Galectin‑3 facilitates the proliferation and migration of nasopharyngeal carcinoma cells via activation of the ERK1/2 and Akt signaling pathways, and is positively correlated with the inflammatory state of nasopharyngeal carcinoma

Li, Mei; Chen, Yu Bin; Liu, Fen; Qu, Jia; Ren, Li; Chai, Jin; Tang, Cong

doi:10.3892/mmr.2021.12009

Cited by 5 publications

(7 citation statements)

References 36 publications

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“…Further research has revealed that Gal-3 can regulate multiple signaling pathways in cancer cells. Li et al ( 28 ) suggested that Gal-3 can regulate the Akt and MEK/ERK1/2 signaling pathways in nasopharyngeal cancer cells, which was consistent with the results of the present study. The present study demonstrated that the expression of Gal-3 was significantly increased in the cytoplasm of cet-R OSCC, which indicated that treatment with cetuximab may activate Gal-3 in OSCC via translocation into the cytoplasm, leading to OSCC progression.…”

Section: Discussionsupporting

confidence: 93%

“…Previous studies have demonstrated that Gal-3 can regulate multiple signaling pathways in cells (27)(28)(29). in the present study, p-erK1/2 and p-Akt expression was significantly increased in cet-r HSc3 tumors compared with that in regular HSc3 tumors, which was significantly inhibited by treatment with GB1107 (Fig.…”

Section: Gal-3 Inhibitor (Gb1107) Inhibits Oscc Via Suppressing the Activity Of The Erk1/2 And Akt Signaling Pathwaysmentioning

confidence: 99%

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Galectin‑3 blockade suppresses the growth of cetuximab‑resistant human oral squamous cell carcinoma

et al. 2021

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oral squamous cell carcinoma (oScc) is a cancer associated with high mortality (accounting for 3.1/100,000 deaths per year in Brazil in 2013) and a high frequency of amplification in the expression of the epidermal growth factor receptor (EGFR). Treatment with the EGFR inhibitor cetuximab leads to drug resistance in patients with oScc due to unknown mechanisms. Galectin-3 (Gal-3) is a β-galactoside binding lectin that regulates multiple signaling pathways in cells. The present study aimed to investigate the effect of Gal-3 in cetuximab-resistant (cet-R) OSCC. The OSCC HSC3 cell line was selected to establish a mouse xenograft model, which was treated with cetuximab to induce resistance. Subsequently, a Gal-3 inhibitor was used to treat cet-r tumors, and the tumor volume was monitored. The expression of Gal-3, phosphorylated (p)-erK1/2 and p-akt was assessed using immunohistochemistry. The combined effect of cetuximab and the Gal-3 inhibitor on HSC3 tumor xenografts was also investigated. HSc3 cells were cultured in vitro to investigate the regulatory effects of Gal-3 on erK1/2 and akt via western blotting. in addition, the effects of the Gal-3 inhibitor on the proliferation, colony formation, invasion and apoptosis of HSc3 cells were investigated by performing cell counting Kit-8, colony formation, Transwell and apoptosis assays, respectively. In cet-R OSCC tumors, increased expression of Gal-3, p-erK1/2 and p-akt was observed. Further research demonstrated that Gal-3 regulated the expression of both erK1/2 and akt in HSc3 cells by promoting phosphorylation. Moreover, the Gal-3 inhibitor decreased the proliferation and invasion, but increased the apoptosis of cet-r HSc3 cells. in addition, the Gal-3 inhibitor suppressed the growth of cet-r tumors. collectively, the results indicated that the Gal-3 inhibitor and cetuximab displayed a synergistic inhibitory effect on oScc tumors. in summary, the present study demonstrated that Gal-3 may serve an important role in cet-r oScc. The combination of cetuximab and the Gal-3 inhibitor may display a synergistic antitumor effect, thereby inhibiting the development of cetuximab resistance in OSCC.

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Section: Discussionsupporting

confidence: 93%

Section: Gal-3 Inhibitor (Gb1107) Inhibits Oscc Via Suppressing the Activity Of The Erk1/2 And Akt Signaling Pathwaysmentioning

confidence: 99%

Galectin‑3 blockade suppresses the growth of cetuximab‑resistant human oral squamous cell carcinoma

et al. 2021

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“…7). ERK1/2, AKT, and p38-MAPK signaling pathways have been reported to be activated in NPC, contributing to tumor progression (Hsieh et al, 2019;Li et al, 2021;Liu et al, 2020;Xu et al, 2021). These results suggest that AE targets multiple cancerassociated signaling pathways by elevating the expression levels of DUSP1, an endogenous inhibitor of these pathways, and inhibits the malignant biological behaviors of NPC cells (Figure 9).…”

Section: These Antitumor Effects Include Induction Of Cell Apoptosis ...mentioning

confidence: 87%

“…In addition, the selective inhibitor of DUSP1 successfully blocked AE‐induced inhibition of the three signaling pathways and partially reversed the inhibitory effects of AE treatment on malignant biological behaviors, such as cell proliferation, apoptosis, cell cycle transition, metastasis, and abnormal growth of transplanted tumors in vivo (Figures 4–7). ERK1/2, AKT, and p38‐MAPK signaling pathways have been reported to be activated in NPC, contributing to tumor progression (Hsieh et al, 2019; Li et al, 2021; Liu et al, 2020; Xu et al, 2021). These results suggest that AE targets multiple cancer‐associated signaling pathways by elevating the expression levels of DUSP1, an endogenous inhibitor of these pathways, and inhibits the malignant biological behaviors of NPC cells (Figure 9).…”

Section: Discussionmentioning

confidence: 99%

Aloe‐emodin targets multiple signaling pathways by blocking ubiquitin‐mediated degradation of DUSP1 in nasopharyngeal carcinoma cells

Chen

Guan

Xie

et al. 2023

Phytotherapy Research

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Aloe‐emodin (AE) has been shown to inhibit the proliferation of several cancer cell lines, including human nasopharyngeal carcinoma (NPC) cell lines. In this study, we confirmed that AE inhibited malignant biological behaviors, including cell viability, abnormal proliferation, apoptosis, and migration of NPC cells. Western blotting analysis revealed that AE upregulated the expression of DUSP1, an endogenous inhibitor of multiple cancer‐associated signaling pathways, resulting in blockage of the extracellular signal‐regulated kinase (ERK)‐1/2, protein kinase B (AKT), and p38‐mitogen activated protein kinase（p38‐MAPK） signaling pathways in NPC cell lines. Moreover, the selective inhibitor of DUSP1, BCI‐hydrochloride, partially reversed the AE‐induced cytotoxicity and blocked the aforementioned signaling pathways in NPC cells. In addition, the binding between AE and DUSP1 was predicted via molecular docking analysis using AutoDock‐Vina software and further verified via a microscale thermophoresis assay. The binding amino acid residues were adjacent to the predicted ubiquitination site (Lys192) of DUSP1. Immunoprecipitation with the ubiquitin antibody, ubiquitinated DUSP1 was shown to be upregulated by AE. Our findings revealed that AE can stabilize DUSP1 by blocking its ubiquitin–proteasome‐mediated degradation and proposed an underlying mechanism by which AE‐upregulated DUSP1 may potentially target multiple pathways in NPC cells.

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“…Gal‐3 has cancer‐promoting effects. Experimental studies have shown the cancer‐inducing and apoptosis‐inhibiting potential of Gal‐3 in nasopharyngeal carcinoma (M. Li et al, 2021). However, pro and antiapoptotic properties of Gal‐3 have also been reported.…”

Section: Galactins: Types Structure and Functionmentioning

confidence: 99%

Unraveling the pathophysiologic role of galectin‐3 in chronically injured liver

Ezhilarasan

2023

Journal Cellular Physiology

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Galectin‐3 (Gal‐3) previously referred to as S‐type lectins, is a soluble protein that specifically binds to β‐galactoside carbohydrates with high specificity. Gal‐3 plays a pivotal role in a variety of pathophysiological processes such as cell proliferation, inflammation, differentiation, angiogenesis, transformation and apoptosis, pre‐mRNA splicing, metabolic syndromes, fibrosis, and host defense. The role of Gal‐3 has also been implicated in liver diseases. Gal‐3 is activated upon a hepatotoxic insult to the liver and its level has been shown to be upregulated in fatty liver diseases, inflammation, nonalcoholic steatohepatitis, fibrosis, cholangitis, cirrhosis, and hepatocellular carcinoma (HCC). Gal‐3 directly interacts with the NOD‐like receptor family, pyrin domain containing 3, and activates the inflammasome in macrophages of the liver. In the chronically injured liver, Gal‐3 secreted by injured hepatocytes and immune cells, activates hepatic stellate cells (HSCs) in a paracrine fashion to acquire a myofibroblast like collagen‐producing phenotype. Activated HSCs in the fibrotic liver secrete Gal‐3 which acts via autocrine signaling to exacerbate extracellular matrix synthesis and fibrogenesis. In the stromal microenvironment, Gal‐3 activates cancer cell proliferation, migration, invasiveness, and metastasis. Clinically, increased serum levels and Gal‐3 expression were observed in the liver tissue of nonalcoholic steatohepatitis, fibrotic/cirrhotic, and HCC patients. The pathological role of Gal‐3 has been experimentally and clinically reported in the progression of chronic liver disease. Therefore, this review discusses the pathological role of Gal‐3 in the progression of chronic liver diseases.

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Galectin‑3 facilitates the proliferation and migration of nasopharyngeal carcinoma cells via activation of the ERK1/2 and Akt signaling pathways, and is positively correlated with the inflammatory state of nasopharyngeal carcinoma

Cited by 5 publications

References 36 publications

Galectin‑3 blockade suppresses the growth of cetuximab‑resistant human oral squamous cell carcinoma

Galectin‑3 blockade suppresses the growth of cetuximab‑resistant human oral squamous cell carcinoma

Aloe‐emodin targets multiple signaling pathways by blocking ubiquitin‐mediated degradation of DUSP1 in nasopharyngeal carcinoma cells

Unraveling the pathophysiologic role of galectin‐3 in chronically injured liver

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