Novel structural approaches concerning HPV proteins: Insight into targeted therapies for cervical cancer (Review)

Pappa, Kalliopi I.; Kontostathi, Georgia; Lygirou, Vasiliki; Zoidakis, Jérôme; Anagnou, Nicholas P.

doi:10.3892/or.2018.6257

Cited by 18 publications

(18 citation statements)

References 58 publications

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“…The occurrence and development of cervical cancer are related to many factors. Persistent human papillomavirus (HPV) infection has been recognized as an important cause of cervical cancer [3][4][5]. HPV16 and HPV18 cause almost 75% of cervical cancer, while HPV31 and HPV45 lead to 10% of cervical cancer [3,4,6].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of SEMA4C Inhibit Epithelial-Mesenchymal Transition (EMT) and the Invasion and Metastasis of Cervical Cancer Cells via Inhibiting Transforming Growth Factor-beta 1 (TGF-β1)-Induced Hela cells p38 Mitogen-Activated Protein Kinase (MAPK) Activation

Yang

Xiong

et al. 2020

Med Sci Monit

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Background: Epithelial-mesenchymal transition (EMT) plays a key role in promoting invasion and metastasis of tumor cells. SEMA4C can regulate the generation of transforming growth factor-beta 1 (TGF-b1)-induced EMT in cervical cancer. This study investigated the relationship between the regulation of SEMA4C on TGF-b1-induced p38 mitogen-activated protein kinase (MAPK) activation and invasion and metastasis of cervical cancer. Material/Methods: Hela-shSEMA4C cell line was established and the success of transfection was confirmed with fluorescence intensity. Cell experiments were divided into 2 groups. Group 1 was Hela, Hela-shNC, and Hela-shSEMA4C; and Group 2 was Hela, Hela-shNC, Hela-shSEMA4C, Hela+TGF-b1, Hela-shNC+TGF-b1, and Hela-shSEMA4C+TGF-b1. Group 1 was detected for SEMA4C mRNA expression by real-time polymerase chain reaction (RT-PCR), cell viability by Cell Counting Kit-8 (CCK-8), F-actin fluorescence intensity by immunofluorescence, cell migration by scratch test, and cell invasion by invasion test. Group 2 was analyzed for E-cadherin fluorescence intensity by immunofluorescence, human fibronectin (FN) content by enzyme-linked immunosorbent assay (ELISA), and SEMA4C, E-cadherin and p-p38 expressions by Western blot. Results: For Group 1, compared with Hela and Hela-shNC subgroups, the SEMA4C mRNA expression, cell viability, F-actin fluorescence intensity, cell migration and invasion ability in the Hela-shSEMA4C subgroup were significantly decreased (P<0.05). For Group 2, compared with Hela and Hela-shNC subgroups, the E-cadherin expression and fluorescence intensity in the Hela-shSEMA4C subgroup were significantly increased (P<0.01), while the FN content, SEMA4C, and p-p38 MAPK expressions were significantly decreased (P<0.01). Compared with Hela-shNC+TGF-b1 and Hela+TGF-b1 subgroups, the E-cadherin expression and fluorescence intensity in the Hela-shSEMA4C+TGF-b1 subgroup were significantly increased (P<0.01), while the FN content, SEMA4C and p-p38 expressions were significantly decreased (P<0.01). Conclusions: Downregulation of SEMA4C can inhibit EMT and the invasion and metastasis of cervical cancer cells via inhibiting TGF-b1-induced Hela cells p38 MAPK activation.

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Section: Introductionmentioning

confidence: 99%

Downregulation of SEMA4C Inhibit Epithelial-Mesenchymal Transition (EMT) and the Invasion and Metastasis of Cervical Cancer Cells via Inhibiting Transforming Growth Factor-beta 1 (TGF-β1)-Induced Hela cells p38 Mitogen-Activated Protein Kinase (MAPK) Activation

Yang

Xiong

et al. 2020

Med Sci Monit

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“…It is widely accepted that HPV is the virtually important cause of cervical cancer development, although the pathogenesis of cervical carcinoma is complex. The cervical tumorigenesis is often initiated by persistent infection of high-risk HPV types, particularly virus types 16 and 18 [7]. More than 100 types of HPV have been identified and the viral typing plays a key role in determining the prognosis of cervical cancer [8].…”

Section: Introductionmentioning

confidence: 99%

Recent Advances on the Molecular Mechanism of Cervical Carcinogenesis Based on Systems Biology Technologies

Lin

Zhou

et al. 2019

Computational and Structural Biotechnology Journal

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Cervical cancer is one of the common malignancies in women worldwide. Exploration of pathogenesis and molecular mechanism of cervical cancer is pivotal for development of effective treatment for this disease. Recently, systems biology approaches based on high-throughput technologies have been carried out to investigate the expression of some genes and proteins in genomics, transcriptomics, proteomics, and metabonomics of cervical cancer. Compared with traditional methods，systems biology technology has been shown to provide large of information regarding prognostic biomarkers and therapeutic targets for cervical cancer. These molecular signatures from system biology technology could be useful to understand the molecular mechanisms of cervical cancer development and progression, and help physicians to design targeted therapeutic strategies for patients with cervical cancer.

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“…8 Unlike breast cancer and lung adenocarcinoma, the effective molecular targets for therapy have yet to be identified in cervical carcinoma. 9,10 Thus, it is necessary to elucidate the underlying mechanisms of cervical carcinoma for developing molecular target therapy in cervical carcinoma.…”

Section: Introductionmentioning

confidence: 99%

CERNA2: A predictor for clinical progression and poor prognosis in cervical carcinoma

Wang

Ouyang

Li³

2019

J of Cellular Biochemistry

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Competing long noncoding RNA 2 (lncRNA 2) for microRNA let-7b (CERNA2) has emerged as an important regulator of tumorigenesis and cancer progression but the clinical value and regulatory function of CERNA2 is yet to be investigated in cervical carcinoma. In our study, we found the CERNA2 expression was obviously increased in cervical carcinoma tissues compared with adjacent normal cervical tissues. In addition, we observed that metastatic lymph nodes exhibited high levels of CERNA2 expression in contrast to primary cervical carcinoma tissues. Furthermore, high CERNA2 expression was associated with advanced clinical stage, lymph node metastasis, distant metastasis poor histological grade, and short overall survival in cervical carcinoma patients. Moreover, high CERNA2 expression acted as an independent unfavorable predictor for overall survival in cervical carcinoma patients. The cell migration and invasion assays in vitro suggested that knockdown of CERNA2 remarkably inhibited cell migration and invasion in cervical carcinoma. In conclusion, CERNA2 functions as an oncogenic lncRNA and may be as a potential therapeutic target in cervical carcinoma. K E Y W O R D S biomarker, cervical carcinoma, competing endogenous long noncoding RNA 2 for microRNA let-7b, long noncoding RNA, metastasis J Cell Biochem. 2019;120:11216-11221. wileyonlinelibrary.com/journal/jcb 11216 |

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Novel structural approaches concerning HPV proteins: Insight into targeted therapies for cervical cancer (Review)

Cited by 18 publications

References 58 publications

Downregulation of SEMA4C Inhibit Epithelial-Mesenchymal Transition (EMT) and the Invasion and Metastasis of Cervical Cancer Cells via Inhibiting Transforming Growth Factor-beta 1 (TGF-β1)-Induced Hela cells p38 Mitogen-Activated Protein Kinase (MAPK) Activation

Downregulation of SEMA4C Inhibit Epithelial-Mesenchymal Transition (EMT) and the Invasion and Metastasis of Cervical Cancer Cells via Inhibiting Transforming Growth Factor-beta 1 (TGF-β1)-Induced Hela cells p38 Mitogen-Activated Protein Kinase (MAPK) Activation

Recent Advances on the Molecular Mechanism of Cervical Carcinogenesis Based on Systems Biology Technologies

CERNA2: A predictor for clinical progression and poor prognosis in cervical carcinoma

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