Project description:Cervical cancer is one of the most common cancers in women worldwide. The role of HPV in cervical cancer is well studied, however, the underlying mechanism promoting cervical tumorigenesis is still not fully understood. Recently, emodin was shown to induce cell cycle arrest, induction of differentiation, downregulation of TGF β signaling pathway and apoptosis in cervical cancer cell lines. Further, recent studies have shown the role of miRNAs in mediating abnormal regulatory mechanisms leading to the pathogenesis of cervical cancer and large scale miRNA profiling studies have examined the use of miRNAs as cervical cancer diagnostic markers. However, to date, there is no study being performed to analyze the changes in miRNAs following emodin treatment to determine whether emodin mediates its effects by regulating the expression of miRNAs. Therefore, the aim of the current study is to perform miRNA profiling in cervical cancer cells following emodin treatment and to analyze the roles of differentially expressed miRNAs in regulating the pathogenesis and treatment of cervical cancer.
Project description:Cervical cancer is the second most common cancer in women worldwide. In addition to the important role played by HPV, the underlying mechanism promoting cervical tumorigenesis is complex and involves deregulation of key signaling pathways. Recently, role of miRNA mediated abnormal regulatory mechanisms is implicated in the pathogenesis of cervical cancer. Micro RNAs are regulatory, non‐coding RNAs about 21–23 nucleotides in length and effects the expression of a number of genes at the post‐transcriptional level. For the past few decades, role of curcumin in inhibiting the growth of cervical cancer and increasing the chemo and radio- sensistivity has been studied extensively. Interestingly, curcumin was shown to downregulate NF-κB, Wnt/β-catenin, TGF‐β and various other signaling pathways in cervical cancer cells. Although, a number of microarray studies have examined the use of miRNAs as cancer diagnostic markers, the regulation of miRNAs upon treatment with curcumin in cervical cancer cells has not been studied. The current study is aimed to perform miRNA profiling in cervical cancer cells following curcumin treatment and to study the role of miRNAs in regulating the different signaling pathways.
Project description:This study is aimed in identification of gene expression profiles in cervical cancer and the role of specific genes in cervical carcinogenesis. Keywords: Gene expression in cervical cancer
Project description:The infection with high-risk human papillomavirus is aetiologically linked to cervical cancer, the role of miRNAs regulated by virus oncogene in cancer progression remain largely unknown. Here, we screened the differentially expressed miRNAs with miRNA array between virus oncogene e6/e7 silenced and not in HPV16-positive cervical cancer cell lines
Project description:Cervical cancer is one of the major cancers that threaten the health of women. CircRNA is an important factor in the regulation of cancer development and progression. The role of circRNA in cervical cancer is less well studied. The aim of this study was to explore the mechanism of circRNA effects on cervical cancer using circRNA-seq technology to study the expression profile data of 9 pairs of primary cervical cancer and paracancerous tissues.
Project description:MicroRNAs (miRNAs or miRs) play essential roles in the initiation and progression of human tumors, including cervical cancer. However, the mechanisms underlying their actions in cervical cancer remain unclear. The present study aimed to evaluate the functional role of miR‑130a‑3p in cervical cancer. Cervical cancer cells were transfected with a miRNA inhibitor (anti‑miR‑130a‑3p) and a negative control. Adhesion‑independent cell proliferation, migration and invasion were evaluated. The findings presented herein demonstrated that miR‑130a‑3p was overexpressed in HeLa, SiHa, CaSki, C‑4I and HCB‑514 cervical cancer cells. The inhibition of miR‑130a‑3p significantly reduced the proliferation, migration and invasion of cervical cancer cells. The canonical delta‑like Notch1 ligand (DLL1) was identified as a possible direct target of miR‑103a‑3p. The DLL1 gene was further found to be significantly downregulated in cervical cancer tissues. On the whole, the present study demonstrates that miR‑130a‑3p contributes to the proliferation, migration and invasion of cervical cancer cells. Therefore, miR‑130a‑3p may be used as a biomarker to determine cervical cancer progression.
Project description:The study examined the infection state of HPV in the Uyghur population with cervical cancer, followed by genotyping to determine the variation in the types of HPV. Using microRNA microarray technology, differential gene expression between HPV-infected cervical cancer and uninfected normal cervical tissues was determined. The microarray results were verified by qRT-PCR using 20 sets of HPV-infected cervical cancer and uninfected cervical tissues.
Project description:Persistent infection by high-risk human papillomaviruses (HPVs) is associated with the development of cervical cancer and a subset of anogenital and head and neck squamous cell carcinomas. Abnormal expression of cellular microRNAs (miRNAs) plays an important role in the development of cancer, including HPV-related tumors. MiRNA expression profile was investigated by microrray analysis in the HPV-positive cervical cancer cell lines SiHa (HPV16-positive cell line derived from a cervical squamous cell carcinoma), CaSki (HPV16-positive cell line derived from a metastatic cervical epidermoid carcinoma), and HeLa (HPV18-positive cell line derived from a cervical adenocarcinoma) and compared with primary HFKs and C33a (HPV-negative cervical cell line).
Project description:Our previous study implied a correlation of inhibitors of differentiation-1 (Id-1) to cervical cancer development. However, how Id-1 contributes to cervical carcinogenesis is unknown. In the present study, we investigated the role of Id-1 in transforming cervical cells with an in vitro transformation model. The human papillomavirus (HPV) immortalized cervical epithelial cells (H8) were successfully transformed by exposure to the carcinogen N-nitrosopyrrolidine (NPYR). The results showed that both Id-1 RNA and protein expression were significantly increased in transformed H8 cells, suggesting a possible role of Id-1 in cervical cell transformation. Ectopic expression of Id-1 in H8 cells potentiated NPYR-induced cell transformation. In contrast, silencing of Id-1 suppressed NPYR-induced H8 cell transformation. A cDNA microarray assay was performed, which identified suggested potential cell signaling pathways for NPYR-induced H8 cell transformation. The results suggest that Id-1 plays an oncogenic role in the cervix, which sheds light on cervical cancer development and implies potential target for cervical cancer prevention and therapy.