scholarly journals Increased Expression of hsa_circ_0002111 and Its Clinical Significance in Papillary Thyroid Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Gongbo Du ◽  
Runsheng Ma ◽  
Hongqiang Li ◽  
Jiao He ◽  
Kaixiang Feng ◽  
...  

Circular RNA (circRNA) is a newly discovered non-coding RNA. Recent reports suggest that circRNAs are key regulators of tumorigenesis because of their special structure. In order to investigate the role of hsa_circ_0002111 in papillary thyroid cancer (PTC), we use quantitative real-time polymerase chain reaction (qRT-PCR) to determine the expression pattern of hsa_circ_0002111 in 82 paired PTC and adjacent non-cancerous thyroid tissues. Cell counting kit-8, colony formation, and transwell assays were conducted to assess the effect of hsa_circ_0002111 on PTC cell proliferation, migration, and invasion. We found that the expression of hsa_circ_0002111 was significantly up-regulated in PTC tissues compared with adjacent non-cancerous tissues (P < 0.0001). Expression of hsa_circ_0002111 was also associated with advanced TNM stage and lymph-node metastasis of patients with PTC. The area under the receiver operating characteristic curve was 0.833. Further, cell function assays showed that hsa_circ_0002111 inhibition significantly suppressed the proliferation and invasion abilities of PTC cells in vitro. In conclusions, the study findings show that the over-expression of hsa_circ_0002111 promotes PTC, and thus hsa_circ_0002111 may be a potential diagnostic biomarker and therapeutic target for PTC.

2020 ◽  
Vol 19 (7) ◽  
pp. 1383-1388 ◽  
Author(s):  
Peng Wang ◽  
Liang Guo ◽  
Zhong Liang ◽  
Jianlin Lou ◽  
Jianqiang Zhao

Purpose: To investigate the therapeutic effect of baicalein on papillary thyroid cancer (PTC) cells in vitro and its underlying molecular mechanism.Methods: The human PTC cell line TPC-1 was divided into five groups and treated with distilled water or baicalein at 10, 20, 50, or 100 μM. Next, miR-206, miR-206 inhibitor, the respective negative controls of miR-206 and miR-206 inhibitor, RAP1B small interfering RNA (siRNA), and control vector siRNA were synthesized and transfected into TPC-1 cells. Cell viability, migration, and invasion were measured using the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and Transwell assays. miR-206 expression and Ras-related protein (RAP1B) levels were assessed by quantitative real-time reverse transcription-polymerase chain reaction and western blotting, respectively.Results: Baicalein inhibited TPC-1 cell viability, migration and invasion, upregulated miR-206 expression, and reduced the RAP1B level in a concentration-dependent manner (p < 0.01). miR-206 negatively regulated RAP1B expression and increased the baicalein-induced reduction of RAP1B expression. Moreover, RAP1B overexpression relieved the suppression of cell viability, migration, and invasion caused by baicalein (p < 0.01).Conclusion: Baicalein suppresses cell growth in PTC cells by regulating the miR-206/RAP1B pathway, providing a new therapeutic strategy for PTC treatment. Keywords: Baicalein, Papillary thyroid cancer (PTC), miR-206, RAP1B, Cell viability, Cell invasion


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Junjie Chu ◽  
Li Tao ◽  
Teng Yao ◽  
Zizheng Chen ◽  
Xiaoxiao Lu ◽  
...  

AbstractPapillary thyroid cancer (PTC) has a continuously increasing incidence and imposes a heavy medical burden to individuals and society due to its high proportion of lymph node metastasis and recurrence in recent years. Circular RNAs, a class of noncoding RNAs, participate in the progression of many cancers, but the role of circRNAs in PTC is still rarely reported. In this study, circRNA deep sequencing was performed to identify differentially expressed circRNAs in PTC. CircRUNX1 was selected for its high expression in PTC, and circRUNX1 silencing was directly associated with the week potential for migration, invasion and proliferation of PTC in vivo and in vitro. Fluorescence in situ hybridization (FISH) was further used to confirm the cytoplasmic localization of circRUNX1, indicating the possible function of circRUNX1 as a ceRNAs in PTC progression through miRNA binding. MiR-296-3p was then confirmed to be regulated by circRUNX1 and to target DDHD domain containing 2 (DDHD2) by luciferase reporter assays. The strong antitumor effect of miR-296-3p and the tumor-promoting effect of DDHD2 were further investigated in PTC, indicating that circRUNX1 modulates PTC progression through the miR-296-3p/DDHD2 pathway. Overall, circRUNX1 plays an oncogenic role in PTC and provides a potentially effective therapeutic strategy for PTC progression.


2020 ◽  
Vol 48 (9) ◽  
pp. 030006052093465
Author(s):  
Sha Luan ◽  
Peng Fu ◽  
Xinyu Wang ◽  
Yue Gao ◽  
Ke Shi ◽  
...  

Objective Papillary thyroid cancer (PTC) is one of the most prevalent endocrine malignancies and the fifth most common cancer in women. Circular RNAs (circRNAs) have been shown to play vital functions in cancers, but few studies have focused on the functions and mechanism of dysregulated circRNAs in PTC. Methods Quantitative reverse transcription PCR was used to measure circ-NCOR2 levels in PTC tissues and cell lines. The functions of circ-NCOR2 in PTC were examined by analysis using the cell counting kit-8, clone forming, flow cytometry, and Transwell experiments. Bioinformatic analysis and dual luciferase reporter gene testing were used to identify the mechanisms of circ-NCOR2. Results Circ-NCOR2 overexpression was observed in PTC tissues and cells. Silenced or overexpressed expression of circ-NCOR2 strikingly attenuated or facilitated, respectively, the growth, migration, and invasion of PTC cells. Mechanistically, miR-615a-5p was identified as the target of circ-NCOR2. Moreover, circ-NCOR2 enhanced the expression of metastasis-associated protein 2 (MTA2) by sponging miR-615a-5p, thereby facilitating PTC cell progression. Conclusions Taken together, our findings reveal a novel circ-NCOR2/miR-615a-5p/MTA2 axis in PTC, which could become a potential therapeutic target for this disease.


2018 ◽  
Vol 50 (5) ◽  
pp. 1659-1672 ◽  
Author(s):  
Fada Xia ◽  
Yong Chen ◽  
Bo Jiang ◽  
Xin Du ◽  
Yao Peng ◽  
...  

Background/Aims: Thyroid cancer is one of the most prevalent endocrine tumors. The present study examined the effects of lncRNA HOXA cluster antisense RNA2 (HOXA-AS2) on the progression of papillary thyroid cancer (PTC), and explored the underlying molecular mechanisms. Methods: Quantitative real-time PCR was used to detect HOXA-AS2, miR-520c-3p and S100 calcium-binding protein A4 (S100A4) expression. Furthermore, the effects of HOXA-AS2 silencing and overexpression on cell proliferation, migration, and invasion were assessed in PTC in vitro by CCK8 and transwell assay. Furthermore, bioinformatics online programs predicted and luciferase reporter assay were used to validate the association of HOXA-AS2 and miR-520c-3p in PTC. Results: We observed that HOXA-AS2 was up-regulated in PTC tissues. In vitro experiments revealed that HOXA-AS2 knockdown significantly inhibited cell growth in PTC in vitro and in vivo. Further functional assays indicated that HOXA-AS2 significantly promoted PTC cell migration and invasion by promoting EMT. Bioinformatics online programs predicted that HOXA-AS2 sponge miR-520c-3p at 3’-UTR with complementary binding sites, which was validated using luciferase reporter assay. HOXA-AS2 could negatively regulate the expression of miR-520c-3p in PTC cells. MiR-520c-3p was down-regulated in PTC tissues, and S100A4 was predicted as a downstream target of miR-520c-3p, which was confirmed by luciferase reporter assay. Conclusion: In summary, our results suggested that the HOXA-AS2/miR-520c-3p/S100A4 axis may play an important role in the regulation of PTC progression, which provides us with new insights into understanding the PTC.


Author(s):  
Ying Ye ◽  
Yanan Song ◽  
Juhua Zhuang ◽  
Saifei He ◽  
Jing Ni ◽  
...  

Long noncoding RNA CCAL has been reported to promote tumor progression in various human cancers, including hepatocellular carcinoma, osteosarcoma, and colorectal cancer. However, the role of CCAL in papillary thyroid cancer remains largely unknown. In the present study, we found that the expression of CCAL was upregulated in papillary thyroid tumor tissues compared to adjacent normal tissues. Moreover, the expression of CCAL was positively related with papillary thyroid cancer severity and TNM stage and predicated poor prognosis. Besides, we found that knockdown of CCAL significantly inhibited papillary thyroid cancer cell proliferation, migration, and invasion in vitro and reduced tumor growth and metastasis in vivo. We found that knockdown of CCAL dramatically decreased the expression of NOTCH1 and suppressed the activation of the NOTCH1 signaling pathway. Furthermore, overexpression of NOTCH1 rescued the proliferation, migration, and invasion in papillary thyroid cancer cells. Taken together, our data indicated that CCAL promoted papillary thyroid cancer development and progression by activation of the NOTCH1 pathway, which provided a new insight on the design of therapeutic targets.


2020 ◽  
Vol 69 (1) ◽  
pp. 66-74
Author(s):  
Su Dong ◽  
Shuai Xue ◽  
Yue Sun ◽  
Zhe Han ◽  
Lele Sun ◽  
...  

MicroRNA-363-3 p (miR-363–3 p) has been reported to play a crucial role in tumor development and progression, and function as a tumor suppressor in many types of cancer. In our previous studies, we found that miRNA-363–3 p inhibited papillary thyroid carcinoma (PTC) progression by targeting PIK3CA. Meanwhile, we found that NIN1/RPN12 binding protein 1 (NOB1) was significantly upregulated in thyroid carcinoma tissue and downregulation of NOB1 expression significantly inhibited cell proliferation, migration and invasion in PTC. However, the correlation of NOB1 and miR-363–3 p has not been investigated. Here, we performed bioinformatic analysis to explore miRNA targeting NOB1. We found that NOB1 was a target of miR-363–3 p and miR-363–3 p regulated NOB1 expression at the translational and transcriptional levels by targeting its 3’ untranslated region (3'-UTR). Further, we showed that miR-363–3 p inhibited tumor progression by targeting NOB1 in vitro and in vivo. We found that overexpression miR-363–3 p or silencing NOB1 significantly increased G0/G1-phase and decreased S-phase in the human papillary thyroid cells, which led to a significant delay in cell proliferation, indicating miR-363–3 p and NOB1 are crucial for human papillary thyroid cancer tumorigenesis. Collectively, our data unveil that miR-363–3 p negatively regulates NOB1 activity by reducing its stability. This study provides a new therapeutic target for regulation of NOB1 stability to modulate human papillary thyroid cancer progression.


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