scholarly journals GHET1 acts as a prognostic indicator and functions as an oncogenic lncRNA in cervical cancer

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Qunchang Zhang ◽  
Yongtao Zhang ◽  
Ying Wang
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Patients ◽  
Cancer Cell ◽  
Human Cancer ◽  
Cervical Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Cancer Cell Proliferation ◽  
Tissue Specimens

AbstractGastric carcinoma proliferation enhancing transcript 1 (GHET1) has been suggested to serve as a promising oncogenic lncRNA in various types of human cancer. However, the role of GHET1 remained unknown in cervical cancer. In our study, we found GHET1 expression was markedly elevated in cervical cancer tissue specimens and cell lines compared with adjacent normal cervical tissue specimens and human normal cervical cell line, respectively. Then, we found high expression of GHET1 is a useful biomarker to discriminate cervical cancer tissues from non-tumorous tissues, and associated with advanced clinical stage, lymph node metastasis, distant metastasis and poor histological grade in cervical cancer patients. The survival analysis showed high GHET1 expression was an independent unfavorable prognostic factor in cervical cancer patients. Knockdown of GHET1 expression markedly inhibits cervical cancer cell proliferation, migration, and invasion. The loss-of-function study indicated knockdown of GHET1 expression markedly inhibits cervical cancer cell proliferation, migration, and invasion. In conclusion, GHET1 acts as an oncogenic lncRNA in cervical cancer.

scholarly journals LINC00511 is associated with the malignant status and promotes cell proliferation and motility in cervical cancer

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Chun-Ling Yu ◽  
Xiao-Ling Xu ◽  
Fang Yuan
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Patients ◽  
Cancer Cell ◽  
Clinical Stage ◽  
Cervical Cancer Cell ◽  
Migration And Invasion ◽  
Epithelial Cell Line ◽  
Cancer Cell Proliferation ◽  
Poor Overall Survival

Abstract LINC00511 is a newly identified lncRNA that is up-regulated in many types of human cancers and may serve as an oncogenic lncRNA. However, there was no report about the role of LINC00511 in cervical cancer. Therefore, we investigated the clinical value of LINC00511 in cervical cancer patients via analyzing the correlation between LINC00511 expression and clinicopathological features. Moreover, we performed loss-of-function study to estimate the effect of LINC00511 on cervical cancer cell proliferation, migration, and invasion. In our study, we found LINC00511 expression levels were increased in cervical cancer tissues and cell lines compared with adjacent normal tissues and normal cervical epithelial cell line, respectively. High LINC00511 expression was correlated with advanced clinical stage, large tumor size, histological type of adenocarcinoma, and present lymph node metastasis, distant metastasis, and poor overall survival in cervical cancer patients. The in vitro studies indicated that knockdown of LINC00511 inhibited cervical cancer cell proliferation, migration, and invasion. In conclusion, LINC00511 acts as oncogenic lncRNA in cervical cancer, and may be a novel biomarker and potential therapeutic target for cervical cancer patients.

TXNIP induced by MondoA, rather than ChREBP, suppresses cervical cancer cell proliferation, migration and invasion

2019 ◽  
Vol 167 (4) ◽  
pp. 371-377 ◽  
Author(s):  
Junhua Zhang ◽  
Xingbo Tian ◽  
Huifang Yin ◽  
Songshu Xiao ◽  
Shuijing Yi ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Hela Cells ◽  
Cervical Cancer Cell ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Cancer Cell Proliferation ◽  
Interacting Protein

Abstract Evidence has indicated the associations between thioredoxin-interacting protein (TXNIP) and cancers. However, the role of TXNIP in cervical cancer remains unclear. Hence, this study aims to investigate the role of TXNIP in regulating cervical cancer cell proliferation, migration and invasion. TXNIP expression can be regulated by either MondoA or ChREBP in a cell- or tissue- dependent manner. Thus, we also explored whether TXNIP expression in cervical cancer can be regulated by MondoA or ChREBP. Our results showed that TXNIP expression was decreased in cervical cancer cells (HeLa, SiHa, CaSki, MS751, C-33A). Furthermore, TXNIP overexpression inhibited cell proliferation, migration and invasion in HeLa cells, whereas TXNIP silencing exerted the opposite effect in C-33A cells. Moreover, TXNIP expression could be induced by MondoA, rather than ChREBP in HeLa cells. Additionally, MondoA overexpression inhibited cell proliferation, migration and invasion through upregulating TXNIP in HeLa cells. In summary, TXNIP induced by MondoA, rather than ChREBP, suppresses cervical cancer cell proliferation, migration and invasion. Our findings provide new ideas for the prevention and treatment of cervical cancer.

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