NGAL protects in nasopharyngeal carcinoma by inducing apoptosis and blocking epithelial‑mesenchymal transition

Guo, Ying; Zhai, Jianhua; Zhang, Jing; Zhou, Hongyu

doi:10.3892/ol.2020.11527

Cited by 5 publications

(9 citation statements)

References 44 publications

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“…Moreover, NGAL is a type of injury-induced transferrin that may improve the activation of intracellular coenzyme iron and regulate various important proteins involved in cellular activities ( 19 ). For example, Guo et al ( 20 ) revealed that NGAL modulates cell apoptosis and epithelial-mesenchymal transition in nasopharyngeal carcinoma. Han et al ( 21 ) demonstrated that NGAL participates in LPS-mediated apoptosis of renal tubular epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

CID16020046, a GPR55 antagonist, attenuates sepsis‑induced acute kidney injury

Chen

Guo

et al. 2022

Mol Med Rep

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acute kidney injury (aKi) is the most common and serious complication of sepsis, and it is also the main cause of mortality in patients with sepsis. The G protein-coupled receptor 55 (GPr55) inhibitor cid16020046 was found to suppress the inflammatory response in sepsis models in mice. The aim of the present study was to investigate the effect of cid16020046 on aKi in sepsis mouse models and elucidate the possible underlying mechanisms. a sepsis model in mice was established by cecal ligation/perforation (clP). The expression levels of GPr55 in the serum of patients with sepsis and the renal tissues of septic mice were determined via reverse transcription-quantitative Pcr and western blot analyses, respectively. The pathological injury of renal tissue was evaluated using H&e and periodic acid-Schiff staining. eliSa was performed to detect the levels of renal injury-related factors, including blood urea nitrogen (Bun), creatinine (cre), kidney injury molecule 1 (KiM1) and neutrophil gelatinase-associated lipocalin (nGal) in septic mice. Moreover, the levels of pro-inflammatory cytokines (TNF-α, il-6 and il-1β) were detected via eliSa and western blotting. apoptosis was determined using Tunel staining and western blotting. The expression levels of rho-associated protein kinase (rocK) pathway-related proteins (ras homolog family member a, rocK1 and rocK2) was measured via western blotting. Finally, H&E staining was used to evaluate the effect of cid16020046 on various organs in mice. compared with the control subjects, the expression level of GPr55 in the serum of patients with sepsis was significantly increased. Compared with the sham group, CID16020046 (20 mg/kg) significantly decreased the levels of Bun and cre in the serum, as well as the contents of KIM1 and NGAL in the urine. Furthermore, CID16020046 significantly decreased the contents of TNF-α, il-6 and il-1β in the serum and renal tissue of septic mice, and reduced cell apoptosis. in addition, cid16020046 effectively suppressed the expression levels of rocK pathway-related proteins, and H&e staining revealed that cid16020046 (20 mg/kg) had no toxic effect on the heart, liver, spleen or lung in normal mice. in conclusion, cid16020046 may prove useful for the development of drugs for the treatment of sepsis-induced aKi.

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Section: Discussionmentioning

confidence: 99%

CID16020046, a GPR55 antagonist, attenuates sepsis‑induced acute kidney injury

Chen

Guo

et al. 2022

Mol Med Rep

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“…NGAL is synthesised during a narrow window of granulocyte maturation in the bone marrow but also may be induced in epithelial cells in the setting of inflammation or malignancy [ 51 , 52 ]. The gene for this protein is located on chromosome 9 [ 53 ].…”

Section: Biomarkers Of Allogeneic Kidney Transplant Rejectionmentioning

confidence: 99%

The Most Promising Biomarkers of Allogeneic Kidney Transplant Rejection

Rogulska

Wojciechowska‐Koszko

Dołęgowska

et al. 2022

Journal of Immunology Research

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Clinical transplantology is a constantly evolving field of medicine. Kidney transplantation has become standard clinical practice, and it has a significant impact on reducing mortality and improving the quality of life of patients. Allogenic transplantation induces an immune response, which may lead to the rejection of the transplanted organ. The gold standard for evaluating rejection of the transplanted kidney by the recipient’s organism is a biopsy of this organ. However, due to the high invasiveness of this procedure, alternative diagnostic methods are being sought. Therefore, the biomarkers may play an essential predictive role in transplant rejection. A review of the most promising biomarkers for early diagnosis and prognosis prediction of allogenic kidney transplant rejection summarizes novel data on neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), C-X-C motif chemokine 10 (CXCL-10), cystatin C (CysC), osteopontin (OPN), and clusterin (CLU) and analyses the dynamics of changes of the biomarkers mentioned above in kidney diseases and the mechanism of rejection of the transplanted kidney.

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“…Previous studies have reported that LCN2 is involved in pathological disorders, especially in inflammation, metabolic disease, neurological disease, and cancers. Recently, an immunohistochemical analysis of NPC tumor specimens demonstrated that LCN2 expression is associated with the survival of NPC patients [ 9 , 10 ]. A high expression of LCN2 has been found to be positively associated with improved 5-year overall survival in NPC patients [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

“…Recently, an immunohistochemical analysis of NPC tumor specimens demonstrated that LCN2 expression is associated with the survival of NPC patients [ 9 , 10 ]. A high expression of LCN2 has been found to be positively associated with improved 5-year overall survival in NPC patients [ 10 ]. Conversely, a recent study showed that a high expression of LCN2 is associated with a poor 5-year relapse-free survival and local relapse-free survival, but not with distant metastasis-free survival, progression-free survival and overall survival between high- and low-LCN2-expression groups in NPC patients [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

“…The invasion of tumor cells into the surrounding microenvironment is a key step in cancer progression, leading to the formation of metastasis of cancer cells in secondary regions. An ectopic expression of LCN2 has been shown to reduce cellular invasion and metastases in colon cancer [ 12 ], in Ras-transformed mouse mammary cells [ 13 ] and in NPC cells [ 10 ]. A variety of signaling pathways, such as Ras [ 14 ], and mitogen-activated protein kinase (MAPK) [ 15 ], have been identified to participate in the metastatic process of many cancers as well as NPC [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

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Lipocalin 2 Reduces MET Levels by Inhibiting MEK/ERK Signaling to Inhibit Nasopharyngeal Carcinoma Cell Migration

Lin

Huang

et al. 2022

Cancers

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Nasopharyngeal carcinoma (NPC) is the most common cancer that occurs in the nasopharynx, and it is difficult to detect early. The main cause of death of NPC patients is cancer metastasis. Lipocalin 2 (LCN2) has been shown to be involved in a variety of carcinogenesis processes. Here, we aimed to study the role of LCN2 in NPC cells and determine its underlying mechanism. We found that LCN2 was expressed differently in NPC cell lines, namely HONE-1, NPC-39, and NPC-BM. The down-regulation of LCN2 levels by siRNA targeting LCN2 (siLCN2) increased cell migration and invasion in HONE-1 cells, while the up-regulation of LCN2 levels by transfection with the LCN2 expression plasmid decreased cell migration and invasion in NPC-BM cells. Furthermore, LCN2 levels negatively regulated the phosphorylation of MEK/ERK pathways. The treatment of the specific MEK/ERK inhibitor, U0126, reduced cell migration in HONE-1 cells, whereas the treatment of tBHQ, an ERK activator, enhanced cell migration in NPC-BM cells. Based on the bioinformatics data, there was a moderately negative correlation between LCN2 and MET in metastatic NPC tissues (r = −0.5946, p = 0.0022). Indeed, the manipulation of LCN2 levels negatively regulated MET levels in these NPC cells. The treatment of U0126 reduced siLCN2-increased MET levels, while the treatment of tBHQ enhanced LCN2-enhanced MET levels. Interestingly, the down-regulation of MET levels by siMET further decreased siLCN2-enhanced MET levels and cell migration. Therefore, LCN2 inhibits NPC cell migration by reducing MET levels through MEK/ERK signaling.

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NGAL protects in nasopharyngeal carcinoma by inducing apoptosis and blocking epithelial‑mesenchymal transition

Cited by 5 publications

References 44 publications

CID16020046, a GPR55 antagonist, attenuates sepsis‑induced acute kidney injury

CID16020046, a GPR55 antagonist, attenuates sepsis‑induced acute kidney injury

The Most Promising Biomarkers of Allogeneic Kidney Transplant Rejection

Lipocalin 2 Reduces MET Levels by Inhibiting MEK/ERK Signaling to Inhibit Nasopharyngeal Carcinoma Cell Migration

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