scholarly journals The Nuclear Farnesoid X Receptor Reduces p53 Ubiquitination and Inhibits Cervical Cancer Cell Proliferation

2021 ◽  
Vol 9 ◽  
Author(s):  
Xiaohua Huang ◽  
Bin Wang ◽  
Runji Chen ◽  
Shuping Zhong ◽  
Fenfei Gao ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Farnesoid X Receptor ◽  
Tumor Xenograft ◽  
G1 Arrest ◽  
Cancer Cell Proliferation ◽  
Small Heterodimer Partner ◽  
Double Minute ◽  
Late Apoptosis ◽  
Murine Double Minute

The role of farnesoid X receptor (FXR) in cervical cancer and the underlying molecular mechanism remain largely unknown. Therefore, this study aimed to assess the mechanism of FXR in cervical cancer. Western blot, qRT-PCR, and immunohistochemistry demonstrated that FXR was significantly reduced in squamous cell carcinoma tissues, although there were no associations of metastasis and TNM stage with FXR. In Lenti-FXR cells obtained by lentiviral transfection, the overexpression of FXR reduced cell viability and colony formation. Compared with the Lenti-Vector groups, the overexpression of FXR induced early and late apoptosis and promoted G1 arrest. With time, early apoptosis decreased, and late apoptosis increased. In tumor xenograft experiments, overexpression of FXR upregulated small heterodimer partner (SHP), murine double minute-2 (MDM2), and p53 in the nucleus. Co-immunoprecipitation (Co-IP) showed that SHP directly interacted with MDM2, which is important to protect p53 from ubiquitination. Nutlin3a increased MDM2 and p53 amounts in the Lenti-Vector groups, without effects in the Lenti-FXR groups. Silencing SHP reduced MDM2 and p53 levels in the Lenti-FXR groups, and Nutlin3a counteracted these effects. Taken together, these findings suggest that FXR inhibits cervical cancer via upregulation of SHP, MDM2, and p53.

scholarly journals miR-145 Contributes to the Progression of Cervical Carcinoma by Directly Regulating FSCN1

2019 ◽  
Vol 28 (9-10) ◽  
pp. 1299-1305 ◽  
Author(s):  
Li Ma ◽  
Ling-Ling Li
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cervical Carcinoma ◽  
Hela Cells ◽  
Underlying Mechanism ◽  
Luciferase Assay ◽  
Cancer Cell Proliferation ◽  
Expression Levels ◽  
Direct Target

The purpose of our study was to investigate the underlying mechanism and functional role of microRNA-145 (miR-145) in cervical cancer. In this study, quantitative real-time PCR (qRT-PCR) was used to detect miR-145 and FSCN1 expression levels in tissues and HeLa cells. Western blotting was performed to determine the protein level of FSCN1. The luciferase assay was used to verify the direct target of miR-145. The CCK-8 assay and 2D colony formation assays were performed to determine the effects of miR-145 mimics or FSCN1 silencing on cell proliferation. miR-145 expression levels were significantly down-regulated, while FSCN1 expression levels were significantly up-regulated in the cervical carcinoma tissues compared with their matched non-cancerous tissues. In addition, FSCN1 expression levels were negatively correlated to miR-145 in tissues. Next, FSCN1 was verified as the direct target of miR-145 in HeLa cells. Moreover, overexpression of miR-145 dramatically inhibited the proliferation of HeLa cells. The silencing of FSCN1 exhibited the similar patterns on cell proliferation as miR-145 overexpression. The miR-145/ FSCN1 axis contributes to the progression of cervical cancer by inhibition of cervical cancer cell proliferation.

scholarly journals The Clinical Significance and Biological Function of PCDH7 in Cervical Cancer

2020 ◽  
Author(s):  
Shitong Zhang ◽  
Xianhu Fu
Keyword(s):  
Cervical Cancer ◽  
Cox Regression ◽  
Prognostic Significance ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Clinical Prognosis ◽  
Kaplan Meier ◽  
Cancer Tissues ◽  
The Relationship

Abstract Background: Cervical cancer is a common malignant tumor in women that is prone to recurrence and metastasis. Recently, many people have explored the role of protocadherin 7 (PCDH7) in cancer, and found that PCDH7 is abnormally expressed in many cancers. The purpose of this study is to investigate the expression and mechanism of PCDH7 in cervical cancer and evaluate its clinical prognostic significance.Methods: The expression of PCDH7 in cervical cancer and cells was detected by qRT-PCR. The relationship between PCDH7 expression and clinical prognosis was calculated by the Kaplan-Meier method and Cox regression analyses. The effects of PCDH7 on cancer cell proliferation, migration, and invasion were studied by MTT assay and transwell assays.Results: The expression of PCDH7 in cervical cancer tissues and cell lines was significantly down-regulated compared with the control. Low PCDH7 expression was associated with low survival rate. PCDH7 expression was significantly correlated with lymph node metastasis, cell differentiation, and FIGO staging. PCDH7 can be used as an independent prognostic factor for cervical cancer. Up-regulation of PCDH7 significantly inhibited the proliferation, migration, and invasion of cancer cells.Conclusions: PCDH7 may be used as a biomarker for the prognosis of cervical cancer.

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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