Low CPNE3 expression is associated with risk of acute myocardial infarction: A feasible genetic marker of acute myocardial infarction in patients with stable coronary artery disease

Tan, Buchuan; Liu, Long; Yang, Yan; Liu, Qian; Yang, Liping; Meng, F.

doi:10.5603/cj.a2017.0155

Cited by 15 publications

(14 citation statements)

References 20 publications

(23 reference statements)

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“…Other studies have confirmed that CPNE3 participates in processes involved in acute myocardial infarction and coronary heart disease by potentially mediating the metabolism of nuclear fatty acids, serum total cholesterol and triglycerides (Tan et al, 2019). In addition, recent studies have also found that CPNE3 is highly expressed in breast cancer, prostate cancer and ovarian cancer and is involved in tumor cell proliferation and metastasis.…”

Section: Cpne3mentioning

confidence: 83%

The CPNE Family and Their Role in Cancers

et al. 2021

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Lung cancer is the leading cause of cancer-related deaths worldwide. Despite significant advances in cancer research and treatment, the overall prognosis of lung cancer patients remains poor. Therefore, the identification for novel therapeutic targets is critical for the diagnosis and treatment of lung cancer. CPNEs (copines) are a family of membrane-bound proteins that are highly conserved, soluble, ubiquitous, calcium dependent in a variety of eukaryotes. Emerging evidences have also indicated CPNE family members are involved in cancer development and progression as well. However, the expression patterns and clinical roles in cancer have not yet been well understood. In this review, we summarize recent advances concerning CPNE family members and provide insights into new potential mechanism involved in cancer development.

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Section: Cpne3mentioning

confidence: 83%

The CPNE Family and Their Role in Cancers

et al. 2021

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“…CPNE3 is a functional protein in many diseases, especially in cancers, such as non-small cell lung cancer, breast cancer, prostate cancer, colorectal cancer and acute myocardial tumor [9][10][11][12][13]. However, the role of CPNE3 in GBM remains poorly understood.…”

Section: Discussionmentioning

confidence: 99%

Cpne3 Regulates the Cell Proliferation and Apoptosis in Human Gbm via the Activation of Pi3k/akt Signaling Pathway

Zhang¹,

Wang²,

Wang³

et al. 2021

Preprint

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Background: Even with decades of intensive study, the signaling regulative network of the progression of GBM remains unclear, a deeper understanding of the molecular crosstalk with pathways in GBM is needed to identify new potential targets for treatment. Methods: To investigated the expression of CPNE3 in GBM, we applied bioinformatic analysis and clinical samples validation. Then the functional validation of carried out in commercially available glioma cell lines and nude mice model. Also, the GSEA analysis was used to identify the relevant pathways. The role of activated pathway was further validated by pharmacology method.Results: We found that CPNE3 was significantly up-regulated in GBM when compared with adjacent normal tissues, and the overexpression of CPNE3 promoted cell proliferation and inhibiting cell apoptosis in vitro and in vivo. Also, the principal protein markers of PI3K/AKT pathway were found to be phosphorylated by CPNE3 over-expression, and pathway inhibitor, LY294002, alleviated the cell proliferation enhancement induced by CPNE3 over-expression. Conclusion: Our results showed that the expression of CPNE3 promotes cell proliferation by inhibiting cell apoptosis via activating PI3K/AKT pathway, thereby enhancing the progression of GBM, which suggesting that CPNE3 may play as a tumorigenesis gene and its crosstalk with PI3K/AKT pathway may become a promising potential therapeutic target for human GBMs.

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“…The CPNE7 protein is a member of the copine family that binds phospholipids and also belongs to the von Willebrand factor A domain-containing proteins (28), which are known to be important in cell adhesion and migration events. Studies on copines suggest that they are associated with coronary artery disease (29) and obesity (30), which indicates that they also function in lipid metabolism pathways. However, whether the high frequency of CPNE7 variants is caused by neutrality or selection needs further investigation.…”

Section: Discussionmentioning

confidence: 99%

Genetic architecture and adaptations of Nunavik Inuit

Zhou

Xie

Quoibion

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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The Canadian Inuit have a distinct population background that may entail particular implications for the health of its individuals. However, the number of genetic studies examining this Inuit population is limited, and much remains to be discovered in regard to its genetic characteristics. In this study, we generated whole-exome sequences and genomewide genotypes for 170 Nunavik Inuit, a small and isolated founder population of Canadian Arctic indigenous people. Our study revealed the genetic background of Nunavik Inuit to be distinct from any known present-day population. The majority of Nunavik Inuit show little evidence of gene flow from European or present-day Native American peoples, and Inuit living around Hudson Bay are genetically distinct from those around Ungava Bay. We also inferred that Nunavik Inuit have a small effective population size of 3,000 and likely split from Greenlandic Inuit ∼10.5 kya. Nunavik Inuit went through a bottleneck at approximately the same time and might have admixed with a population related to the Paleo-Eskimos. Our study highlights population-specific genomic signatures in coding regions that show adaptations unique to Nunavik Inuit, particularly in pathways involving fatty acid metabolism and cellular adhesion (CPNE7, ICAM5, STAT2, and RAF1). Subsequent analyses in selection footprints and the risk of intracranial aneurysms (IAs) in Nunavik Inuit revealed an exonic variant under weak negative selection to be significantly associated with IA (rs77470587; P = 4.6 × 10−8).

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Low CPNE3 expression is associated with risk of acute myocardial infarction: A feasible genetic marker of acute myocardial infarction in patients with stable coronary artery disease

Abstract: Background: Gene COPINE III may be related to a phosphoprotein with intrinsic kinase

Cited by 15 publications

References 20 publications

The CPNE Family and Their Role in Cancers

The CPNE Family and Their Role in Cancers

Cpne3 Regulates the Cell Proliferation and Apoptosis in Human Gbm via the Activation of Pi3k/akt Signaling Pathway

Genetic architecture and adaptations of Nunavik Inuit

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