scholarly journals Bibliometric Insights in Advances of Anaplastic Thyroid Cancer: Research Landscapes, Turning Points, and Global Trends

2021 ◽  
Vol 11 ◽  
Author(s):  
Hanyu Wang ◽  
Yuxin Yu ◽  
Kang Wang ◽  
Hui Sun

BackgroundThyroid cancers are the most common endocrine malignancies with a dramatic increase in incidences. Anaplastic thyroid cancer is a rare but deadly form among thyroid cancers. To better understand of this field, we assessed the global scientific outputs and tried to depict its overview via bibliometric methods.MethodsApproximately 1,492 science publications published between 1997 and 2020 were included by systematic retrieval in the WoS database. The general information of them was characterized, and the developmental skeleton and research frontiers were explored.ResultsThe article number in this field has been increasing in the past 24 years. North America, East Asia, and Western Europe have reached remarkable achievements. Mutations of BARF and TERT and their downstream pathways have attracted researchers’ attention, where genetic diagnosis provides new clinical insight and several targeted therapeutic approaches have been on the clinical trial.ConclusionsNumerous efforts have been made to figure out gene expression reprogramming of anaplastic thyroid cancer and key mechanism in driving its dedifferentiation, invasion and migration process. Targeted therapy, immunotherapy, and systematic combination therapy are the recent current research hotspots. These results provide insightful clues for the funding direction and the potential breakthrough direction of the anaplastic thyroid cancer study.

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Wei Zhang ◽  
Wenyue Ji ◽  
Xudong Zhao

Abstract Background Anaplastic thyroid cancer (ATC) is considered to be a rare type of thyroid cancer but takes up the most important proportion of thyroid cancer-related deaths. Therefore, the development of molecular targeted therapy is an exciting strategy in the management of ATC. Methods miR-155 and SOCS1 expression were measured by qRT-PCR as well as western blot analysis. 8305c and FRO cells were transfected and cultured for apoptosis assays, transwell, MTT on miR-155 or SOCS1 suppression and overexpression. Dual-luciferase reporter assays and SOCS1 restoration experimentswas implemented for define the relation between SOCS1 and miR-155. In addition, the correlation between miR-155 expression and patients’ clinicopathological features were also explored. Results Aberrant miR-155 and SOCS1 expression and inverse correlation were found in ATC samples. In addition, it indicated that miR-155 expression correlated with cervical metastasis as well as extrathyroidal invasion. Moreover, we demonstrated that miR-155 inhibited 8305c and FRO cells apoptosis, promoted proliferation, invasion and migration. Furthermore, miR-155 inhibition was associated with a significant overexpression of SOCS1. Additionally, luciferase reporter assays presented that miR-155 could bind to SOCS1 3′-UTR, influencing its stability negatively and finally lowering SOCS1 levels. Moreover, it was illustrated that the impacts of miR-155 suppression were reversed by the inhibition of SOCS1 on cell proliferation, apoptosis as well as invasion. Conclusions Aberrant miR-155/SOCS1 expression has been included in ATC progression: miR-155 overexpression leads to SOCS1 suppression and develops ATC progression. Thus, miR-155 has been considered to be an underlying therapeutic target for ATC.


Oncotarget ◽  
2017 ◽  
Vol 8 (66) ◽  
pp. 110552-110565 ◽  
Author(s):  
Honggang Sun ◽  
Liqin He ◽  
Lan Ma ◽  
Tao Lu ◽  
Jianguo Wei ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 125 ◽  
Author(s):  
Hye-Ji Shin ◽  
Kyung-A Hwang ◽  
Kyung-Chul Choi

Thyroid cancers developed from the tissues of the thyroid gland are classified into papillary (PTC), follicular (FTC), medullary (MTC), and anaplastic thyroid cancer (ATC). Although thyroid cancers have been generally known as mild forms of cancer, undifferentiated MTC and ATC have a more unfavorable prognosis than differentiated PTC and FTC because they are more aggressive and early metastatic. A variety of therapies such as surgery, radiotherapy, and chemotherapy have been currently used to treat thyroid cancer, but they still have limitations including drug resistance or unfavorable side effects. Phytochemicals are plant-derived chemicals having various physiological activities that are expected to be effective in cancer treatment. In this review, anticancer efficacy of phytochemicals, such as resveratrol, genistein, curcumin, and other substances in each type of thyroid cancer was introduced with their chemopreventive mechanisms. English articles related with thyroid cancer and anti-thyroid cancer of phytochemicals were searched from PubMed and Google Scholar. This article mainly focused on in vitro or animal studies on phytochemicals with anti-thyroid cancer activity. These various phytochemicals have been shown to induce apoptosis in all types of thyroid cancer cells, inhibit cell proliferation and invasion, and to be helpful in enhancing the effect of radioiodine therapy that is a typical therapy to thyroid cancer. These results suggest that thyroid cancer can be more effectively treated by the combinations of phytochemicals and the existing therapies or substances.


2017 ◽  
Vol 442 ◽  
pp. 68-80 ◽  
Author(s):  
Ping Zhu ◽  
Ling-Yao Liao ◽  
Ting-Ting Zhao ◽  
Xiao-Mei Mo ◽  
George G. Chen ◽  
...  

2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Kai Liu ◽  
Wen Huang ◽  
Dan-Qing Yan ◽  
Qing Luo ◽  
Xiang Min

The study evaluated the ability of long intergenic noncoding RNA LINC00312 (LINC00312) to influence the proliferation, invasion, and migration of thyroid cancer (TC) cells by regulating miRNA-197-3p. TC tissues and adjacent normal tissues were collected from 211 TC patients. K1 (papillary TC), SW579 (squamous TC), and 8505C (anaplastic TC) cell lines were assigned into a blank, negative control (NC), LINC00312 overexpression, miR-197-3p inhibitors, and LINC00312 overexpression + miR-197-3p mimics group. The expression of LINC00312, miR-197-3p, and p120 were measured using quantitative real-time PCR (qRT-PCR) and Western blotting. Cell proliferation was assessed via CCK8 assay, cell invasion through the scratch test, and cell migration via Transwell assay. In comparison with adjacent normal tissues, the expression of LINC00312 is down-regulated and the expression of miR-197-3p is up-regulated in TC tissues. The dual luciferase reporter gene assay confirmed that P120 is a target of miR-197-3p. The expression of LINC00312 and p120 was higher in the LINC00312 overexpression group than in the blank and NV groups. However, the expression of miR-197-3p was lower in the LINC00312 overexpression group than in the blank and NC groups. The miR-197-3p inhibitors group had a higher expression of miR-197-3p, but a lower expression of p120 than the blank and NC groups. The LINC00312 overexpression and miR-197-3p inhibitor groups had reduced cell proliferation, invasion and migration than the blank and NC groups. These results indicate that a LINC00312 overexpression inhibits the proliferation, invasion, and migration of TC cells and that this can be achieved by down-regulating miR-197-3p.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Sunwang Xu ◽  
Caiqin Mo ◽  
Junyu Lin ◽  
Yixing Yan ◽  
Xiaoyu Liu ◽  
...  

AbstractPapillary thyroid cancer (PTC) is the main histological type of thyroid cancer and accounts for almost all increased cases worldwide. Patients with PTC exhibit a favorable prognosis, but the fact that PTC is often accompanied by a high prevalence of lymph node metastasis (LNM) means that the overall recurrence-free survival rate in PTC patients is relatively low. Herein, we identified that ID3 expression is subdued in PTC tissues and closely associated with LNM and a poor disease-free survival outcome in PTC patients. The main contributor to this gene repression is the hypermethylation of the CpG island at the promoter of ID3. Besides, we uncovered that a loss of ID3 promotes invasion and migration of PTC cells, while an ectopic overexpression of ID3 inhibits invasion and migration. Mechanistically, ID3 exhibits tumor suppressor functions in PTC cells by interacting with E47 to form heterodimers that prevent E47 binding to CDH1 promoter and maintaining CDH1 transcription and epithelial phenotype in PTC cells. Taken together, our study demonstrates that ID3 plays a tumor suppressor role in PTC and impedes metastasis by inhibiting E47-mediated epithelial to mesenchymal transition.


2017 ◽  
Vol 18 (12) ◽  
pp. 2690 ◽  
Author(s):  
Mei-Chieh Chen ◽  
Yuan-Chin Tsai ◽  
Jen-Ho Tseng ◽  
Jr-Jiun Liou ◽  
Steve Horng ◽  
...  

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