scholarly journals High expression of prolactin receptor is associated with cell survival of cervical cancer cells

2013 ◽  
Vol 4 ◽  
Author(s):  
L�pez Pulido Edgar ◽  
Mu�oz Valle Jos� ◽  
Pereira Su�rez Ana ◽  
Del Toro Arreola Susana ◽  
Ascencio Cedillo Rafael ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Prolactin Receptor ◽  
High Expression ◽  
Cervical Cancer Cells

scholarly journals High expression of prolactin receptor is associated with cell survival in cervical cancer cells

2013 ◽  
Vol 13 (1) ◽  
pp. 103 ◽  
Author(s):  
Edgar I Lopez-Pulido ◽  
José F Muñoz-Valle ◽  
Susana Del Toro-Arreola ◽  
Luis F Jave-Suárez ◽  
Miriam R Bueno-Topete ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Prolactin Receptor ◽  
High Expression ◽  
Cervical Cancer Cells

scholarly journals High expression of TMEM33 predicts poor prognosis and promotes cell proliferation in cervical cancer

2022 ◽  
Author(s):  
Hanxiang Chen ◽  
Yongqing Li ◽  
Shaoming Zhang ◽  
Yunshan Wang ◽  
Lili Wang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Gene Networks ◽  
Cox Regression ◽  
Interaction Analysis ◽  
Transmembrane Protein ◽  
Functional Enrichment ◽  
High Expression ◽  
Cervical Cancer Cells

Abstract Background As one of the most common cancer among women worldwide, the prognosis of patients with advanced cervical cancer remains unsatisfactory. A study indicated that transmembrane protein 33 (TMEM33) was implicated in tumor recurrence, while its role in cervical cancer has not been elucidated. Methods TMEM33 expression in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) was primarily screened in The Cancer Genome Altas (TCGA), and further validated in Gene Expression Omnibus (GEO) database. The Kaplan–Meier plotter analysis and Cox regression were constructed to evaluate the prognostic value of TMEM33 in CESC. Functional enrichment analysis was performed with GO, KEGG and GSEA tools. Protein-protein interaction analysis and correlated gene networks were conducted using STING and GEPIA2 websites, respectively. The expression of TMEM33 in cervical cancer cells were examined by immunoblotting and RT-qPCR. Finally, CCK-8 assay and colony formation assay were performed to investigate the role of TMEM33 in cervical cancer cell proliferation. Results TMEM33 expression was significantly elevated in CESC compared with normal tissues. High expression of TMEM33 was associated with poor prognostic clinical characteristics in CESC patients. KM-plotter analysis revealed that patients with increased TMEM33 had shorter overall survival (OS), progress free interval (PFI), and disease specific survival (DSS). Moreover, Multivariate Cox analysis further confirmed that high TMEM33 expression was an independent risk factor for OS in patients with CESC. TMEM33 was associated with immune cell infiltration, and its expression was correlated with tumorigenesis-related genes RNF4, OCIAD1, TMED5, DHX15, MED28 and LETM1. More importantly, knockdown of TMEM33 in cervical cancer cells decreased the expression of those genes and inhibited cell proliferation. Conclusions Increased TMEM33 in cervical cancer can serve as an independent prognostic marker and might play a role in tumorigenesis by promoting cell proliferation.

scholarly journals 17β‑estradiol‑induced mitochondrial dysfunction and Warburg effect in cervical cancer cells allow cell survival under metabolic stress

2019 ◽  
Author(s):  
Annie Riera Leal ◽  
Pablo Ortiz‑Lazareno ◽  
Luis Jave‑Su�rez ◽  
Adri�n Ram�rez De Arellano ◽  
Adriana Aguilar‑Lemarroy ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Mitochondrial Dysfunction ◽  
Cell Survival ◽  
Cancer Cells ◽  
Warburg Effect ◽  
Metabolic Stress ◽  
Cervical Cancer Cells ◽  
17Β Estradiol

Eriodictyol Suppresses Survival of Cervical Cancer Cells Through Mediation of PTEN/Akt Signaling Pathway

2019 ◽  
Vol 18 (2) ◽  
pp. 196-200
Author(s):  
Yu Lixiao ◽  
Liu Xiaoyun
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Hela Cells ◽  
Akt Signaling ◽  
Dependent Manner ◽  
Akt Signaling Pathway ◽  
Cervical Cancer Cells

Cervical cancer is one of the most malignant cancers of the female reproductive system with high morbidity and mortality. In the current study, we have examined the effect of eriodictyol on cell survival including cell growth, cell cycle and apoptosis of cervical cancer cells and also explored the underlying mechanism(s). To this end, CCK-8 assay, flow cytometry and western blotting assays were performed in cervical cancer HeLa cells. Eriodictyol significantly inhibited cell survival including impeding the cell viability, arresting the cell cycle at the G1 phase and potentiating cell apoptosis in a concentration-dependent manner. Also, ERI activated PTEN, P21, cleaved caspase-3/-9 expression and downregulated P-Akt and cyclin D1 expression in a dose-dependent manner. In conclusion, ERI can inhibit cervical cancer HeLa cells viability via impeding cell cycle and inducing apoptosis by regulating PTEN/Akt signaling pathway.

scholarly journals ER-α36 Promotes the Malignant Progression of Cervical Cancer Mediated by Estrogen via HMGA2

2021 ◽  
Vol 11 ◽  
Author(s):  
Chunyan Wang ◽  
Tianli Zhang ◽  
Kun Wang ◽  
Shuo Zhang ◽  
Qing Sun ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Poor Prognosis ◽  
High Mobility ◽  
High Expression ◽  
Cervical Cancer Cells

ObjectivesEstrogen is proven to promote the malignant behaviors of many cancers via its receptors. Estrogen receptor alfa 36 (ER-α36) is a newly identified isoform of estrogen receptor alfa (ER-α), the role of ER-α36 in regulating the effects of estrogen and its potential impact on human cervical cancer is poorly understood.MethodsImmunohistochemistry staining was used to evaluate the expression of ER-α36, estrogen receptor alfa 66 (ER-α66) and their prognostic values in cervical cancer. The effects of ER-α36 and ER-α66 on the proliferation and metastasis of cervical cancer were measured in vitro. A xenograft tumor assay was used to study the tumorigenesis role of ER-α36 in vivo. Furthermore, the functional gene at the downstream of ER-α36 was obtained via next-generation sequencing, and the biological functions of high mobility group A2 (HMGA2) in cervical cancer cells were investigated in vitro.ResultsER-α36 was over-expressed in cervical cancer tissues and elevated ER-α36 expression was associated with poor prognosis in cervical cancer patients. High expression of ER-α36 promoted the proliferation, invasion and metastasis of cervical cancer cells mediated by estrogen, while silencing ER-α36 had the opposite effects. Further research showed that HMGA2 was a downstream target of ER-α36 in cervical cancer cells. The oncogenic effect of ER-α36 was attenuated after HMGA2 knockdown.ConclusionsHigh expression of ER-α36 was correlated with a poor prognosis in cervical cancer by regulating HMGA2. ER-α36 could be a prognostic biomarker and a target for cervical cancer treatment.

scholarly journals Elevated Expression of Programmed Death-1 and Programmed Death Ligand-1 Negatively Regulates Immune Response against Cervical Cancer Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Zhifang Chen ◽  
Nannan Pang ◽  
Rong Du ◽  
Yuejie Zhu ◽  
Lingling Fan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Immune Response ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Peripheral Blood ◽  
High Expression ◽  
Programmed Death Ligand 1 ◽  
Programmed Death ◽  
Cervical Cancer Cells ◽  
Programmed Death 1

The present study is to measure the expression of programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1), as well as its clinical significance in cervical cancer patients. Our results showed that different T cell subsets in patients with cervical cancer had high expression of PD-1, and DCs had high expression of PD-L1. High expression of PD-1 on Treg cells in cervical cancer patients facilitated the production of TGF-βand IL-10 but inhibited the production of IFN-γ. Cervical cancer elevated the expression of PD-1 and PD-L1 in mRNA level. PD-1 expression in peripheral blood of cervical cancer patients was related with tumor differentiation, lymph node metastasis, and invasiveness. PD-1/PD-L1 pathway inhibited lymphocyte proliferation but enhanced the secretion of IL-10 and TGF-βin vitro. In summary, our findings demonstrate that elevated levels of PD-1/PD-L1, TGF-β, and IL-10 in peripheral blood of cervical cancer patients may negatively regulate immune response against cervical cancer cells and contribute to the progression of cervical cancer. Therefore, PD-1/PD-L1 pathway may become an immunotherapy target in the future.

Water-soluble amphiphilic ruthenium(ii) polypyridyl complexes as potential light-activated therapeutic agents

2020 ◽  
Vol 56 (65) ◽  
pp. 9332-9335
Author(s):  
Sandra Estalayo-Adrián ◽  
Salvador Blasco ◽  
Sandra A. Bright ◽  
Gavin J. McManus ◽  
Guillermo Orellana ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cellular Uptake ◽  
Therapeutic Agents ◽  
Water Soluble ◽  
Polypyridyl Complexes ◽  
Cervical Cancer Cells

Two new water-soluble amphiphilic Ru(ii) polypyridyl complexes were synthesised and their photophysical and photobiological properties evaluated; both complexes showed a rapid cellular uptake and phototoxicity against HeLa cervical cancer cells.

The Antitumor Efficiency of Zinc Finger Nuclease Combined with Cisplatin and Trichostatin A in Cervical Cancer Cells

2020 ◽  
Vol 20 (17) ◽  
pp. 2125-2135
Author(s):  
Ci Ren ◽  
Chun Gao ◽  
Xiaomin Li ◽  
Jinfeng Xiong ◽  
Hui Shen ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Zinc Finger ◽  
Hela Cells ◽  
Colony Formation ◽  
Trichostatin A ◽  
Combined Therapy ◽  
Hpv E7 ◽  
Anti Cancer ◽  
Cervical Cancer Cells

Background: Persistent infection with the high-risk of human papillomavirus (HR-HPVs) is the primary etiological factor of cervical cancer; HR-HPVs express oncoproteins E6 and E7, both of which play key roles in the progression of cervical carcinogenesis. Zinc Finger Nucleases (ZFNs) targeting HPV E7 induce specific shear of the E7 gene, weakening the malignant biological effects, hence showing great potential for clinical transformation. Objective: Our aim was to develop a new comprehensive therapy for better clinical application of ZFNs. We here explored the anti-cancer efficiency of HPV targeted ZFNs combined with a platinum-based antineoplastic drug Cisplatin (DDP) and an HDAC inhibitor Trichostatin A (TSA). Methods: SiHa and HeLa cells were exposed to different concentrations of DDP and TSA; the appropriate concentrations for the following experiments were screened according to cell apoptosis. Then cells were grouped for combined or separate treatments; apoptosis, cell viability and proliferation ability were measured by flow cytometry detection, CCK-8 assays and colony formation assays. The xenograft experiments were also performed to determine the anti-cancer effects of the combined therapy. In addition, the HPV E7 and RB1 expressions were measured by western blot analysis. Results: Results showed that the combined therapy induced about two times more apoptosis than that of ZFNs alone in SiHa and HeLa cells, and much more inhibition of cell viability than either of the separate treatment. The colony formation ability was inhibited more than 80% by the co-treatment, the protein expression of HPV16/18E7 was down regulated and that of RB1 was elevated. In addition, the xenografts experiment showed a synergistic effect between DDP and TSA together with ZFNs. Conclusion: Our results demonstrated that ZFNs combined with DDP or TSA functioned effectively in cervical cancer cells, and it provided novel ideas for the prevention and treatment of HPV-related cervical malignancies.

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