The role of calgranulin B gene on the biological behavior of squamous cervical cancer in vitro and in vivo
CANCER MANAGEMENT AND RESEARCH
Authors: Zhang, Wenwen; Chen, Miaomiao; Cheng, Huihui; Shen, Qi; Wang, Ying; Zhu, Xueqiong
Abstract
Objective: The objective of the study was to explore the role of calgranulin B gene on the biological behavior of squamous cervical cancer. Methods: Differential transcription in calgranulin B gene between human papillomavirus (HPV)-positive and negative cervical cancer groups was identified, and the relationship between calgranulin B gene and matrix metalloproteinase (MMP) genes were explored using The Cancer Genome Atlas database. Subsequently, the role of calgranulin B on the cell proliferation, apoptosis, invasion and migration was investigated, through overexpression and/or underexpression of calgranulin B in cervical cancer cells. In addition, the effect of calgranulin B on the growth of the cervical cancer was studied via constructing xenograft model in BALB/c nude mice that either overexpressed or underexpressed calgranulin B. Results: Calgranulin B gene transcription in cervical cancer was highly correlated with the high-risk HPV-16 and HPV-45. In addition, overexpression of calgranulin B increased cell proliferation, invasion and migration, whereas it did not significantly affect cell apoptosis. This effect was also confirmed by calgranulin B knockdown assay. Additionally, we found that the transcription of calgranulin B gene was negatively correlated with MMP15 and MMP24 genes, but positively associated with MMP25 genes in cervical cancer. Furthermore, calgranulin B significantly promoted the growth of cervical cancer in vivo. Conclusion: Calgranulin B promotes cell proliferation, migration and invasion of squamous cervical cancer, possibly via regulation of MMPs. Whether there are synergistic actions between calgranulin B and HPV-16/HPV-45 infection on the squamous cervical carcinogenesis or progression need further study.
Weighted Gene Co-expression Network Analysis of Key Biomarkers Associated With Bronchopulmonary Dysplasia
FRONTIERS IN GENETICS
Authors: Cai, Yao; Ma, Fei; Qu, LiuHong; Liu, Binqing; Xiong, Hui; Ma, Yanmei; Li, Sitao; Hao, Hu
Abstract
Bronchopulmonary dysplasia (BPD) is a complex disorder resulting from interactions between genes and the environment. The accurate molecular etiology of BPD remains largely unclear. This study aimed to identify key BPD-associated genes and pathways functionally enriched using weighted gene co-expression network analysis (WGCNA). We analyzed microarray data of 62 pre-term patients with BPD and 38 pre-term patients without BPD from Gene Expression Omnibus (GEO). WGCNA was used to construct a gene expression network, and genes were classified into definite modules. In addition, the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of BPD-related hub genes were performed. Firstly, we constructed a weighted gene co-expression network, and genes were divided into 10 modules. Among the modules, the yellow module was related to BPD progression and severity and included the following hub genes:MMP25,MMP9,SIRPA,CKAP4,SLCO4C1, andSLC2A3; and the red module included some co-expression molecules that displayed a continuous decline in expression with BPD progression and included the following hub genes:LEF1,ITK,CD6,RASGRP1,IL7R,SKAP1,CD3E, andICOS. GO and KEGG analyses showed that high expression of inflammatory response-related genes and low expression of T cell receptor activation-related genes are significantly correlated with BPD progression. The present WGCNA-based study thus provides an overall perspective of BPD and lays the foundation for identifying potential pathways and hub genes that contribute to the development of BPD.