Family with Sequence Similarity 83 Member H Promotes the Viability and Metastasis of Cervical Cancer Cells and Indicates a Poor Prognosis
10.3349/ymj.2019.60.7.611
- Author:
Chao CHEN
1
;
Hua Feng LI
;
Yu Jie HU
;
Meng Jie JIANG
;
Qing Sheng LIU
;
Jia ZHOU
Author Information
1. Department of Radiotherapy, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, China.
- Publication Type:Original Article
- Keywords:
Cervical cancer;
FAM83H;
prognosis;
proliferation;
migration
- MeSH:
Blotting, Western;
Carcinogenesis;
Cell Line;
Cell Proliferation;
Genome;
Humans;
Methods;
Multivariate Analysis;
Neoplasm Metastasis;
Polymerase Chain Reaction;
Prognosis;
Proportional Hazards Models;
Reverse Transcription;
Uterine Cervical Neoplasms
- From:Yonsei Medical Journal
2019;60(7):611-618
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Family with sequence similarity 83 member H (FAM83H) plays key roles in tumorigenesis. However, the specific roles of FAM83H in cervical cancer (CC) have not been well studied. MATERIALS AND METHODS: The RNA-seq data of 306 CC tissues and three normal samples downloaded from The Cancer Genome Atlas were used to analyze the expression of FAM83H. The Kaplan-Meier method was used to draw survival curves. Associations between FAM83H expression and clinicopathological factors were analyzed by chi-square test. Cox proportional hazards model was used to analyze prognostic factors. Loss-of-function assays were conducted to discover the biological functions of FAM83H in cell proliferation, colony formation, invasion, and migration. Real-time Quantitative Reverse Transcription PCR (qRT-PCR) and Western blotting were used to measure the expression levels of FAM83H in CC cell lines. RESULTS: Our results demonstrated that FAM83H is overexpressed in CC tissues and that high FAM83H expression is associated with worse overall survival (OS). High FAM83H expression in CC was associated with clinical stage, pathologic tumor, and pathologic node. Univariate analysis suggested that FAM83H expression was significantly related to the OS of CC patients. Although multivariate analysis showed that FAM83H expression was not an independent prognostic factor for the OS of CC patients, the effects of FAM83H on CC cell growth and motility was significant. Loss-of-function experiments demonstrated that knockdown of FAM83H inhibited proliferation, colony formation, migration, and invasion of CC cells by inactivating PI3K/AKT pathway. CONCLUSION: FAM83H might play a crucial role in CC progression and could act as a novel therapeutic target in CC.
