title: CHIP promotes thyroid cancer proliferation via activation of the MAPK and AKT pathways.
abstract: The carboxyl terminus of Hsp70-interacting protein (CHIP) is a U box-type ubiquitin ligase that plays crucial roles in various biological processes, including tumor progression. To date, the functional mechanism of CHIP in thyroid cancer remains unknown. Here, we obtained evidence of upregulation of CHIP in thyroid cancer tissues and cell lines. CHIP overexpression markedly enhanced thyroid cancer cell viability and colony formation in vitro and accelerated tumor growth in vivo. Conversely, CHIP knockdown impaired cell proliferation and tumor growth. Notably, CHIP promoted cell growth through activation of MAPK and AKT pathways, subsequently decreasing p27 and increasing cyclin D1 and p-FOXO3a expression. Our findings collectively indicate that CHIP functions as an oncogene in thyroid cancer, and is therefore a potential therapeutic target for this disease.
authors.affiliation: Department of Pharmacy, Urumchi General Hospital of Lanzhou Military Region, Urumchi, Xinjiang 830000, China.
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Medical College of Soochow University, Suzhou, Jiangsu 215123, China; Department of Endocrinology, Shanghai Punan Hospital, Shanghai 200125, China.
authors.forename: Lianyong
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Endocrinology, Urumchi General Hospital of Lanzhou Military Region, Urumchi, Xinjiang 830000, China.
authors.forename: Xiaohua
authors.initials: X
authors.lastname: He
authors.affiliation: Department of Endocrinology, Urumchi General Hospital of Lanzhou Military Region, Urumchi, Xinjiang 830000, China.
authors.forename: Yunling
authors.initials: Y
authors.lastname: Shen
authors.affiliation: Department of Endocrinology, Urumchi General Hospital of Lanzhou Military Region, Urumchi, Xinjiang 830000, China.
authors.forename: Xuerong
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of Endocrinology, Urumchi General Hospital of Lanzhou Military Region, Urumchi, Xinjiang 830000, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Wei
authors.affiliation: Department of Endocrinology, Urumchi General Hospital of Lanzhou Military Region, Urumchi, Xinjiang 830000, China.
authors.forename: Fang
authors.initials: F
authors.lastname: Yu
authors.affiliation: Department of Endocrinology, Urumchi General Hospital of Lanzhou Military Region, Urumchi, Xinjiang 830000, China. Electronic address: jianqing0991@163.com.
authors.forename: Jianqing
authors.initials: J
authors.lastname: Tian
mesh_terms: D002352:Carrier Proteins / Q000235:genetics / Q000502:physiology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000502:physiology*; D004789:Enzyme Activation; D020868:Gene Silencing; D006801:Humans; D020935:MAP Kinase Signaling System; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D013964:Thyroid Neoplasms / Q000201:enzymology / Q000473:pathology*; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000502:physiology*; D015854:Up-Regulation; D018832:Molecular Chaperones
chemical_list: D002352:Carrier Proteins; D051057:Proto-Oncogene Proteins c-akt; D025521:Tumor Suppressor Proteins; C101119:ST13 protein, human; D018832:Molecular Chaperones
keywords: AKT pathway; CHIP; MAPK pathway; Proliferation; Thyroid cancer