MicroRNA-133a suppresses the proliferation, migration, and invasion of laryngeal carcinoma cells by targeting CD47

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.

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

Bioscience Reports ◽

10.1042/bsr20182480 ◽

2019 ◽

Vol 39 (7) ◽

Cited By ~ 3

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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RNA interference (RNAi) mediated stable knockdown of protein casein kinase 2-alpha (CK2α) inhibits migration and invasion and enhances cisplatin-induced apoptosis in HEp-2 laryngeal carcinoma cells

Acta Histochemica ◽

10.1016/j.acthis.2014.04.001 ◽

2014 ◽

Vol 116 (6) ◽

pp. 1000-1006 ◽

Cited By ~ 8

Author(s):

Fang Zhang ◽

Bo Yang ◽

Shengli Shi ◽

Xuejun Jiang

Keyword(s):

Rna Interference ◽

Laryngeal Carcinoma ◽

Casein Kinase ◽

Casein Kinase 2 ◽

Carcinoma Cells ◽

Migration And Invasion ◽

Induced Apoptosis

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Faculty Opinions recommendation of Targeting of urokinase plasminogen activator receptor in human pancreatic carcinoma cells inhibits c-Met- and insulin-like growth factor-I receptor-mediated migration and invasion and orthotopic tumor growth in mice.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1033797.388968 ◽

2006 ◽

Author(s):

Arthur Frankel

Keyword(s):

Growth Factor ◽

Tumor Growth ◽

Pancreatic Carcinoma ◽

Plasminogen Activator ◽

Urokinase Plasminogen Activator ◽

Carcinoma Cells ◽

Migration And Invasion ◽

Urokinase Plasminogen Activator Receptor ◽

Factor I ◽

Plasminogen Activator Receptor

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Overexpression of p62 Induces Autophagy and Promotes Proliferation, Migration and Invasion of Nasopharyngeal Carcinoma Cells through Promoting ERK Signaling Pathway

Current Cancer Drug Targets ◽

10.2174/1568009620666200424145122 ◽

2020 ◽

Vol 20 (8) ◽

pp. 624-637 ◽

Cited By ~ 3

Author(s):

Qiong Wu ◽

Manlin Xiang ◽

Kun Wang ◽

Zhen Chen ◽

Lu Long ◽

...

Keyword(s):

Nasopharyngeal Carcinoma ◽

Clinical Analysis ◽

Carcinoma Cells ◽

Immunofluorescent Staining ◽

Clinicopathological Parameters ◽

Migration And Invasion ◽

Extracellular Signal Regulated Kinase ◽

Extracellular Signal ◽

Potential Biomarker

Background: Increasing evidence has shown that p62 plays an important role in tumorigenesis. However, relatively little is known about the association between p62 and tumor invasion and metastasis; in addition, its role in NPC (nasopharyngeal carcinoma, NPC) has been rarely investigated. Objective: To investigate the effect of p62 on tumorigenesis and metastasis in nasopharyngeal carcinoma. Methods: Western blotting, immunofluorescent staining and immunohistochemistry were used to evaluate p62 protein expression. Subsequently, cell viability, colony formation, migration, invasion and autophagy assays were performed. anti-p62 autoantibodies in sera were detected by ELISA. These data were correlated with clinicopathological parameters. Results: We confirmed that p62 was significantly up-regulated in NPC tissues. Furthermore, high expression of p62 was observed in NPC cell lines, and especially in the highly metastatic 5-8F cells. In vitro, down-regulation of p62 inhibited proliferation, clone forming ability, autophagy, migration, and invasion in 5-8F cells, whereas p62 overexpression resulted in the opposite effects in 6-10B cells. Moreover, we confirmed that p62 promotes NPC cell proliferation, migration, and invasion by activating ERK (extracellular signal-regulated kinase, ERK). Clinical analysis indicated that high p62 expression correlates with lymph node and distant metastasis (P<0.05). Serum anti-p62 autoantibodies were increased in NPC patients and levels were associated with metastasis. Conclusion : Our data establish p62 targeting ERK as potential determinant in the NPC, which supplies a new pathway to treat NPC. Furthermore, p62 is a potential biomarker which might be closely related to the tumorigenesis and metastasis in NPC.

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