A MAP3k1 SNP Predicts Survival of Gastric Cancer in a Chinese Population

Wei, Xiaowei; En-ke, Zhang; Wang, Chun; Gu, Dongying; Song, Lili; Wang, Meilin; Xu, Zhi; Gong, Weida; Tang, Cuiju; Gao, Jinglong; Chen, Jinfei; Zhang, Zhengdong

doi:10.1371/journal.pone.0096083

Cited by 9 publications

(15 citation statements)

References 32 publications

(36 reference statements)

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“…MAP3K1 is a component of an evolutionarily conserved signal transduction cascade, which can activate mitogen-activated protein kinases (MAPKs) (39). It has been previously revealed that the single nucleotide polymorphism MAP3K1 rs889312 is closely associated with the risk of breast cancer and outcome among patients with diffuse-type gastric cancer (40).…”

Section: Discussionmentioning

confidence: 99%

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miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

et al. 2017

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Abstract. Lung cancer is one of the most common types of tumors and the leading cause of cancer-associated mortality in the world. Additionally, non-small cell lung cancer (NSCLC) accounts for ~80% of all lung cancer cases. Epithelialmesenchymal transition (EMT) is an important cell biological process, which is associated with cancer migration, metastasis, asthma and fibrosis in the lung. In the present study, it was revealed that miR-145-5p was able to suppress EMT by inactivating the c-Jun N-terminal kinase (JNK) signaling pathway in NSCLC cells. Mitogen-activated protein kinase kinase kinase 1 (MAP3K1) was predicted and confirmed to be a novel target of miR-145-5p. Overexpression of MAP3K1 was able to reverse the inhibition of EMT induced by miR-145-5p via the JNK signaling pathway. Overall, the results revealed that miR-145-5p inhibits EMT via the JNK signaling pathway by targeting MAP3K1 in NSCLC cells.

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Section: Discussionmentioning

confidence: 99%

“…GAPDH was used as endogenous control to normalize the expression data. Reactions were incubated for 10 min at 95˚C, followed by 40 (19).…”

Section: Reverse Transcription Quantitative Polymerase Chain Reactionmentioning

confidence: 99%

miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

et al. 2017

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“…Recently, MAP3K1 rs889312 has been identified as a low-penetrant risk factor for breast cancer, both for ER+ or ER− breast cancer [ 18 ]. It was also demonstrated to be an independent risk factor for poor survival in diffuse-type gastric cancer in an overdominant model [ 19 ]. However, two similar investigations failed to prove this variant was associated with BC clinical outcome [ 6 , 7 ], although neither of them carried out survival analysis on the basis of BC intrinsic subtypes.…”

Section: Discussionmentioning

confidence: 99%

Subtype-specific associations between breast cancer risk polymorphisms and the survival of early-stage breast cancer

Fu¹,

Guo²,

Lin³

et al. 2018

J Transl Med

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BackgroundLimited evidence suggests that inherited predisposing risk variants might affect the disease outcome. In this study, we analyzed the effect of genome-wide association studies—identified breast cancer-risk single nucleotide polymorphisms on survival of early-stage breast cancer patients in a Chinese population.MethodsThis retrospective study investigated the relationship between 21 GWAS-identified breast cancer-risk single nucleotide polymorphisms and the outcome of 1177 early stage breast cancer patients with a long median follow-up time of 174 months. Cox proportional hazards regression models were used to estimate the hazard ratios and their 95% confidence intervals. Primary endpoints were breast cancer special survival and overall survival while secondary endpoints were invasive disease free survival and distant disease free survival.ResultsMultivariate survival analysis showed only the rs2046210 GA genotype significantly decreased the risk of recurrence and death for early stage breast cancer. After grouping breast cancer subtypes, significantly reduced survival was associated with the variant alleles of rs9485372 for luminal A and rs4415084 for triple negative breast cancer. Importantly, all three single-nucleotide polymorphisms, rs889312, rs4951011 and rs9485372 had remarkable effects on survival of luminal B EBC, either individually or synergistically. Furthermore, statistically significant multiplicative interactions were found between rs4415084 and age at diagnosis and between rs3803662 and tumor grade.ConclusionsOur results demonstrate that breast cancer risk susceptibility loci identified by GWAS may influence the outcome of early stage breast cancer patients’ depending on intrinsic tumor subtypes in Chinese women.Electronic supplementary materialThe online version of this article (10.1186/s12967-018-1634-0) contains supplementary material, which is available to authorized users.

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“…Only the SNP rs4135385 AG/AA genotypes were significantly associated with a favorable GC survival compared with the GG genotype (adjusted hazard ratio = 0.80; 95% confidence interval = 0.66-0.97), and the association was more prominent among patients with non-cardia GC than those with cardia GC (log-rank p = 0.007 for non-cardia GC and 0.417 for cardia GC). Polymorphisms in genes such as SCRN1, MTHFR, MAP3K1, TLR-9 and pri-let-7a-2 also have been demonstrated to be useful prognostic biomarkers for GC patients [32,41,42,43,44,45,46]. …”

Section: Discussionmentioning

confidence: 99%

Genetic Variations and Gastric Cancer

Yu¹,

Chen²

2015

Gastrointest Tumors

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Background: Gastric cancer (GC) has an apparent hereditary component. However, in a large fraction of gastric cases, no known genetic syndrome or family history can be identified, suggesting the presence of ‘missing heritability' in GC etiology. Genome-wide association studies (GWAS) and traditional candidate gene studies have both led to the identification of multiple replicable common genetic variants associated with GC risk. Summary: We summarize the genetic variants associated with GC risk identified up to date. Achievements derived from translational cancer research including the following aspects: (a) contribution to the our understanding of gastric tumorigenesis, (b) guidance to individualized treatment and (c) prediction of patient prognosis. We also prospect future research direction such as post-GWAS analyses and rare variants studies. Key Message: Many genetic variants were found through GWAS or candidate gene studies, and interpreting their underlying mechanisms will help us translate risk profiles generated from these variations into use in the clinical setting for targeted screening and treatment. Practical Implications: Investigation of the potential use of genetic variations as prognostic and predictive markers is a developing field. Many people could benefit from a better understanding of genetic polymorphisms to potentially identify a priori individuals who might have the best chance of survival and therefore derive most clinical benefit from treatment. Outcomes of particular scientific interest for molecular epidemiologic studies should include overall survival, recurrence- and progression-free survival, response to treatment, and early and late toxicities stemming from chemotherapy and radiation.

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A MAP3k1 SNP Predicts Survival of Gastric Cancer in a Chinese Population

Cited by 9 publications

References 32 publications

miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

Subtype-specific associations between breast cancer risk polymorphisms and the survival of early-stage breast cancer

Genetic Variations and Gastric Cancer

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