&lt;p&gt;The Roles And Signaling Pathways Of Phosphatidylethanolamine-Binding Protein 4 In Tumors&lt;/p&gt;

Luo, Zi-Kang; Chen, Qiongfeng; Qu, Xiaoqin; Zhou, Xiaoyan

doi:10.2147/ott.s216161

Cited by 9 publications

(9 citation statements)

References 46 publications

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“…As multiple studies have demonstrated, dysregulation of metabolism is considered one of the hallmarks of cancer in general [ 29 ], and aberrant metabolism of different lipids classes is among the main metabolic disorders in cancer cells [ 30 ]. The importance of phospholipid in metabolic alterations within BC has been explored in a few works [ 31 , 32 , 33 , 34 ], and it seems to correlate with our findings. Phospholipids synthesis is frequently increased in BC, and it has been related to oncogenesis and tumor progression [ 31 ]; particularly, an increase in PE plays a major role in some BC tumors [ 31 , 32 ].…”

Section: Resultssupporting

confidence: 85%

LC–MS Based Lipidomics Depict Phosphatidylethanolamine as Biomarkers of TNBC MDA-MB-231 over nTNBC MCF-7 Cells

Estrada-Pérez

Bakalara

García-Vázquez

et al. 2022

IJMS

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Breast cancer (BC) is the first malignant neoplasm in women, with a high death rate despite early diagnoses and treatment advances. Significant differences exist between the most common BC and triple-negative breast cancer (TNBC). TNBC presents molecular differences such as lacking expression of the estrogen receptor (ER), progesterone receptor (PR), and HER2 proteins, making this cancer have a poor clinical prognostic and lack clear strategies for its treatment. However, growing evidence points to metabolic dysregulation as another differential process between stages and types of BC. Therefore, the study of this crucial hallmark could identify new therapeutic targets to treat this aggressive form of BC. These differences induce an in vitro exploration of the metabolic behavior of the MCF7 cells (nTNBC) and MDA-MB-231 (TNBC) cells under lipidomic based LC–MS. The results show more significant differences in lipid regulation (phosphatidylethanolamine) that could be associated with the aggressiveness and difficulties of the treatment of TNBC.

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Section: Resultssupporting

confidence: 85%

LC–MS Based Lipidomics Depict Phosphatidylethanolamine as Biomarkers of TNBC MDA-MB-231 over nTNBC MCF-7 Cells

Estrada-Pérez

Bakalara

García-Vázquez

et al. 2022

IJMS

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“…In addition, PEBP4 is reported to be involved in the activation of sonic hedgehog (SHH) pathway (Jian et al, 2019). These research indicate that PEBP4 is potentially involved in many molecular pathways to modulate tumor pathogenesis (Luo et al, 2019), but its potential role in other diseases like hepatic fibrosis has not yet been discussed.…”

Section: Introductionmentioning

confidence: 99%

“…Phosphatidylethanolamine-binding protein 4 (PEBP4) is a newly discovered secreted protein of the PEBP family, and is expressed in multiple human tissues such as the heart, lung, colon, prostate, and liver (He et al, 2016;Luo et al, 2019). Existing studies have revealed the effects of PEBP4 on multiple human cancers.…”

Section: Introductionmentioning

confidence: 99%

Phosphatidylethanolamine-binding protein 4 deficiency exacerbates carbon tetrachloride-induced liver fibrosis by regulating the NF-κB signaling pathway

Luo

Ling

et al. 2022

Front. Pharmacol.

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Liver fibrosis is a pathological process which can progress to hepatocirrhosis, even hepatocellular carcinoma. Phosphatidylethanolamine-binding protein 4 (PEBP4) is a secreted protein involved in regulating many molecular pathways, whereas its roles in diseases including hepatic fibrosis remain undefined. The nuclear factor-κappa B (NF-κB) signaling pathway has been found to be involved in the development of liver fibrosis. In this study, we generated a hepatocyte-conditional knockout (CKO) mouse model of PEBP4, and explored the potential functions of PEBP4 on liver fibrosis and the NF-κB signaling pathway in a mouse model of carbon tetrachloride (CCl4)-induced liver fibrosis. We demonstrated that PEBP4 CKO aggravated CCl4-triggered liver fibrosis, as evidenced by altered histopathology, an increase in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and hydroxyproline (HYP) levels, and more collagen deposition, as well as by enhanced expression of fibrotic markers including α-smooth muscle actin (α-SMA), collagen I and collagen III. Mechanistically, PEBP4 deficiency activated the NF-κB signaling pathway, as indicated by increased phosphorylation of NF-κB p65 and inhibitor protein κB inhibitor-α (IκB-α), and nuclear NF-κB p65 expression in the fibrotic liver. Notably, the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) partially blocked the activation of the NF-κB pathway, and reversed the pro-fibrotic effect of PEBP4 deletion in CCl4-treated mice. Together, these results suggest that PEBP4 deficiency results in aggravation of liver fibrosis and activation of the NF-κB signaling pathway, supporting a novel concept that PEBP4 is a crucial player in hepatic fibrosis, but also might be a negative regulator of the NF-κB signaling in liver fibrosis.

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“…Several studies have shown that the inhibition of apoptosis induced by tumor necrosis factor-α (TNF-α) and the upregulation of hPEBP4 plays a vital role in tumor progression in various types of cancer [ 26 , 27 , 28 , 29 ]. Qiu et al investigated hPEBP4 as an independent biomarker for predicting rectal cancer response to radiotherapy treatment ( p = 0.001).…”

Section: Resultsmentioning

confidence: 99%

Tissue-Based Markers as a Tool to Assess Response to Neoadjuvant Radiotherapy in Rectal Cancer—Systematic Review

Smolskas

Mikulskytė

Sileika

et al. 2022

IJMS

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According to current guidelines, the current treatment for locally advanced rectal cancer is neoadjuvant therapy, followed by a total mesorectal excision. However, radiosensitivity tends to differ among patients due to tumor heterogeneity, making it difficult to predict the possible outcomes of the neoadjuvant therapy. This review aims to investigate different types of tissue-based biomarkers and their capability of predicting tumor response to neoadjuvant therapy in patients with locally advanced rectal cancer. We identified 169 abstracts in NCBI PubMed, selected 48 reports considered to meet inclusion criteria and performed this systematic review. Multiple classes of molecular biomarkers, such as proteins, DNA, micro-RNA or tumor immune microenvironment, were studied as potential predictors for rectal cancer response; nonetheless, no literature to date has provided enough sufficient evidence for any of them to be introduced into clinical practice.

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<p>The Roles And Signaling Pathways Of Phosphatidylethanolamine-Binding Protein 4 In Tumors</p>

Cited by 9 publications

References 46 publications

LC–MS Based Lipidomics Depict Phosphatidylethanolamine as Biomarkers of TNBC MDA-MB-231 over nTNBC MCF-7 Cells

LC–MS Based Lipidomics Depict Phosphatidylethanolamine as Biomarkers of TNBC MDA-MB-231 over nTNBC MCF-7 Cells

Phosphatidylethanolamine-binding protein 4 deficiency exacerbates carbon tetrachloride-induced liver fibrosis by regulating the NF-κB signaling pathway

Tissue-Based Markers as a Tool to Assess Response to Neoadjuvant Radiotherapy in Rectal Cancer—Systematic Review

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