Transcriptome profiling of the cancer and adjacent nontumor tissues from cervical squamous cell carcinoma patients by RNA sequencing

Abstract

Cervical cancer is the third most common cancer and the fourth leading cause of cancer deaths among women in the world. The discovery of vital diagnostic and therapeutic markers against cervical squamous cell carcinoma (CSCC) would broaden our understanding on the molecular basis of CSCC. In this study, we thoroughly analyzed the transcriptome of CSCC and matched adjacent nontumor (ATN) tissue. RNA sequencing was performed to screen the differentially expressed genes (DEGs) of three pairs of CSCC and ATN tissues. Functional enrichment analysis was used to uncover the biological functions of DEGs. Protein interaction network was carried out to reveal interaction of DEGs. Quantitative real-time PCR was conducted to validate the expression of DEGs. Immunohistochemistry was used to detect the relationship between clinicopathological parameters of CSCC and DEGs. There were a total of 347 significantly common DEGs in the three paired examples, including 104 consistent upregulated and 148 consistent downregulated DEGs. The 347 DEGs were categorized into 73 functional categories by Gene Ontology (GO) analysis. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis suggested six significantly signal pathways. The protein interaction network uncovered three important DEGs, including retinol dehydrogenase 12 (RDH12), ubiquitin D (UBD), and serum amyloid A1 (SAA1). We found that RDH12 expression was decreased in 74.5 % of CSCC tissues. RDH12 expression was negatively associated with tumor size and depth of cervical invasion. The UBD was overexpressed in 61.7 % of CSCC tissues and was positively related with tumor size and lymphatic metastasis. The SAA1 protein was overexpressed in 57.4 % of CSCC tissues and was positively related with clinicopathological parameters of tumor size, lymphatic metastasis, and depth of cervical invasion. The RDH12, UBD, and SAA1 genes might participate in the progression of CSCC.

Triage of high-risk HPV positive women in cervical cancer screening

“…It has been previously demonstrated that HPV infection alone is insufficient for development of cervical cancer; abnormal host genes play an important role in carcinogenesis [62]. The mRNA-based expression profile of normal cervical tissue is known to change during carcinogenesis, and expression of single genes or gene profiles might be used as molecular biomarker to distinguish between different stages of carcinogenesis or indicate response to particular treatment.…”

Improvement in RNA quantity and quality in cervico-vaginal cytology

“…Previous studies have demonstrated the important role of long non-coding RNAs, circular RNAs, microRNAs and mRNAs in cervical cancer development and progression [2][3][4]. High-quality RNA is a pre-requisite for gene expression studies.…”

Serum amyloid A1 in combination with integrin αVβ3 increases glioblastoma cells mobility and progression

“…The study revealed that SAA1 was upregulated 10 to 60 times in patients with glioblastomas compared with patients with non-neoplastic and other grades of astrocytoma. However, the elevation of SAA1 in serum can be directly correlated with the unfavorable outcomes for many types of cancer such as lung cancer and cervical cancer (Kim et al, 2015;Peng et al, 2015;Sung et al, 2011). The exact concentration of serum SAA1 that serves as the threshold for GBM diagnosis has yet to be determined.…”

“…Plasma levels of SAA1 are elevated following injury, inflammation, and brain trauma, as well as cancer Milan et al, 2012;Sung et al, 2011;Villapol et al, 2015). A transcriptomic analysis of patients with cervical squamous cell carcinoma revealed that SAA1 levels were associated with tumor size, lymphatic metastasis, and cancer cell invasion (Peng et al, 2015;Ren et al, 2014). SAA1 has also been proposed as a lung cancer biomarker, and patients with lung cancer who have higher levels of plasma SAA1 have less favorable outcomes (Kim et al, 2015;Milan et al, 2012;Sung et al, 2011).…”