PLOD2 in cancer research

Du, Hongzhi; Pang, Mao; Hou, Xiaoying; Yuan, Shengtao; Sun, Li

doi:10.1016/j.biopha.2017.04.023

Cited by 70 publications

(68 citation statements)

References 52 publications

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“…In addition, fat tissue accumulation may contribute to enhance the expression of PLOD2 [69]. The availability of PLOD2 is one way by which IL-6 and leptin may influence collagen re-organization to create a "highway" for cancer cell migration and invasion to promote metastasis [78].…”

Section: Leptin and Bone Metastasismentioning

confidence: 99%

Leptin, Adiponectin, and Sam68 in Bone Metastasis from Breast Cancer

Maroni

2020

IJMS

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The most serious aspect of neoplastic disease is the spread of cancer cells to secondary sites. Skeletal metastases can escape detection long after treatment of the primary tumour and follow-up. Bone tissue is a breeding ground for many types of cancer cells, especially those derived from the breast, prostate, and lung. Despite advances in diagnosis and therapeutic strategies, bone metastases still have a profound impact on quality of life and survival and are often responsible for the fatal outcome of the disease. Bone and the bone marrow environment contain a wide variety of cells. No longer considered a passive filler, bone marrow adipocytes have emerged as critical contributors to cancer progression. Released by adipocytes, adipokines are soluble factors with hormone-like functions and are currently believed to affect tumour development. Src-associated in mitosis of 68 kDa (Sam68), originally discovered as a protein physically associated with and phosphorylated by c-Src during mitosis, is now recognised as an important RNA-binding protein linked to tumour onset and progression of disease. Sam68 also regulates splicing events and recent evidence reports that dysregulation of these events is a key step in neoplastic transformation and tumour progression. The present review reports recent findings on adipokines and Sam68 and their role in breast cancer progression and metastasis.

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Section: Leptin and Bone Metastasismentioning

confidence: 99%

Leptin, Adiponectin, and Sam68 in Bone Metastasis from Breast Cancer

Maroni

2020

IJMS

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“…The consequent hydroxylysyl groups become sites of carbohydrate adherence in collagen and are therefore essential for intermolecular crosslink stability (39). The effect of PLOD2 on cancer has been previously reviewed (39). In the present study, Plod2 mRNA levels were upregulated both in AL-09 peptide-treated and patient serum-treated cardiomyocytes, which in turn may contribute to abnormal collagen accumulation in cardiac amyloidosis.…”

Section: Discussionmentioning

confidence: 50%

“…The myocardial biopsy with Masson's trichrome stain from the patient in the present study showed abundant collagen accumulation. Lysyl hydroxylases 2 (encoded by the Plod2 gene) is a vital enzyme that mediates stabilized collagen crosslink formation; it is localized to the cisternae of the rough endoplasmic reticulum and catalyzes the lysyl residues hydroxylation in collagen-like peptides (39). The consequent hydroxylysyl groups become sites of carbohydrate adherence in collagen and are therefore essential for intermolecular crosslink stability (39).…”

Section: Discussionmentioning

confidence: 99%

Analysis of gene expression profiling of amyloidogenic immunoglobulin light‑chains on cultured rat cardiomyocytes

Wang

et al. 2020

Exp Ther Med

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The present study aimed to investigate the toxic effects of different amyloidogenic light-chains (LCs) on cardiomyocytes, and demonstrate the differentially expressed genes (DEGs) and signaling pathways that participate in this process. Cultured cardiomyocytes were treated with recombinant κ LC peptide (AL-09) or with serum from a patient diagnosed with multiple myeloma (λ LC) with cardiac involvement. The 6xHis peptide or serum from healthy patients was used as peptide control or serum control, respectively. Cell viability was determined using CCK-8 assay and apoptosis was analyzed by flow cytometry. The DEGs were detected by RNA sequencing (RNA-Seq), followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Changes in gene expression levels were confirmed by reverse transcription-quantitative PCR. The cell viability in the AL-09 peptide-treated (0.2 mg/ml) and patient serum-treated (1:10 dilution) cardiomyocytes decreased to 42 and-72% of the corresponding control groups. The extent of cell apoptosis increased in AL-09-treated cardiomyocytes compared with the control group. RNA-Seq showed 256 DEGs co-existed in the two paired groups, including 127 upregulated and 88 downregulated genes. The KEGG pathways for upregulated expressed genes included the 'TGF-β signaling pathway', the 'Hedgehog signaling pathway', the 'ErbB signaling pathway' and 'lysine degradation'. The higher mRNA expression of bone morphogenetic protein (Bmp) 4, Bmp6, prostaglandin G/H synthase (Ptgs)1, Ptgs2, epiregulin, Tgfa and procollagen-lysine,2-oxoglutarate 5-dioxygenase 2 were confirmed. The KEGG pathways of downregulated expressed genes included genes involved with the 'p53 signaling pathway' and the 'cell cycle'. The mRNA expression levels of E3 ubiquitin-protein ligase CCNB1IP1 showed significant downregulation in the AL-09 peptide group compared with those in the 6xHis peptide group. In conclusion, cardiomyocytes treated with amyloidogenic λ and κ LCs presented with decreased cell viability compared with controls. Cell apoptosis increased in κ LC-treated cells compared with controls. The gene expression profiles associated with transforming growth factor-β-bone morphogenetic protein, the receptor tyrosine-protein kinase erbB-2 signaling pathways, prostaglandins, collagen production, the p53 signaling pathway and the cell cycle were altered in light-chain-treated cardiomyocytes.

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“…PLOD2 has been reported up-regulated in many tumors, which affect collagen remodeling through affecting HIF-1α, TGF-β and microRNA-26a/b [37][38][39]. In breast cancer tumorigenesis, high expression of PLOD2 was positively associated with poorer prognosis [40].…”

Section: Disccussionmentioning

confidence: 99%

Comprehensive Analysis of PLOD Family Members in Low-grade Gliomas Using Bioinformatics Methods

Zhao

Zhang

Yao

2020

Preprint

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Abstract Low-grade gliomas (LGGs) is a primary invasive brain tumor that grows slowly but is incurable and eventually develops into high malignant glioma. Novel biomarkers for the tumorigenesis and lifetime of LGG are critically demanded to be investigated. In this study, the expression levels of procollagen-lysine, 2-oxoglutarate 5-dioxygenases (PLODs) were analyzed by ONCOMINE, HPA and GEPIA. The GEPIA online platform was applied to evaluate the interrelation between PLODs and survival index in LGG. Furthermore, functions of PLODs and co-expression genes were inspected by the DAVID. Moreover, we used TIMER, cBioportal, GeneMINIA and NetworkAnalyst analysis to reveal the mechanism of PLODs in LGG. We found that expression levels of each PLOD family members were up-regulated in patients with LGG. Higher expression of PLODs was closely related to shorter disease-free survival (DFS) and overall survival (OS). The findings showed that LGG cases with or without alterations were significantly correlated with the OS and DFS. The mechanism of PLODs in LGG may be involved in response to hypoxia, oxidoreductase activity, Lysine degradation and immune cell infiltration. In general, this research has investigated the values of PLODs in LGG, which could serve as biomarkers for diagnosis, prognosis and potential therapeutic targets of LGG patients.

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PLOD2 in cancer research

Cited by 70 publications

References 52 publications

Leptin, Adiponectin, and Sam68 in Bone Metastasis from Breast Cancer

Leptin, Adiponectin, and Sam68 in Bone Metastasis from Breast Cancer

Analysis of gene expression profiling of amyloidogenic immunoglobulin light‑chains on cultured rat cardiomyocytes

Comprehensive Analysis of PLOD Family Members in Low-grade Gliomas Using Bioinformatics Methods

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