4149/neo_2016_418

Cited by 11 publications

(8 citation statements)

References 26 publications

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“…30 Also, a polymorphism in the KCNJ4 gene, which encodes another potassium channel, is associated with prostate cancer. 4 The research on membrane channels and transporters in cancer is still in the initial phase and can fill more gaps in the years to come.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 More recently, the nature and function of specific ion channels have been suggested to be involved in tumor development and progression. [3][4][5][6][7][8] Moreover, elevated levels of potassium and lowered levels of sodium have been found in patients with various types of cancer, 3,[9][10][11] probably due to oxidative damage 12 or cancer cell lysis. 13,14 Thus, extracellular electrolyte concentration may be linked to the diagnosis of cancer, either because the electrolyte composition may facilitate cancer development or result from an ongoing undetected cancer disease.…”

Section: Introductionmentioning

confidence: 99%

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<p>Fasting Serum Levels of Potassium and Sodium in Relation to Long-Term Risk of Cancer in Healthy Men</p>

Falk¹,

Heir²,

Robsahm³

et al. 2020

CLEP

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Purpose: To examine whether serum levels of potassium and sodium were associated with long-term cancer risk in initially healthy men. Patients and Methods: A cohort of 1994 initially healthy men with no use of medication, aged 40-59 years, was followed for cancer during 40 years of follow-up. Associations between fasting electrolyte levels and cancer risk were assessed with incidence rates and Cox proportional hazards models. Results: Potassium, but not sodium, was linearly associated with cancer risk. This association remained significant after adjustment of several potential confounding factors, and also after excluding the first 10 years of follow-up. The age-adjusted risk of all-site cancer increased with 16% for each SD increase in potassium level. Men with hyperkalemia showed an incidence rate that was 40% higher than for men with normal potassium levels. Conclusion: Fasting serum potassium level in healthy men was positively associated with long-term cancer risk. Potassium or potassium ion channels may have a role in cell proliferation or differentiation. These findings might imply future cancer strategies for targeting individuals with high serum potassium levels.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

<p>Fasting Serum Levels of Potassium and Sodium in Relation to Long-Term Risk of Cancer in Healthy Men</p>

Falk¹,

Heir²,

Robsahm³

et al. 2020

CLEP

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“…Second, CHRNA5 – CHRNA3 – CHRNB4 within chromosome 15q25.1 has been documented to modify some pathways of gated channel activity and ion channel activity, and therefore to play a crucial role in leading to and maintaining malignant phenotypes 43 . Finally, the majority of genes which were chosen as the significant or selected genes in the current GWAS pathway analyses, such as KCNJ4 44 , CACNB2 45 , and SLC14A 46 , have been reported to be involved in cancer etiology and development. In addition, our finding that genes from our susceptibility transporter activity GO terms jointly affected the chromosome 15q25.1-related lung cancer risk also supported the hypothesis that these pathways were implicated in the mechanisms of lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Identification of susceptibility pathways for the role of chromosome 15q25.1 in modifying lung cancer risk

Bossé

Landi

et al. 2018

Nat Commun

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Genome-wide association studies (GWAS) identified the chromosome 15q25.1 locus as a leading susceptibility region for lung cancer. However, the pathogenic pathways, through which susceptibility SNPs within chromosome 15q25.1 affects lung cancer risk, have not been explored. We analyzed three cohorts with GWAS data consisting 42,901 individuals and lung expression quantitative trait loci (eQTL) data on 409 individuals to identify and validate the underlying pathways and to investigate the combined effect of genes from the identified susceptibility pathways. The KEGG neuroactive ligand receptor interaction pathway, two Reactome pathways, and 22 Gene Ontology terms were identified and replicated to be significantly associated with lung cancer risk, with P values less than 0.05 and FDR less than 0.1. Functional annotation of eQTL analysis results showed that the neuroactive ligand receptor interaction pathway and gated channel activity were involved in lung cancer risk. These pathways provide important insights for the etiology of lung cancer.

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“…NEIL3 also serves important roles in cancer ( 18 ). For example, Kim et al ( 19 ) reported that polymorphisms in NEIL3 increased the risk of prostate cancer. In glioblastoma, loss of NEIL3 increased replication-associated double strand breaks in DNA strands ( 20 ).…”

Section: Introductionmentioning

confidence: 99%

NEIL3 contributes toward the carcinogenesis of liver cancer and regulates PI3K/Akt/mTOR signaling

et al. 2021

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Liver cancer is one of the top three fatal types of cancer and it causes several thousands of mortalities each year. The main treatment is surgical resection which shows little benefit for patients with recurrence or metastasis. NEIL3 promotes progression and predicts survival in cancer. However, its role in liver cancer remains unclear. Based on data in the TCGA database, NEIL3 exhibited much higher expression in liver cancer tissues and was clinically correlated with tumor grade in patients with liver cancer. Furthermore, high NEIL3 expression caused shorter survival times. In liver cancer cell lines, NEIL3 showed abundant expression. When NEIL3 was knocked down in HepG2 and Huh-7 cells, cell abilities including proliferation, growth, migration and invasion, exhibited deficiency to different extents. Cell cycle transition was blocked at the G2 phase and the cell apoptotic rate increased notably. In addition, the phosphorylation levels of Akt, PI3K and mTOR were increased following NEIL3-overexpression but decreased following NEIL3-knockdown. In conclusion, NEIL3 contributes toward development and/or progression in liver cancer and regulates PI3K/Akt/mTOR signaling.

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Genetic variants and risk of prostate cancer using pathway analysis of a genome-wide association study

Cited by 11 publications

References 26 publications

<p>Fasting Serum Levels of Potassium and Sodium in Relation to Long-Term Risk of Cancer in Healthy Men</p>

<p>Fasting Serum Levels of Potassium and Sodium in Relation to Long-Term Risk of Cancer in Healthy Men</p>

Identification of susceptibility pathways for the role of chromosome 15q25.1 in modifying lung cancer risk

NEIL3 contributes toward the carcinogenesis of liver cancer and regulates PI3K/Akt/mTOR signaling

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