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Abstract
Increasing evidence shows that hepatocellular carcinoma (HCC) is a principal cause of cancer-related mortality globally, especially among Asian and African populations. Collagen type I α1 (COL1A1) is the major component of type I collagen. While aberrant expression of COL1A1 and COL1A2 is implicated in numerous cancers, the differential role of COL1A1 in malignant, premalignant and normal tissues remains unclear, and its clinical significance in HCC has not been elucidated. In this study, using bioinformatics analysis of publicly-available HCC microarray data from Gene Expression Omnibus (GEO) and RNAseq data from The Cancer Genome Atlas (TCGA) database, we determined that COL1A1 is significantly upregulated in HCC tumor tissues in comparison to normal tissues. Our analysis also revealed that COL1A1 confers survival advantage and enhanced oncogenicity on HCC cells. Interestingly, the siRNA-mediated silencing of COL1A1 expression (siCOLIA1) suppressed HCC cells clonogenicity, motility, invasiveness and tumorsphere formation. Concomitantly, siCOL1A1 abrogated Slug-dependent epithelial-to-mesenchymal transition (EMT) and HCC stemness gene-signature, by attenuating expression of stemness markers SOX2, OCT4 and CD133. The present study provides some mechanistic insight into COL1A1 activity in HCC and highlights its putative role as an important diagnostic biomarker and potential therapeutic target in early development and metastasis of HCC.
Highlights
Hepatocellular cancer (HCC) is the fifth most common cause of cancer-related death.The fact that its incidence matches mortality reflects the poor prognosis of this disease [1]
COL1A2 in normal epithelium, premalignant and tumor lesions of the stomach is rarely mentioned, and while type I collagen has been associated with hepatic fibrosis [20], there is a dearth of information on the clinical significance of COL1A1 in patients with hepatocellular cancer (HCC), the present study investigate the role of COL1A1 in HCC
Gene expression profile analysis using heatmap generated from the GSE14323 dataset showed 543 upregulated genes in cirrhosis, and 89 downregulated genes in HCC, with 87 of these genes commonly expressed in both cirrhosis and HCC
Summary
Hepatocellular cancer (HCC) is the fifth most common cause of cancer-related death.The fact that its incidence matches mortality reflects the poor prognosis of this disease [1]. Hepatocellular cancer (HCC) is the fifth most common cause of cancer-related death. HCC is diagnosed in more than half a million people worldwide [2]. Despite advances in diagnostic and therapeutic strategies in the last two decades, the management of patients with HCC remains a therapeutic challenge; this is evident in the abysmal median survival time of ≤1 year for patients with advanced HCC, and a five-year relative survival rate ≤9% [3]. Many strategies are available to extend the survival time of liver cancer patients, such as transplantation, surgical resection, target drugs including sorafenib, lenvatinib or regorafenib and immunotherapy (nivolumab) [4]. Surgical resection remains the treatment of choice for patients with well-preserved liver function, and liver transplantation is viewed as the most effective way to improve survival in patients with
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