scholarly journals Photodynamic therapy of cervical cancer by eradication of cervical cancer cells and cervical cancer stem cells

Oncotarget ◽  
2019 ◽  
Vol 10 (43) ◽  
pp. 4380-4396 ◽  
Author(s):  
Elvin Peter Chizenga ◽  
Rahul Chandran ◽  
Heidi Abrahamse
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Photodynamic Therapy ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Cervical Cancer Cells

scholarly journals Reciprocal Regulation Between Indoleamine 2,3-Dioxigenase 1 and Notch1 Involved in Radiation Response of Cervical Cancer Stem Cells

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1547 ◽  
Author(s):  
Hui-Ying Low ◽  
Yueh-Chun Lee ◽  
Yi-Ju Lee ◽  
Hui-Lin Wang ◽  
Yu-I Chen ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Radiation Treatment ◽  
Tryptophan Metabolism ◽  
Breakdown Product ◽  
Regulation Mechanism ◽  
Reciprocal Regulation ◽  
Cervical Cancer Cells

Cervical cancer is the fourth most common cancer in women around the world. Cancer stem cells (CSCs) are responsible for cancer initiation, as well as resistance to radiation therapy, and are considered as the effective target of cancer therapy. Indoleamine 2,3-dioxygenase 1 (IDO1) mediates tryptophan metabolism and T cell suppression, but the immune-independent function of IDO1 in cancer behavior is not fully understood. Using tumorsphere cultivation for enriched CSCs, we firstly found that IDO1 was increased in HeLa and SiHa cervical cancer cells and in these two cell lines after radiation treatment. The radiosensitivity of HeLa and SiHa tumorsphere cells was increased after the inhibition of IDO1 through RNA interference or by the treatment of INCB-024360, an IDO1 inhibitor. With the treatment of kynurenine, the first breakdown product of the IDO1-mediated tryptophan metabolism, the radiosensitivity of HeLa and SiHa cells decreased. The inhibition of Notch1 by shRNA downregulated IDO1 expression in cervical CSCs and the binding of the intracellular domain of Notch (NICD) on the IDO1 promoter was reduced by Ro-4929097, a γ-secretase inhibitor. Moreover, the knockdown of IDO1 also decreased NICD expression in cervical CSCs, which was correlated with the reduced binding of aryl hydrocarbon receptor nuclear translocator to Notch1 promoter. In vivo treatment of INCB-0234360 sensitized SiHa xenograft tumors to radiation treatment in nude mice through increased DNA damage. Furthermore, kynurenine increased the tumorsphere formation capability and the expression of cancer stemness genes including Oct4 and Sox2. Our data provide a reciprocal regulation mechanism between IDO1 and Notch1 expression in cervical cancer cells and suggest that the IDO1 inhibitors may potentially be used as radiosensitizers.

scholarly journals Cervical Cancer Cells with Positive Sox2 Expression Exhibit the Properties of Cancer Stem Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e87092 ◽  
Author(s):  
Xiao-Fang Liu ◽  
Wen-Ting Yang ◽  
Rui Xu ◽  
Jun-Tian Liu ◽  
Peng-Sheng Zheng
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Sox2 Expression ◽  
Cervical Cancer Cells

scholarly journals TAB2 Promotes the Stemness and Biological Functions of Cervical Squamous Cell Carcinoma Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yijia Zhou ◽  
Yuandong Liao ◽  
Chunyu Zhang ◽  
Junxiu Liu ◽  
Wei Wang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Cell Function ◽  
Chemotherapy Resistance ◽  
Cervical Squamous Cell Carcinoma ◽  
Published Data ◽  
Cell Functions

Cancer stem cells are a key population participating in the promotion of the cervical cancer progression through interacting with cancer cells. Existing studies have preliminary revealed that cervical cancer stem cells contribute to tumor recurrence and chemotherapy resistance. However, the specific mechanisms involved in regulating cell functions remain largely unknown. Here, we analyzed published data from public databases and our global transcriptome data, thus identifying cancer-related signaling pathways and molecules. According to our findings, upregulated TAB2 was correlated to stem cell-like properties of cervical cancer. Immunohistochemistry staining of TAB2 in normal and cervical cancer tissues was performed. The cell function experiments demonstrated that knockdown of TAB2 reduced the stemness of cervical cancer cells and, importantly, prevented cervical cancer progression. Collectively, the therapeutic scheme targeting TAB2 may provide an option for overcoming tumor relapse and chemoresistance of cervical cancer via obstructing stemness maintenance.

scholarly journals Photodynamic therapy combined to cisplatin potentiates cell death responses of cervical cancer cells

BMC Cancer ◽  
2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Laura Marise de Freitas ◽  
Rodolfo Bortolozo Serafim ◽  
Juliana Ferreira de Sousa ◽  
Thaís Fernanda Moreira ◽  
Cláudia Tavares dos Santos ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Cancer Cells ◽  
Cervical Cancer Cells

scholarly journals NF-YA Transcriptionally Activates the Expression of SOX2 in Cervical Cancer Stem Cells

2019 ◽  
Author(s):  
Wen-Ting Yang ◽  
Zong-Xia Zhao ◽  
Bin Li ◽  
Peng-Sheng Zheng
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Cancer Stem Cell ◽  
Transcriptional Activation ◽  
Luciferase Reporter ◽  
Cis Element ◽  
Cervical Cancer Cells ◽  
Ccaat Box

AbstractRoles for SOX2 have been extensively studied in several types of cancer, including colorectal cancer, glioblastoma and breast cancer, with particular emphasis placed on the roles of SOX2 in cancer stem cell. Our previous study identified SOX2 as a marker in cervical cancer stem cells driven by a full promoter element of SOX2 EGFP reporter. Here, dual-luciferase reporter and mutagenesis analyses were employed, identifying key cis-elements in the SOX2 promoter, including binding sites for SOX2, OCT4 and NF-YA factors in SOX2 promoter. Mutagenesis analysis provided additional evidence to show that one high affinity-binding domain CCAAT box was precisely recognized and bound by the transcription factor NF-YA. Furthermore, overexpression of NF-YA in primitive cervical cancer cells SiHa and C33A significantly activated the transcription and the protein expression of SOX2. Collectively, our data identified NF-YA box CCAAT as a key cis-element in the SOX2 promoter, suggesting that NF-YA is a potent cellular regulator in the maintenance of SOX2-positive cervical cancer stem cell by specific transcriptional activation of SOX2.

scholarly journals microRNA-375 released from extracellular vesicles of bone marrow mesenchymal stem cells exerts anti-oncogenic effects against cervical cancer

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Feng Ding ◽  
Jinhua Liu ◽  
Xiaofei Zhang
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cancer Cells ◽  
Extracellular Vesicles ◽  
Cervical Cancer Cells ◽  
Marrow Mesenchymal Stem Cells

Abstract Background Cervical cancer is the most prevalent gynecological malignancies accompanied by high mortality, where finding a more effective therapeutic option for cervical cancer is necessary. The inhibitory role of microRNAs (miRNAs) derived from the extracellular vesicles (EVs) of the bone marrow mesenchymal stem cells (BMSCs) was analyzed in cervical cancer. Methods Expression of miR-375 was examined by RT-qPCR in cervical cancer cell lines. The targeting relation between miR-375 and maternal embryonic leucine zipper kinase (MELK) was predicted by bioinformatics analysis and verified by dual-luciferase reporter gene assay. Isolated BMSCs were transfected with lentivirus-mediated vectors, followed by EV extraction. The morphology of EVs was then identified using a NanoSight particle size analyzer and transmission electron microscope (TEM). The biological properties of cervical cancer cells were evaluated using Transwell, EdU, and TUNEL assays, respectively. Xenograft tumors in nude mice were observed to assess cervical tumorigenesis in vivo. Results Low expression of miR-375 and high expression of MELK were detected in cervical cancer samples. MELK was identified as the target gene of miR-375, which was negatively correlated with miR-375 levels. Overexpression of miR-375 suppressed proliferation, migration, and invasion of cervical cancer cells, but enhanced cell apoptosis by cooperating with downregulated MELK expression. miR-375 transferred from BMSC-derived EVs exerted the same effects on cell biological activities. Xenograft assays in vivo proved that miR-375 from BMSC-derived EVs inhibited tumor growth. Conclusion The present study highlighted the role of miR-375 from BMSC-derived EVs in suppressing the progression of cervical cancer, which may contribute to the discovery of novel potential biomarkers for cervical cancer therapy.

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