Long non‐coding RNA DNM3OS/miR‐204‐5p/HIP1 axis modulates oral cancer cell viability and migration

2020 ◽  
Vol 49 (9) ◽  
pp. 865-875
Author(s):  
Xiaodan Fang ◽  
Zhangui Tang ◽  
Haixia Zhang ◽  
Hongzhi Quan
Keyword(s):  
Oral Cancer ◽  
Cell Viability ◽  
Cancer Cell ◽  
Oral Cancer Cell ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis

2021 ◽  
Vol 61 (1) ◽  
Author(s):  
Binfeng Wang ◽  
Xiangwei Liu
Keyword(s):  
Cell Viability ◽  
Inverse Correlation ◽  
Luciferase Reporter ◽  
Relative Expression ◽  
Downstream Target ◽  
Non Coding Rna ◽  
Ecm Degradation ◽  
Post Traumatic ◽  
And Migration ◽  
Long Non Coding Rna

Abstract Background Osteoarthritis (OA) is defined as a degenerative disease. Pivotal roles of long non-coding RNA (lncRNAs) in OA are widely elucidated. Herein, we intend to explore the function and molecular mechanism of lncRNA KCNQ1OT1 in CHON-001 cells. Methods Relative expression of KCNQ1OT1, miR-126-5p and TRPS1 was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was examined by MTT assay. The migratory ability of chondrocytes was assessed by transwell assay. Western blot was used to determine relative protein expression of collagen II, MMP13 and TRPS1. Dual-luciferase reporter (DLR) assay was applied to test the target of lncRNA KCNQ1OT1 or miR-126-5p. Results Relative expression of KCNQ1OT1 and TRPS1 was reduced, whereas miR-126-5p was augmented in cartilage tissues of post-traumatic OA patients compared to those of subjects without post-traumatic OA. Increased KCNQ1OT1 or decreased miR-126-5p enhanced cell viability and migration, and repressed extracellular matrix (ECM) degradation in CHON-001 cells. MiR-126-5p was the downstream target of KCNQ1OT1, and it could directly target TRPS1. There was an inverse correlation between KCNQ1OT1 and miR-126-5p or between miR-126-5p and TRPS1. Meantime, there was a positive correlation between KCNQ1OT1 and TRPS1. The promoting impacts of KCNQ1OT1 on cell viability and migration as well as the suppressive impact of KCNQ1OT1 on ECM degradation were partially abolished by miR-126-5p overexpression or TRPS1 knockdown in CHON-001 cells. Conclusions Overexpression of KCNQ1OT1 attenuates the development of OA by sponging miR-126-5p to target TRPS1. Our findings may provide a possible therapeutic strategy for human OA in clinic.

scholarly journals The long non-coding RNA HOTTIP enhances pancreatic cancer cell proliferation, survival and migration

Oncotarget ◽  
2015 ◽  
Vol 6 (13) ◽  
pp. 10840-10852 ◽  
Author(s):  
Yating Cheng ◽  
Indira Jutooru ◽  
Gayathri Chadalapaka ◽  
J. Christopher Corton ◽  
Stephen Safe
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna

scholarly journals NGAL is Downregulated in Oral Squamous Cell Carcinoma and Leads to Increased Survival, Proliferation, Migration, and Chemoresistance

2018 ◽  
Author(s):  
Javadi Monisha ◽  
Nand Kishor Roy ◽  
Ganesan Padmavathi ◽  
Kishore Banik ◽  
Devivasha Bordoloi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Oral Cancer ◽  
Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Public Health Burden ◽  
Normal Tissues ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Oral Cancer Cell ◽  
Signaling Axis ◽  
And Migration

Oral cancer is a major public health burden worldwide. The lack of biomarkers for early diagnosis has increased the difficulty in managing this disease. Recent studies have reported that neutrophil gelatinase-associated lipocalin (NGAL), a secreted glycoprotein, is upregulated in various tumors. In our study we found that NGAL was significantly downregulated in primary malignant and metastatic tissues of oral cancer compared to normal tissues. The downregulation of NGAL was strongly correlated with the degree of differentiation and stage (I-IV), and can serve as a prognostic biomarker for oral cancer. Tobacco carcinogens were also found to be involved in the downregulation of NGAL. Mechanistic studies revealed that knockdown of NGAL increased oral cancer cell proliferation, survival, and migration, and also induced resistance against cisplatin. Silencing of NGAL activated mTOR signaling and reduced autophagy by the LKB1-AMPK-p53-Redd1 signaling axis. Moreover, cyclin-D1, Bcl-2, and MMP-9 were upregulated, and caspase-9 was downregulated, suggesting that silencing of NGAL increases oral cancer cell proliferation, survival, and migration. Thus, from our study it is evident that downregulation of NGAL activates the mTOR pathway and helps in the progression of oral cancer.

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