scholarly journals The expression and significance of AKR1B10 in laryngeal squamous cell carcinoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jixuan Liu ◽  
Hongyan Ban ◽  
Yafang Liu ◽  
Jinsong Ni
Keyword(s):  
Laryngeal Cancer ◽  
Laryngeal Carcinoma ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Lipid Synthesis ◽  
Prognostic Indicator ◽  
Carcinoma Cells ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Ki 67 ◽  
Degree Of Differentiation

AbstractAldosterone reductase family 1 member B10 (AKR1B10) is a nicotinamide adenine dinucleotide phosphate (reduced coenzyme II)-dependent oxidoreductase, and its biological functions include carbonyl detoxification, hormone metabolism, osmotic adjustment, and lipid synthesis. Studies suggested that AKR1B10 is a new biomarker for cancer based on its overexpression in epithelial tumors, such as breast cancer, cervical cancer, and lung cancer. At present, studies on the expression of AKR1B10 in laryngeal cancer have not been reported. However, we found that AKR1B10 is upregulated in laryngeal carcinoma, and its expression was negatively correlated with the degree of differentiation. In addition, AKR1B10 expression was positively correlated with tumor size; lymph node metastasis; alcohol use; and Ki-67, mutant p53, and matrix metalloproteinase 2 expression. AKR1B10 was overexpressed in Hep-2 laryngeal carcinoma cells. Oleanolic acid inhibited AKR1B10 activity and expression in Hep-2 cells and suppressed Hep-2 cell proliferation, migration, and invasion. Therefore, AKR1B10 may be related to the development of laryngeal carcinoma, suggesting its use as a prognostic indicator for laryngeal cancer.

scholarly journals The expression and significance of AKR1B10 in laryngeal squamous cell carcinoma

2021 ◽  
Author(s):  
Jixuan Liu ◽  
Hongyan Ban ◽  
Yafang Liu ◽  
Jinsong Ni
Keyword(s):  
Laryngeal Cancer ◽  
Laryngeal Carcinoma ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Lipid Synthesis ◽  
Prognostic Indicator ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Ki 67 ◽  
Degree Of Differentiation

Abstract Aldosterone reductase family 1 member B10 (AKR1B10) is a nicotinamide adenine dinucleotide phosphate (NADPH) (reduced coenzyme II)-dependent oxidoreductase, and its biological functions include carbonyl detoxification, hormone metabolism, osmotic adjustment, and lipid synthesis. Studies suggested that AKR1B10 is a new biomarker for cancer based on its overexpression in epithelial tumors, such as breast cancer, cervical cancer, and lung cancer. At present, studies on the expression of AKR1B10 in laryngeal cancer have not been reported. However, we found that AKR1B10 is upregulated in laryngeal carcinoma, and its expression was negatively correlated with the degree of differentiation. In addition, AKR1B10 expression was positively correlated with tumor size; lymph node metastasis; long-term drinking; and Ki-67, mutant p53, and matrix metalloproteinase 2 expression. AKR1B10 was overexpressed in Hep-2 laryngeal carcinoma cells. Oleanolic acid inhibited AKR1B10 activity and expression in Hep-2 cells and suppressed Hep-2 cell proliferation, migration, and invasion. Therefore, AKR1B10 may be related to the development of laryngeal carcinoma, suggesting its use as a prognostic indicator for laryngeal cancer.

Anti-invasive effect of gambogic acid in MDA-MB-231 human breast carcinoma cells

2008 ◽  
Vol 86 (5) ◽  
pp. 386-395 ◽  
Author(s):  
Qi Qi ◽  
Na Lu ◽  
Xiao-tang Wang ◽  
Hong-yan Gu ◽  
Yong Yang ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Carcinoma Cells ◽  
Human Breast Carcinoma ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Gambogic Acid ◽  
Human Breast ◽  
Breast Carcinoma Cells ◽  
Human Breast Carcinoma Cells

Gambogic acid (GA) has been known to have antitumor activity in vitro and in vivo. In the present study, we investigated the anti-invasive effects of GA in MDA-MB-231 human breast carcinoma cells. The results indicated that GA significantly inhibited the adhesion, migration, and invasion of the cells in vitro tested by the heterotypic adhesion assay, wound migration assay, and chamber invasion assay. Results of Western blotting and immunocytochemistry analysis showed that GA could suppress the expressions of matrix metalloproteinase 2 (MMP-2) and 9 (MMP-9) in MDA-MB-231 cells. Furthermore, gelatin zymography revealed that GA decreased the activities of MMP-2 and MMP-9. Additionally, GA exerted an inhibitory effect on the phosphorylation of ERK1/2 and JNK, while it had no effect on p38. Taken together, our results demonstrated the anti-invasive property of GA for the first time and indicated it could serve as a promising drug for the treatment of cancer metastasis.

scholarly journals Indole-thiazolidinone conjugate inhibits nasopharyngeal carcinoma cell migration and invasion by targeting NF κB pathway

2021 ◽  
Vol 18 (3) ◽  
pp. 519-525
Author(s):  
Guoping Zhang ◽  
Sheng Zhang
Keyword(s):  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Matrix Metalloproteinase ◽  
Carcinoma Cells ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Nuclear Fraction ◽  
Invasion And Migration ◽  
Migration Potential ◽  
And Migration

Purpose: To investigate the effect of indole-thiazolidinone on metastasis in HK1 nasopharyngeal carcinoma cells. Methods: HK1 cell proliferation was determined colorimetrically using 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. Invasion and migration of HK1 cells were assessed using Matrigel™ chamber coated invasion and wound healing assays, respectively. Results: Indole-thiazolidinone suppressed proliferation of HK1 and NPC 039 NPC cell lines at 72 h. The degree of proliferation of HK1 cells on treatment with 0.25, 0.5, 1.0, 1.5, 2.0, 2.5 and 3.0 μM indolethiazolidinone was 99, 87, 71, 64, 49, 38 and 31 %, respectively. In HK1 cell cultures, migration potential was reduced to 58.32, 47.54, 28.91 and 17.65 %, on exposure to 1.5, 2.0, 2.5 and 3.0 μM indole-thiazolidinone, respectively. Incubation with 1.5, 2.0, 2.5 and 3.0 μM indole-thiazolidinone resulted in cell invasion values of 63.41, 49.37, 35.12 and 19.67 %, respectively. There was a marked decrease in the expressions of matrix metalloproteinase 2 and matrix metalloproteinase 9 in HK1 cells on treatment with indole-thiazolidinone (p < 0.05). In addition, indole-thiazolidinone treatment resulted in decrease in p65 and p50 in nuclear fraction. Treatment of HK1 and NPC 039 cells with indolethiazolidinone and henenalin synergistically decreased cell proliferation. Indole-thiazolidinone treatment caused significant decrease in tumor growth in mice (p < 0.05). Conclusion: Indole-thiazolidinone inhibits proliferation and metastasis in nasopharyngeal carcinoma cells. Therefore, it has potential for development as a therapeutic management of nasopharyngeal carcinoma in humans.

scholarly journals Notch1 Signaling Modulates Hypoxia-induced Multidrug Resistance of Human Laryngeal Cancer Cells

2021 ◽  
Author(s):  
Dawei Li ◽  
Dan Xu ◽  
Penghui Chen ◽  
Jin Xie
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Laryngeal Cancer ◽  
Laryngeal Carcinoma ◽  
Drug Transport ◽  
Malignant Tumors ◽  
Carcinoma Cells ◽  
Cell Counting ◽  
Apoptosis Resistance ◽  
Notch1 Signaling

Abstract Background: Laryngeal carcinoma is one of the common malignant tumors of the head and neck. Multidrug resistance (MDR) remains a critical problem in the chemotherapy for patients with laryngeal cancer. This study aims to clarify the role and mechanisms of Notch1 signaling on MDR induced by hypoxia in laryngeal cancer cells.Methods and Results: Laryngeal carcinoma cells were cultured under normoxia or hypoxia. Notch1 expression was inhibited by small interfering RNA (siRNA). The expression of Notch1, Hes1, Hey1, MDR1 and survivin mRNA was determined by Real-time PCR. The expression of Notch1, Notch1 intracellular domain (N1ICD), MDR1/P-gp and survivin protein was detected by Western blot. Current research showed that hypoxia could upregulate Notch1 expression and the activity of Notch1 signaling. Furthermore, suppression of Notch1 expression could effectively down-regulate the activity of Notch1 signaling and the expression of MDR and survivin genes in laryngeal cancer cells under hypoxia (P<0.05). Cell Counting Kit-8 (CCK-8) assay confirmed that the sensitivity of hypoxic laryngeal cancer cells to a variety of drugs could be up-regulated by suppressing Notch1 expression (P<0.05). Additionally, flow cytometry (FCM) showed that suppression of Notch1 expression significantly increased cisplatin-induced apoptosis and intracellular Rh123 (Rh123) accumulation in hypoxic laryngeal carcinoma cells (P<0.05). Conclusions: Notch1 signalling could be regarded as a pivotal regulator for mediating hypoxia-induced MDR in laryngeal cancer cells by regulating survivin-mediated apoptosis resistance and MDR1/P-gp-mediated drug transport.

scholarly journals Ginsenoside Rg3 Inhibits Migration and Invasion of Nasopharyngeal Carcinoma Cells and Suppresses Epithelial Mesenchymal Transition

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Dingkun Wang ◽  
Cheng Wu ◽  
Dongbo Liu ◽  
Linli Zhang ◽  
Guoxian Long ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Ginsenoside Rg3 ◽  
Antitumor Effects ◽  
Mesenchymal Transition ◽  
Marker Proteins

Nasopharyngeal carcinoma (NPC) is a highly invasive and metastatic head and neck cancer. Distant metastasis becomes the predominant mode of treatment failure in NPC patients. Ginsenoside Rg3 (Rg3), an active pharmaceutical component extracted from traditional Chinese medicine ginseng, shows antitumor effects in various cancers. In this study, we aimed to determine whether Rg3 inhibits the migration and invasion activity of NPC cells and to explore the possible mechanisms. Our results revealed that Rg3 hampers cell migration and invasion in both HNE1 and CNE2 cell lines. A reduced level of matrix metalloproteinase-2 (MMP-2) and MMP-9 was induced by Rg3 treatment. In addition, Rg3 significantly altered the expression of epithelial mesenchymal transition (EMT) markers with increased E-cadherin but decreased Vimentin and N-cadherin expression. Transforming growth factorβ- (TGF-β-) induced morphological transition and marker proteins change of EMT were reversed by Rg3. What is more, Rg3 suppressed the expression of EMT-related transcription factors, especially the Zinc Finger E-Box Binding Homeobox 1 (ZEB1). In summary, our data suggested that Rg3 could inhibit migration and invasion of NPC cells. This effect of Rg3 might be mediated through regulating MMP-2 and MMP-9 expressions and suppressing EMT. Thus, Rg3 may be a potentially effective agent for the treatment of NPC.

scholarly journals PRMT5/Wnt4 axis promotes lymph-node metastasis and proliferation of laryngeal carcinoma

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Nan Wang ◽  
Honghong Yan ◽  
Di Wu ◽  
Zheng Zhao ◽  
Xiaoqi Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Signaling Pathway ◽  
Laryngeal Cancer ◽  
Lymphatic Metastasis ◽  
Laryngeal Carcinoma ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Tumor Stages

Abstract Metastasis is the main cause of laryngeal cancer-related death; its molecular mechanism remains unknown. Here we identify protein arginine methyltransferase 5 (PRMT5) as a new metastasis-promoting factor in laryngeal carcinoma, and explore its underlying mechanism of action in regulating laryngeal cancer progression. We illustrated that PRMT5 expression was positively correlated with tumor stages, lymphatic metastasis, and unfavorable outcome. Functional assays revealed that PRMT5 promoted laryngeal carcinoma cell proliferation, migration, and invasive capacity in vitro, as well as lymph-node metastasis in vivo. The ectopic expression of PRMT5 induced EMT with downregulation of E-cadherin and upregulation of N-cadherin, snail, and MMP9. Mechanistic results revealed that the metastatic effects could be attributed to PRMT5-mediated activation of Wnt signaling, and Wnt4 is an important driver of Wnt/β-catenin signaling pathway. Wnt4 silencing could reverse PRMT5-induced cell proliferation, migration, and invasion capacities. Furthermore, inhibition of the Wnt/β-catenin signaling pathway abolished the effect of PRMT5-induced proliferation, whereas activation of the pathway enhanced the effect of PRMT5 overexpression on cell proliferation. These results demonstrated that the oncogenic role of PRMT5 could be attributed to PRMT5/Wnt4 axis-mediated activation of the Wnt/β-catenin signaling pathway. PRMT5 may serve as a novel prognostic marker and a therapeutic target for lymphatic metastasis of laryngeal carcinoma.

scholarly journals Down-regulation of SOX18 inhibits laryngeal carcinoma cell proliferation, migration, and invasion through JAK2/STAT3 signaling

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Yice Xu ◽  
Qingyuan Zhang ◽  
Jie Zhou ◽  
Zhaolong Li ◽  
Junyu Guo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Laryngeal Carcinoma ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Down Regulation ◽  
Invasion And Migration ◽  
Stat3 Signaling ◽  
And Migration

AbstractLaryngeal carcinoma is one of the most common malignant tumors of the head, neck, and respiratory tract. The aim of the present study is to explore the biological function of SRY-related HMG-box 18 (SOX18) in laryngeal carcinoma cells and study the molecular mechanism involved. Initial findings indicate that the expression of SOX18 was increased in laryngeal carcinoma cell lines and tissues. The effect of SOX18 on laryngeal carcinoma cell proliferation, cell cycle, apoptosis, invasion, and migration was also identified. The results indicated that down-regulation of SOX18 significantly inhibited cell proliferation, migration, and invasion, and induced cell-cycle arrest in G0/G1 phase and apoptosis of laryngeal carcinoma cells. However, overexpression of SOX18 promoted cell proliferation, invasion, and migration, and inhibited cell apoptosis. The expression of cyclin D1, active-caspase-3, N-cadherin, MTA1, MMP-2, and MMP-7 was also regulated by the overexpression of siSOX18 or SOX18. In addition, it was found that SOX18 could also accelerate the phosphorylation of JAK2/STAT3 signaling in laryngeal carcinoma cells. Furthermore, our study indicated that SOX18 could stimulate cell proliferation, migration, and invasion of laryngeal carcinoma cells via regulation of JAK2/STAT3 signaling, which could provide a new strategy for laryngeal carcinoma diagnosis and molecular therapies.

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