科研成果详情

题名S100A6 promotes the development of thyroid cancer and inhibits apoptosis of thyroid cancer cells through the PI3K/AKT/mTOR pathway
作者
发表日期2023-02
发表期刊Pathology, research and practice   影响因子和分区
语种英语
原始文献类型Journal Article
关键词Biomarker Migration PI3K/AKT/mTOR pathway Proliferation Thyroid cancer
其他关键词PHOSPHATIDYLINOSITOL 3-KINASE/AKT ; PROTEIN S100A6 ; UP-REGULATION ; EXPRESSION ; PROLIFERATION ; MIGRATION ; PAPILLARY ; ACTIVATION ; CARCINOMA
摘要High levels of S100A6 have been associated with progression in some types of human cancers. Cancers related to S100A6 have been reported to include lung cancer, cervical cancer, pancreatic cancer, gastric cancer, colon cancer, etc., but its role in the molecular pathogenesis of these cancers is largely unknown. This study investigated the expression and functional roles of S100A6 in human thyroid cancer. The expression level of S100A6 in thyroid cancer cells was determined by bioinformatics and transcriptomic analysis. Furthermore, the potential functions of S100A6 in tumorigenesis were analyzed by cell proliferation, migration, invasion, and Western blot assays in human thyroid cancer cells. Public database queries revealed high S100A6 expression in thyroid cancer. In addition, we also found that high expression of S100A6 was positively correlated with malignant clinicopathological characteristics of thyroid cancer in The Cancer Genome Atlas database. qPCR results confirmed the high expression of S100A6 in thyroid cancer cells. S100A6 silencing inhibited cell proliferation, migration, and invasion. Western blot assays and response experiments showed that S100A6 promotes cell proliferation and tumorigenicity partly through the PI3K/AKT/mTOR signaling pathway. These results suggest that S100A6 affects the progression of thyroid cancer and can be used as a target in the future treatment of thyroid cancer.
资助项目Zhejiang Provincial Natural Science Foundation of China [LQ17H260004]
出版者ELSEVIER GMBH
ISSN0344-0338
EISSN1618-0631
卷号242
DOI10.1016/j.prp.2023.154325
页数10
WOS类目Pathology
WOS研究方向Pathology
WOS记录号WOS:000972849500001
收录类别PUBMED ; SCIE ; SCOPUS
在线发表日期2023-01
URL查看原文
PubMed ID36680929
SCOPUSEID2-s2.0-85146553529
通讯作者地址[Tang, Kaifu]Key Laboratory of Diagnosis and Treatment of Severe Hepatopancreatic Diseases Province,The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China
Scopus学科分类Pathology and Forensic Medicine;Cell Biology
引用统计
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/172470
专题附属第一医院_骨科
附属第一医院_重症医学科(ICU)
第一临床医学院(信息与工程学院)、附属第一医院_浙江省胰脏肝脏危重性疾病重点实验室
通讯作者Tang, Kaifu
作者单位
1.Department of Breast Surgery,The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China;
2.Department of Orthopaedics,The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China;
3.Key Laboratory of Diagnosis and Treatment of Severe Hepatopancreatic Diseases Province,The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China;
4.Department of ICU,The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,China;
5.Department of General Surgery,Breast and Thyroid Unit,Tribhuvan University Teaching Hospital,Kathmandu,Nepal;
6.Department of Obstetrics and Gynecology,Kulhudhuffushi Regional Hospital,Kulhudhuffushi,Maldives
第一作者单位附属第一医院;  第一临床医学院(信息与工程学院)、附属第一医院
通讯作者单位附属第一医院;  第一临床医学院(信息与工程学院)、附属第一医院
第一作者的第一单位附属第一医院
推荐引用方式
GB/T 7714
Chen, Buran,Zheng, Danni,Liu, Conghui,et al. S100A6 promotes the development of thyroid cancer and inhibits apoptosis of thyroid cancer cells through the PI3K/AKT/mTOR pathway[J]. Pathology, research and practice,2023,242.
APA Chen, Buran., Zheng, Danni., Liu, Conghui., Bhandari, Adheesh., Hirachan, Suzita., ... & Zhang, Wei. (2023). S100A6 promotes the development of thyroid cancer and inhibits apoptosis of thyroid cancer cells through the PI3K/AKT/mTOR pathway. Pathology, research and practice, 242.
MLA Chen, Buran,et al."S100A6 promotes the development of thyroid cancer and inhibits apoptosis of thyroid cancer cells through the PI3K/AKT/mTOR pathway".Pathology, research and practice 242(2023).

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